Zoonotic Implications
Abbott, A. and D. Cyranoski (2004). Bird flu
sparks worldwide bid to prevent human pandemic. Nature 427(6972): 274. ISSN: 1476-4687.
NAL
Call Number: 472 N21
Descriptors: influenza prevention and control, influenza
veterinary, poultry diseases epidemiology, zoonoses epidemiology, Asia
epidemiology, influenza epidemiology, influenza transmission, influenza A
virus, avian isolation and purification, poultry diseases prevention and
control, poultry diseases transmission, poultry diseases virology, World Health
Organization, zoonoses transmission, zoonoses virology.
Akkina, R.K. (1990). Antigenic reactivity and
electrophoretic migrational heterogeneity of the three polymerase proteins of
type A human and animal influenza viruses. Archives of Virology
111(3-4): 187-97. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Antigenic reactivity of the three polymerase
proteins PB1, PB2, and PA of type A influenza viruses of animal and human
origin were analysed by radioimmunoprecipitation using monospecific antisera.
Each of the polymerase monospecific antisera made against the polymerase
proteins of the human A/WSN/33 (H1N1) influenza virus reacted efficiently with
the homologous proteins of all the known thirteen HA subtype viruses of avian
influenza virus, three subtypes of human influenza virus, swine and equine
influenza viruses. This broad reactivity of each of the antisera indicated that
the polymerase proteins are antigenically related among the type A influenza
viruses and therefore can be considered as type specific antigens similar to
the other viral internal proteins nucleoprotein (NP) and matrix protein (M). No
electrophoretic migrational heterogeneity was found among the PB2 proteins of
different subtype viruses, whereas PB1 protein exhibited minor variation.
However, PA protein from among various viral subtypes showed considerable
heterogeneity. Each of the polymerase antisera also immunoprecipitated
additional antigenically related polypeptides with distinct electrophoretic
mobilities from cells infected with each of the influenza viral subtypes.
Descriptors: DNA directed RNA polymerases immunology,
influenza A virus human enzymology, influenza A virus enzymology, viral
proteins immunology, antigens, viral immunology, human immunology, influenza A
virus immunology, precipitin tests.
Alexander, D.J. (1998). Avian influenza viruses
and pandemic influenza in humans. State Veterinary Journal (United
Kingdom) 8(3): 8-10.
NAL
Call Number: SF601.S8
Descriptors: avian influenza virus, viroses, mankind,
zoonoses, pathogenicity, biological properties, infectious diseases, influenza
virus, microbial properties, orthomyxoviridae, viruses, influenza.
Alexander, D.J. (2000). How dangerous are avian
influenza viruses for humans? World Poultry (Special): 11-12. ISSN: 1388-3119.
NAL
Call Number: SF481.M54
Descriptors: zoonoses, pathogenesis, avian influenza
virus, poultry, humans, dangers.
Alexander, D.J. (1988). Influenza A isolations
from exotic caged birds. Veterinary Record 123(17): 442. ISSN: 0042-4900.
NAL
Call Number: 41.8 V641
Descriptors: birds microbiology, fowl plague epidemiology,
influenza A virus avian isolation and purification, England, fowl plague
microbiology, quarantine.
Altmuller, A., W.M. Fitch, and C. Scholtissek (1989).
Biological and genetic evolution of the nucleoprotein gene of human
influenza A viruses. Journal of General Virology 70(Pt. 8): 2111-9.
ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: There is a significant difference in the
ability of human influenza A virus H1N1 strains isolated up to 1977 and those
isolated later to rescue temperature-sensitive mutants of fowl plague virus
with a defect in the nucleoprotein (NP) gene. Therefore the NP genes of five
human H1N1 and H3N2 influenza A virus strains, isolated between 1950 and 1978,
have been sequenced. By comparison with previous and more recent isolates, an
evolutionary pathway has been established. Three amino acid replacements were
found which might be responsible for the functional difference between the USSR
(1977) and the Brazil (1978) strains. The California (H1N1) strain isolated in
1978 had acquired by reassortment the NP gene of a human H3N2 virus circulating
at about 1977 as had been previously suggested by investigations involving
RNase fingerprint or hybridization techniques.
Descriptors: evolution, genes viral, influenza A virus
human genetics, nucleoproteins genetics, viral core proteins, viral proteins
genetics, amino acid sequence, base sequence, chick embryo, chickens, influenza
A virus avian genetics, molecular sequence data, mutation, sequence homology,
nucleic acid.
Altmuller, A., M. Kunerl, K. Muller, V.S. Hinshaw,
W.M. Fitch, and C. Scholtissek (1992). Genetic relatedness of the
nucleoprotein (NP) of recent swine, turkey, and human influenza A virus (H1N1)
isolates. Virus Research 22(1): 79-87. ISSN: 0168-1702.
NAL
Call Number: QR375.V6
Abstract: The sequences of nucleoprotein (NP) genes of
recent human and turkey isolates of influenza A viruses, which serologically
could be correlated to contemporary swine viruses, were determined. These
sequences were closely related to the NPs of these swine viruses and they
formed a separate branch on the phylogenetic tree. While the early swine virus
from 1931 resembled the avian strains in consensus amino acids of the NP and in
its ability to rescue NP ts mutants of fowl plague virus in chicken embryo
cells, the later strains on that branch were different: at 15 positions they
have their own amino acids and they rescued the NP ts mutants only poorly. Of
the NPs of the human New Jersey/76 isolates analysed, one clustered with the
recent H1N1 swine viruses of the U.S.A., the other one with contemporary human
strains. Since the NP is one of the main determinants of species specificity it
is concluded that, although the H1N1 swine isolates from the U.S.A. form their
own branch in the phylogenetic tree, they can be transmitted to humans and
turkeys, but they do not spread further in these populations and so far have
not contributed to human pandemics. It is not very likely that they will do so
in future, since its branch in the phylogenetic tree develops further away from
the human and avian branch.
Descriptors: influenza A virus avian genetics, human
genetics, porcine genetics, nucleoproteins genetics, fowl plague microbiology,
influenza microbiology, phylogeny, sequence homology, nucleic acid, turkeys.
Anonymous (1999). Avian strain of influenza A
virus isolated from humans in Hong Kong. Communicable Disease Report.
CDR Weekly 9(15): 131, 134. ISSN:
1350-9357.
Descriptors: disease outbreaks, influenza epidemiology,
influenza A virus avian, child, preschool, Hong Kong epidemiology, infant.
Anonymous (1998). From the Centers for Disease
Control and Prevention. Isolation of avian influenza A(H5N1) viruses from
humans--Hong Kong, May-December 1997. JAMA the Journal of the American
Medical Association 279(4): 263-4.
ISSN: 0098-7484.
NAL
Call Number: 448.9 Am37
Descriptors: influenza epidemiology, influenza A virus
avian isolation and purification, adolescent, adult, child, child, preschool,
Hong Kong epidemiology, influenza virology, middle aged.
Anonymous (1998). From the Centers for Disease
Control and Prevention. Update: isolation of avian influenza A(H5N1) viruses
from humans--Hong Kong, 1997-1998. JAMA the Journal of the American
Medical Association 279(5): 347-8.
ISSN: 0098-7484.
NAL
Call Number: 448.9 Am37
Descriptors: influenza epidemiology, influenza virology,
influenza A virus avian isolation and purification, Hong Kong epidemiology,
seroepidemiologic studies.
Anonymous (1997). Influenza A virus subtype H5N1
infection in humans. Communicable Disease Report. CDR Weekly 7(50):
441. ISSN: 1350-9357.
Descriptors: fowl plague transmission, influenza
epidemiology, influenza A virus avian classification, adolescent, bacterial
typing techniques, chickens, child,
preschool, fowl plague epidemiology, Hong Kong epidemiology, incidence, avian
isolation and purification, middle aged, survival rate.
Anonymous (1998). Isolation of avian influenza
A(H5N1) viruses from humans - Hong Kong, 1997-1998. MMWR. Morbidity and
Mortality Weekly Report 46(52/53): 1245-1247. ISSN: 0149-2195.
NAL
Call Number: RA407.3.M56
Descriptors: avian influenza, human infection,
transmission, Hong Kong.
Anonymous (1997). Isolation of avian influenza
A(H5N1) viruses from humans--Hong Kong, May-December 1997. MMWR.
Morbidity and Mortality Weekly Report 46(50): 1204-7. ISSN: 0149-2195.
NAL
Call Number: RA407.3.M56
Abstract: A strain of influenza virus that previously
was known to infect only birds has been associated with infection and illness
in humans in Hong Kong. The first known human case of influenza type A(H5N1)
occurred in a 3-year-old child who died from respiratory failure in May 1997.
In Hong Kong, the virus initially was identified as influenza type A, but the
subtype could not be determined using standard reagents. By August, CDC; the
National Influenza Center, Rotterdam, the Netherlands; and the National
Institute for Medical Research, London, United Kingdom, had independently
identified the virus as influenza A(H5N1). An investigation conducted during
August-September by the Hong Kong Department of Health and CDC excluded the
possibility of laboratory contamination. Since this initial case was
identified, six additional persons in Hong Kong have been confirmed to have influenza
A(H5N1) infection, and two possible cases have been identified. This report
summarizes the nine cases identified thus far and describes preliminary
findings from the ongoing investigation, which indicate that multiple influenza
A(H5N1) infections have occurred and that both the source and mode of
transmission are uncertain at this time.
Descriptors: influenza epidemiology, influenza A virus
avian isolation and purification, adolescent, adult, child, child, preschool,
Hong Kong epidemiology, influenza virology, middle aged.
Anonymous (2004). Lessons from the outbreak of
avian influenza across Asia. Indian Veterinary Journal 81(3):
A9. ISSN: 0019-6479.
NAL
Call Number: 41.8 In2
Descriptors: avian influenza virus infection, quarantine,
clinical techniques, Food and Agriculture Organization, United Nations, World
Health Organization, Office International des Epizooties, Asia.
Anonymous (1998). Update: isolation of avian
influenza A(H5N1) viruses from humans--Hong Kong, 1997-1998. MMWR.
Morbidity and Mortality Weekly Report 46(52-53): 1245-7. ISSN: 0149-2195.
NAL
Call Number: RA407.3.M56
Abstract: As of January 6, 1998, a total of 16
confirmed and three suspected cases of human infection with avian influenza
A(H5N1) viruses have been identified in Hong Kong. Confirmed cases are those
from which an influenza A(H5N1) virus was isolated or in which a seroconversion
to influenza A(H5N1) virus was detected by a neutralization assay. Suspected
cases are those with influenza-like illness (ILI) and preliminary laboratory
evidence of influenza A(H5N1) infection. This report summarizes interim
findings from the ongoing epidemiologic and laboratory investigation of
influenza A(H5N1) cases by health officials in Hong Kong and by CDC.
Descriptors: influenza epidemiology, influenza virology,
influenza A virus avian isolation and purification, Hong Kong epidemiology,
seroepidemiologic studies.
Austin, F.J. and R.G. Webster (1986). Antigenic
mapping of an avian H1 influenza virus haemagglutinin and interrelationships of
H1 viruses from humans, pigs and birds. Journal of General Virology
67(Pt. 6): 983-92. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: Monoclonal antibodies to the haemagglutinin
(HA) of the avian H1 influenza virus A/duck/Alberta/35/76 were used to
construct an operational antigenic map of the HA molecule and to study the
interrelationships of H1 viruses from different hosts. Haemagglutination
inhibition tests between the monoclonal antibodies and variants selected by
them provided evidence of four antigenic regions which overlap to varying
degrees. Avian H1 influenza viruses displayed a spectrum of reactivities to the
monoclonal antibody panel. Representatives of the epidemic strains of human H1
influenza viruses and early swine influenza viruses showed little or no
reactivity with the monoclonal antibodies but swine influenza-like viruses
isolated from pigs and humans in the last decade reacted with 11 of 17
antibodies. The antigenic similarity of these viruses to many avian isolates suggests
that there has been a transfer of HA genetic information between mammalian and
avian H1 influenza viruses.
Descriptors: hemagglutinins viral immunology, influenza A
virus avian immunology, antibodies, monoclonal diagnostic use, epitopes, human
immunology, porcine immunology, species specificity.
Aymard, M., A.R. Douglas, M. Fontaine, J.M. Gourreau,
C. Kaiser, J. Million, and J.J. Skehel (1985). Antigenic characterization of
influenza A (H1N1) viruses recently isolated from pigs and turkeys in France.
Bulletin of the World Health Organization 63(3): 537-42. ISSN: 0042-9686.
NAL
Call Number: 449.9 W892B
Descriptors: antigens, viral analysis, influenza A virus
avian immunology, porcine immunology, immunology, swine microbiology, turkeys
microbiology, France, avian isolation and purification, porcine isolation and
purification.
Ayoub, N.N.K., G. Heider, H. Glathe, K. Ziedler, D.
Ebner, and E. Prusas (1974). Influenza-A-Antikorper (human) beim Geflugel.
[Influenza A antibodies (human) in poultry]. Monatshefte Fur
Veterinarmedizin 29(4): 139-143.
ISSN: 0026-9263.
NAL
Call Number: 41.8 M742
Descriptors: avian influenza virus, serum samples,
turkeys, fowl, zoonoses, human strains,
Hong Kong strain, Singapore strain, antibodies.
Banbura, M.W., Y. Kawaoka, T.L. Thomas, and R.G.
Webster (1991). Reassortants with equine 1 (H7N7) influenza virus
hemagglutinin in an avian influenza virus genetic background are pathogenic in
chickens. Virology 184(1): 469-471.
ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Reassortants possessing the hemagglutinin
(HA) gene from A/Equine/London/1416/73 (H7N7) [Eq/Lond) and five or more genes
from A/Chicken/Pennsylvania/1370/83 (H5N2) [Ck/Penn] were lethal in chickens.
This result demonstrates that horses can maintain influenza viruses whose HAs
are capable of promoting virulence. Thus, reassortment of equine and avian
influenza virus genes could generate viruses that might be lethal in domestic
poultry.
Descriptors: fowls, horses, avian influenza virus, equine
influenza virus, hemagglutinins, genes, amino acids, virulence, pathogenicity,
mortality, molecular sequence data, EMBL m58657, GENBANK m58657.
Banks, J., E. Speidel, and D.J. Alexander (1998). Characterisation
of an avian influenza A virus isolated from a human--is an intermediate host
necessary for the emergence of pandemic influenza viruses? Archives of
Virology 143(4): 781-7. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: The partial sequencing of the internal and
the neuraminidase genes of isolate 268/96 obtained from a woman with
conjunctivitis showed all seven to have closest homology with avian influenza
viruses. The entire nucleotide sequence of the haemagglutinin gene of 268/96
had close, 98.2%, homology with an H7N7 virus isolated from turkeys in Ireland
in 1995. This appears to be the first reported case of isolation of an
influenza A virus from a human being infected as a result of direct natural
transmission of an avian influenza virus from birds.
Descriptors: influenza virology, influenza A virus avian
genetics, adult, birds virology, genes viral, influenza epidemiology, influenza
transmission, avian classification, influenza A virus avian isolation and
purification, Ireland, molecular sequence data, phylogeny, turkeys virology.
Barclay, W.S. and M. Zambon (2004). Pandemic risks
from bird flu. BMJ Clinical Research 328(7434): 238-9. ISSN: 1468-5833.
Descriptors: disease outbreaks, fowl plague epidemiology,
influenza epidemiology, Asia, Southeastern epidemiology, birds, chickens,
influenza A virus avian, human.
Baumeister, E.G. and V.L. Savy (1998). Human
circulation of avian influenza (H5N1) in Hong Kong. Boletín De La
Asociación Argentina De Microbiología (129): 12-13. ISSN: 0325-6480.
Descriptors: human diseases, influenza virus A, epidemics,
clinical aspects, diagnosis, reviews,
Hong Kong.
Beare, A.S. and R.G. Webster (1991). Replication
of avian influenza viruses in humans. Archives of Virology 119(1-2):
37-42. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Volunteers inoculated with avian influenza
viruses belonging to subtypes currently circulating in humans (H1N1 and H3N2)
were largely refractory to infection. However 11 out of 40 volunteers
inoculated with the avian subtypes, H4N8, H6N1, and H10N7, shed virus and had
mild clinical symptoms: they did not produce a detectable antibody response.
This was presumably because virus multiplication was limited and insufficient
to stimulate a detectable primary immune response. Avian influenza viruses
comprise hemagglutinin (HA) subtypes 1-14 and it is possible that HA genes not
so far seen in humans could enter the human influenza virus gene pool through
reassortment between avian and circulating human viruses.
Descriptors: influenza A virus avian pathogenicity, adult,
antibodies, viral blood, hemagglutinin glycoproteins, influenza virus,
hemagglutinins viral immunology, avian isolation and purification, avian
physiology, middle aged, species specificity, virus replication.
Beckford Ball, J. (2004). Building awareness of
the avian flu outbreak and its symptoms. Nursing Times 100(6):
28-9. ISSN: 0954-7762.
Abstract: The current outbreak of avian influenza in
South East Asia has resulted in a small number of human deaths. Avian flu can
pass from birds to humans, although the number of humans infected is low. The
fear is that the avian flu virus could mutate in a human who was also infected
with a common flu virus, creating a new strain that could pass from human to
human. Nurses, especially those working in travel health, should keep
themselves informed of the latest developments.
Descriptors: avian flu, outbreak, symptoms, South East
Asia, human deaths, birds.
Belshe, R.B. (1998). Influenza as a zoonosis: how
likely is a pandemic? Lancet 351(9101): 460-1. ISSN: 0140-6736.
NAL
Call Number: 448.8 L22
Descriptors: disease outbreaks, fowl plague transmission,
influenza transmission, influenza virology,
influenza A virus avian, zoonoses, Asia epidemiology, chickens virology,
Hong Kong epidemiology, influenza epidemiology.
Bender, C., H. Hall, J. Huang, A. Klimov, N. Cox, A.
Hay, V. Gregory, K. Cameron, W. Lim, and K. Subbarao (1999). Characterization
of the surface proteins of influenza A (H5N1) viruses isolated from humans in
1997-1998. Virology 254(1):
115-23. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: hemagglutinin glycoproteins, influenza virus
genetics, influenza virology, influenza A virus human genetics, neuraminidase
genetics, adolescent, adult, antigens, viral immunology, base sequence, child,
preschool, DNA, viral, disease outbreaks, genes viral, Hong Kong epidemiology,
infant, influenza epidemiology, human growth and development, human immunology,
human isolation and purification, middle aged, molecular sequence data,
phylogeny.
Berg, M., L. Englund, I.A. Abusugra, B. Klingeborn,
and T. Linne (1990). Close relationship between mink influenza (H10N4) and
concomitantly circulating avian influenza viruses. Archives of Virology
113(1-2): 61-71. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Strains of an influenza H10N4 virus have been
isolated during an outbreak of a respiratory disease in mink on the south-east
coast of Sweden. This was the first example of a disease in mammals caused by
the H10 subtype. We compared the A/mink/Sweden/84 strain with two recent avian
H10N4 isolates, one from fowl and another from a mallard, both isolated in
Great Britain in 1985 as well as the prototype A/chicken/Germany/N/49 (H10N7).
The comparison was carried out by genomic analysis of the strains by
oligonucleotide fingerprinting and in bioassays on mink. The oligonucleotide
fingerprint analysis revealed a high degree of genomic homology of around 98%
between the viruses from mink, mallard and fowl. Only the recent avian
isolates, that from the mallard and fowl could infect mink by contact, causing
similar pathological and clinical signs and inducing seroconversion as did the
mink virus. However, the susceptibility of mink to the fowl and mallard viruses
by contact was less pronounced than that to the mink virus. Both the genomic
homology and the similarities from the infectivity and pathogenicity studies
between the mink virus and the recent avian isolates point to a direct invasion
of the mink population by an avian H10N4 virus.
Descriptors: influenza A virus avian genetics, mink,
orthomyxoviridae infections veterinary, chickens microbiology, disease
outbreaks veterinary, ducks microbiology, fowl plague microbiology, fowl plague
transmission, genes viral, avian isolation and purification, avian
pathogenicity, nucleotide mapping, orthomyxoviridae infections microbiology,
orthomyxoviridae infections transmission, RNA, viral, Sweden epidemiology.
Bikour, M.H., E.H. Frost, S. Deslandes, B. Talbot,
and Y. Elazhary (1995). Persistence of a 1930 swine influenza A (H1N1) virus
in Quebec. Journal of General Virology 76(Pt. 10): 2539-47. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: Two antigenically distinct H1N1 influenza A
viruses were isolated during an outbreak of respiratory disease in Quebec swine
in 1990/91. Analysis of haemagglutinin and partial nucleoprotein sequences
indicated that one was a variant of the swine H1N1 influenza virus circulating
in the American Midwest whereas the other was very similar to virus isolated
from swine in 1930. The existence of this latter isolate supports the concept
that influenza viruses can be maintained for long periods in swine, perhaps in
geographically limited pockets. Serological evidence indicates that these
distinct strains continued to circulate widely in south-central Quebec until at
least 1993.
Descriptors: influenza A virus, porcine genetics,
influenza A virus, porcine immunology, orthomyxoviridae infections veterinary,
phylogeny, swine diseases virology, amino acid sequence, antigenic variation, antigens, viral
analysis, base sequence, capsid genetics, disease outbreaks, hemagglutinin
glycoproteins, influenza virus, hemagglutinins viral analysis, hemagglutinins
viral genetics, avian genetics, human genetics, molecular sequence data,
orthomyxoviridae infections epidemiology, orthomyxoviridae infections virology,
quebec epidemiology, sequence analysis, DNA, sequence homology, amino acid,
swine, swine diseases epidemiology, viral core proteins genetics.
Blinov, V.M., O.I. Kiselev, S.M. Resenchuk, A.I.
Brovkin, A.G. Bukrinskaia, and L.S. Sandakhchiev (1993). Analiz potentsial'nykh
uchastkov rekombinatsii v genakh gemaggliutinina virusov grippa zhivotnykh v
otnoshenii ikh adaptatsii k novomu khoziainu--cheloveku. [An analysis of the
potential areas of recombination in the hemagglutinin genes of animal influenza
viruses in relation to their adaptation to a new host--man]. Voprosy
Virusologii 38(6): 263-8. ISSN:
0507-4088.
NAL
Call Number: 448.8 P942
Abstract: The authors tried to decode the mechanism of
influenza viruses species adaptation in the process of host changing. The functionally
important replacement in the surface pocket domains were revealed, particularly
in the conservative region 221-241, involving fibronectin-like part. Close
replacements were revealed in the region 141-161. The method of construction of
heteroduplexes between hemagglutinin RNA of duck, pig, and human viruses was
used. The method showed that all heteroduplexes formed recombinogene
structures. An unexpected effect of directional recombination was elicited for
hemagglutinin RNA heteroduplexes in cases of duck-pig and human-pig viruses.
During the directional recombination the following processes took place: the
receptor-binding site of animal type was transmitted to the duck virus, while
the human receptor-binding site was transmitted to the pig virus. According to
the experimental data, a new hypothesis is formulated: the cascade mechanism of
directional recombination for duck, animal and human viruses makes it possible
for the recombinant viruses to overcome interspecies barriers.
Descriptors: adaptation, physiological genetics, genes
viral genetics, hemagglutinins viral genetics, influenza A virus avian
genetics, porcine genetics, recombination, genetic genetics, amino acid
sequence, ducks microbiology, human genetics, molecular sequence data, nucleic acid heteroduplexes genetics, RNA
viral genetics, swine microbiology, variation genetics genetics.
Bonin, J. and C. Scholtissek (1983). Mouse
neurotropic recombinants of influenza A viruses. Archives of Virology
75(4): 255-68. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Recombinants with known gene constellations
between fowl plague virus (FPV) and various prototype influenza virus strains
have been examined for neurovirulence in suckling mice. Strongly neurotropic
recombinants were obtained from crosses between FPV and the strains virus N,
Hong Kong, and PR8, but not between FPV and equi 2 or swine viruses. All highly
neurotropic recombinants had RNA segment 4 (HA) derived from FPV and RNA
segment 2 (Ptra gene) from the other prototype strain. The derivation of two
other RNA segments of the polymerase complex, namely RNA segments 3 (Pol 2) and
5 (NP) and also segment 8 (NS) can modulate these properties. For example, if
in recombinants between FPV and virus N in addition to RNA segment 2 also RNA
segments 3 and/or 8 are derived from virus N, neurovirulence is further
enhanced, while replacement of RNA segment 5 of FPV by the corresponding
segment of virus N decreases or abolishes neurovirulence. The derivation of the
other genes does not seem to be relevant for neurovirulence in the crosses
mentioned above. Of the prototype strains tested, the turkey England (t. Engl.)
strain is the only one which was highly neurotropic for suckling mice.
Recombinants between FPV and t. Engl. which have kept the HA gene of t. Engl.
were still neurotropic, while those with the HA gene of FPV were completely
avirulent. The results obtained demonstrated that 1. the creation of influenza
virus recombinants neurotropic for mice is not a rare event; 2. one of the
parents should multiply well in mouse lungs; 3. the presence of a cleavable
hemagglutinin is necessary, but not sufficient. In the pair FPV/turkey England
the hemagglutinin of turkey England seems to determine neurovirulence.
Descriptors: influenza A virus, genetics, recombination,
genetic, brain microbiology, cultured cells, embryo microbiology, fibroblasts,
genes viral, avian genetics, pathogenicity, kidney, lung microbiology, mice,
virulence.
Bonn, D. (2004). Avian influenza: the whole
world's business. Lancet Infectious Diseases 4(3): 128. ISSN: 1473-3099.
Descriptors: ducks virology, avian influenza transmission,
poultry diseases transmission, zoonoses, Asia epidemiology, food contamination,
avian influenza epidemiology, poultry diseases epidemiology, public health.
Borek, A. and C. Sauter (1975). Fowl plague virus
adapted to human leukemia cells: interaction with normal human leukocytes and
plastic surfaces. Pathologia Et Microbiologia 43(1): 62-73. ISSN: 0031-2959.
NAL
Call Number: 448.8 Sch9
Abstract: An avian influenza A virus which grows well
in human leukemic myeloblasts was unable to replicate in normal human
leukocytes. The virus adhered during the first hours of incubation to plastic
surfaces and to leukocytes and was then released into the supernatant; care
should be taken not to confuse this with viral growth.
Descriptors: influenza A virus, avian growth and
development, leukocytes microbiology, adaptation, physiological, adsorption,
adult, cell adhesion, granulocytes microbiology, leukemia, myelocytic, acute,
lymphocytes microbiology, monocytes microbiology, plastics, tissue culture,
virus replication.
Bricaire, F. (2004). La grippe aviaire, quel
risque de transmission interhumaine? [Avian flu, what are the risks of
inter-human transmission?]. Presse Medicale Paris, France 1983
33(6): 366-7. ISSN: 0755-4982.
Descriptors: disease outbreaks, influenza A virus, avian
influenza, avian influenza epidemiology, avian influenza transmission,
zoonoses, human, porcine, avian influenza prevention and control, poultry, risk
factors, swine.
Bridges, C.B., W. Lim, J. Hu Primmer, L. Sims, K.
Fukuda, K.H. Mak, T. Rowe, W.W. Thompson, L. Conn, X. Lu, N.J. Cox, and J.M.
Katz (2002). Risk of influenza A (H5N1) infection among poultry workers,
Hong Kong, 1997-1998. Journal of Infectious Diseases 185(8):
1005-10. ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Abstract: In 1997, outbreaks of highly pathogenic
influenza A (H5N1) among poultry coincided with 18 documented human cases of
H5N1 illness. Although exposure to live poultry was associated with human
illness, no cases were documented among poultry workers (PWs). To evaluate the
potential for avian-to-human transmission of H5N1, a cohort study was conducted
among 293 Hong Kong government workers (GWs) who participated in a poultry
culling operation and among 1525 PWs. Paired serum samples collected from GWs
and single serum samples collected from PWs were considered to be anti-H5
antibody positive if they were positive by both microneutralization and Western
blot testing. Among GWs, 3% were seropositive, and 1 seroconversion was
documented. Among PWs, approximately 10% had anti-H5 antibody. More-intensive
poultry exposure, such as butchering and exposure to ill poultry, was
associated with having anti-H5 antibody. These findings suggest an increased
risk for avian influenza infection from occupational exposure.
Descriptors: influenza etiology, influenza A virus,
occupational diseases etiology, poultry virology, adolescent, adult, case
control studies, Hong Kong epidemiology,
influenza epidemiology, middle aged, occupational exposure, risk factors,
seroepidemiologic studies, time factors.
Bright, R.A., D.S. Cho, T. Rowe, and J.M. Katz
(2003). Mechanisms of pathogenicity of influenza A (H5N1) viruses in mice.
Avian Diseases 47(Special Issue): 1131-1134. ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: Avian-like H5N1 influenza viruses isolated
from humans in 1997 were shown to have two distinct pathogenic phenotypes in
BALB/c mice, after intranasal inoculation and without prior adaptation to this
host. To further understand the mechanisms of H5N1 pathogenicity, we
investigated the consequences of the route of viral inoculation on morbidity
and mortality, viral replication in pulmonary and systemic organs, and
lymphocyte depletion. This study demonstrates the importance of extrapulmonary
spread and replication, particularly in the brain, for the lethality of H5N1
viruses.
Descriptors: infection, avian influenza, infectious
disease, respiratory system disease, viral disease, inoculation clinical
techniques, therapeutic and prophylactic techniques, morbidity, mortality,
pathogenic phenotypes, pathogenicity mechanisms, viral replication.
Brown, H. (2004). WHO confirms human-to-human
avian flu transmission. Lancet 363(9407): 462. ISSN: 1474-547X.
NAL
Call Number: 448.8 L22
Descriptors: disease transmission, horizontal statistics
and numerical data, fowl plague transmission, Asia epidemiology, fowl plague
epidemiology, fowl plague prevention and control, influenza A virus avian,
poultry, World Health Organization, zoonoses epidemiology, zoonoses
transmission.
Brown, I.H., P.A. Harris, J.W. McCauley, and D.J.
Alexander (1998). Multiple genetic reassortment of avian and human influenza
A viruses in European pigs, resulting in the emergence of an H1N2 virus of
novel genotype. Journal of General Virology 79(Pt. 12):
2947-55. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract:
Novel H1N2 influenza A viruses which
were first detected in pigs in Great Britain in 1994 were examined
antigenically and genetically to determine their origins and establish the
potential mechanisms for genetic reassortment. The haemagglutinin (HA) of all
swine H 1 N2 viruses examined was most closely related to, but clearly
distinguishable both antigenically and genetically from, the HA of human H1N1
viruses which circulated in the human population during the early 1 980s.
Phylogenetic analysis of the HA gene revealed that the swine H 1 N2 viruses
formed a distinct branch on the human lineage and were probably introduced to
pigs shortly after 1980. Following apparent transfer to pigs the HA gene
underwent genetic variation resulting in the establishment and cocirculation of
genetically and antigenically heterogeneous virus populations. Genetic analyses
of the other RNA segments of all swine H1N2 viruses indicated that the
neuraminidase gene was most closely related to those of early 'human-like'
swine H3N2 viruses, whilst the RNA segments encoding PB2, PB1, PA, NP, M and NS
were related most closely to those of avian viruses, which have been
circulating recently in pigs in Northern Europe. The potential mechanisms and
probable progenitor strains for genetic reassortment are discussed, but we
propose that the swine H1N2 viruses examined originated following multiple
genetic reassortment, initially involving human H1N1 and 'human-like' swine
H3N2 viruses, followed by reassortment with 'avian-like' swine H1N1 virus.
These findings suggest multiple reassortment and replication of influenza
viruses may occur in pigs many years before their detection as clinical
entities.
Descriptors: influenza A virus avian genetics, human
genetics, recombination, genetic, antigens, viral immunology, base sequence,
DNA, viral, Europe, genes viral, genotype, hemagglutination inhibition tests,
hemagglutinin glycoproteins, influenza virus genetics, avian immunology, human
immunology, molecular sequence data, phylogeny, sequence analysis, DNA, swine.
Brownlee, G.G. and E. Fodor (2001). The predicted
antigenicity of the haemagglutinin of the 1918 Spanish influenza pandemic
suggests an avian origin. Philosophical Transactions of the Royal
Society of London. Series B Biological Sciences 356(1416): 1871-1876. ISSN: 0962-8436.
NAL
Call Number: 501 L84Pb
Abstract: In 1982 we characterized the antigenic sites
of the haemagglutinin of influenza A/PR/8/34, which is an influenza strain of
the H1 subtype that was isolated from humans in 1934, by studying mutants which
escaped neutralization by antibody. Four antigenic sites, namely Cb, Sa, Sb and
Ca, were found to be located near the tip of the trimeric haemagglutinin spike.
Based on the sequence of the haemagglutinin of the 1918 Spanish influenza, we
can now specify the extent of divergence of antigenic sites of the
haemagglutinin during the antigenic drift of the virus between 1918 and 1934.
This divergence was much more extensive (40%) than the divergence (20%) in
predicted antigenic sites between the 1918 Spanish influenza and an avian H1
subtype consensus sequence. These results support the hypothesis that the human
1918 pandemic originated from an avian virus of the Hl subtype that crossed the
species barrier from birds to humans and adapted to humans, presumably by
mutation and/or reassortment, shortly before 1918.
Descriptors: epidemiology, infection, molecular genetics,
avian influenza, viral disease, pandemic influenza, epidemiology, respiratory
system disease, viral disease, 1918 Spanish influenza pandemic, age related
mortality, antigenic drift, antigenic site divergence, mortality rate, species
barrier.
Bucher, D.J., I.G. Kharitonenkov, D.K. Lvov, T.V.
Pysina, and H.M. Lee (1980). Comparative study of influenza virus H2 (Asian)
hemagglutinins isolated from human and avian sources. InterVirology
14(2): 69-77. ISSN: 0300-5526.
NAL
Call Number: QR355.I5
Abstract: The hemagglutinin of an influenza virus
isolated from a wild duck (Pintail, Anas acuta) in the USSR in 1976 had
been found to be antigenically indistinguishable from the hemagglutinin of H2N2
viruses of human origin isolated in 1957. The hemagglutinins from viral
preparations of the A/Anas acuta/Primorie/695/76 (H2Nav2) and
A/Singapore/1/57 (H2N2) strains were purified by SDS gel chromatography as the
subunits HA1 and HA2. Comparison of amino acid compositions and peptide maps of
tryptic peptides containing [14C]-carboxymethylcysteine showed a striking
degree of similarity between the H2 hemagglutinins.
Descriptors: hemagglutinins viral analysis, influenza A
virus avian immunology, human immunology, amino acids analysis, ducks
microbiology, peptides analysis.
Buckler White, A.J. and B.R. Murphy (1986). Nucleotide sequence analysis of the
nucleoprotein gene of an avian and a human influenza virus strain identifies
two classes of nucleoproteins. Virology 155(2): 345-55. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The nucleotide sequences of RNA segment 5 of
an avian influenza A virus, A/Mallard/NY/6750/78 (H2N2), and a human influenza
A virus, A/Udorn/307/72 (H3N2), were determined and the deduced amino acid
sequences of the nucleoprotein (NP) of these viruses were compared to two other
avian and two other human influenza A NP sequences. The results indicated that
there are separate classes of avian and human influenza A NP genes that can be
distinguished on the basis of sites containing amino acids specific for avian
and human influenza viruses and also by amino acid composition. The human
influenza A virus NP genes appear to follow a linear pathway of evolution with
the greatest homology (96.9%) between A/NT/60/68 (H3N2) and A/Udorn/72,
isolated only 4 years apart, and the least homology (91.1%) between A/PR/8/34
(H1N1) and A/Udorn/72, isolated 38 years apart. Furthermore, 84% of the
nucleotide substitutions between A/PR/8/34 and A/NT/60/68 are preserved in the
NP gene of the A/Udorn/72 strain. In contrast, a distinct linear pathway is not
present in the avian influenza NP genes since the homology (90.3%) between the
two avian influenza viruses A/Parrot/Ulster/73 (H7N1) and A/Mallard/78 isolated
only 5 years apart is not significantly greater than the homology (90.1%)
between strains A/FPV/Rostock/34 and A/Mallard/78 isolated 44 years apart and
only 49% of the nucleotide substitutions between A/FPV/34 and A/Parrot/73 are
found in A/Mallard/78. A determination of the rate of evolution of the human
influenza A virus NP genes suggested that there were a greater number of
nucleotide substitutions per year during the first several years immediately
following the emergence of a new subtype in 1968.
Descriptors: influenza A virus genetics, nucleoproteins
genetics, viral proteins genetics, amino acid sequence, base sequence,
evolution, genes viral, nucleoproteins classification, RNA viral genetics,
sequence homology, nucleic acid, viral proteins classification.
Buckler White, A.J., C.W. Naeve, and B.R. Murphy
(1986). Characterization of a gene coding for M proteins which is involved
in host range restriction of an avian influenza A virus in monkeys. Journal
of Virology 57(2): 697-700. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: The nucleotide sequence of the region of RNA
segment 7 coding for the M1 and M2 proteins of avian influenza A/Mallard/New
York/6750/78 was determined, and the deduced amino acid sequences were compared
to other avian and human M protein sequences. The M2 proteins of the avian and
human viruses have diverged much more than the M1 proteins, although amino
acids specific for avian and human viruses were found in both M1 and M2
proteins.
Descriptors: genes viral, influenza A virus avian
genetics, RNA viral genetics, viral proteins genetics, amino acid sequence,
haplorhini microbiology, avian growth and development, messenger genetics.
Butterfield, W.K., C.H. Campbell, and K.F.
Shortridge. (1978). Identification of nonavid influenza A viruses containing
human subtypes of haemagglutinin and neuraminidase isolated from poultry in
Hong Kong. In: Proceedings. Eighty second annual meeting of the United
States Animal Health Association, Buffalo, New York, p. 325-331.
NAL
Call Number: 49.9
UN3R
Descriptors: disease surveys, avian influenza
virus, humans, poultry, Hong Kong.
Buxton Bridges, C., J.M. Katz, W.H. Seto, P.K. Chan,
D. Tsang, W. Ho, K.H. Mak, W. Lim, J.S. Tam, M. Clarke, S.G. Williams, A.W.
Mounts, J.S. Bresee, L.A. Conn, T. Rowe, J. Hu Primmer, R.A. Abernathy, X. Lu,
N.J. Cox, and K. Fukuda (2000). Risk of influenza A (H5N1) infection among
health care workers exposed to patients with influenza A (H5N1), Hong Kong.
Journal of Infectious Diseases 181(1): 344-8. ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Abstract: The first outbreak of avian influenza A
(H5N1) occurred among humans in Hong Kong in 1997. To estimate the risk of person-to-person
transmission, a retrospective cohort study was conducted to compare the
prevalence of H5N1 antibody among health care workers (HCWs) exposed to H5N1
case-patients with the prevalence among nonexposed HCWs. Information on H5N1
case-patient and poultry exposures and blood samples for H5N1-specific antibody
testing were collected. Eight (3.7%) of 217 exposed and 2 (0.7%) of 309
nonexposed HCWs were H5N1 seropositive (P=.01). The difference remained
significant after controlling for poultry exposure (P=.01). This study presents
the first epidemiologic evidence that H5N1 viruses were transmitted from
patients to HCWs. Human-to-human transmission of avian influenza may increase
the chances for the emergence of a novel influenza virus with pandemic potential.
Descriptors: antibodies, viral blood, disease outbreaks,
disease transmission, patient to professional, influenza transmission,
influenza A virus avian immunology, adult, carrier state, cohort studies, avian
classification, middle aged, retrospective studies, seroepidemiologic studies.
Cameron, K.R., V. Gregory, J. Banks, I.H. Brown, D.J.
Alexander, A.J. Hay, and Y.P. Lin (2000). H9N2 subtype influenza A viruses
in poultry in Pakistan are closely related to the H9N2 viruses responsible for
human infection in Hong Kong. Virology 278(1): 36-41. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: disease outbreaks veterinary, influenza
veterinary, influenza A virus avian classification, human classification,
poultry diseases virology, antigens, viral genetics, antigens, viral
immunology, cloning, molecular, genome, viral, hemagglutination inhibition
tests, hemagglutinins viral genetics, Hong Kong epidemiology, influenza
epidemiology, avian genetics, avian immunology, human genetics, human immunology,
molecular sequence data, Pakistan epidemiology, phylogeny, poultry diseases
epidemiology, sequence analysis, protein, viral proteins genetics, viral
proteins immunology.
Campbell, C.H., R.G. Webster, and S.S.J. Breese
(1970). Fowl plague virus from man. Journal of Infectious Diseases
122(6): 513-6. ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Descriptors: influenza A virus avian isolation and
purification, antigens analysis, chick embryo, chickens, cross reactions,
hemagglutination inhibition tests, immune sera analysis, avian classification,
avian immunology, avian pathogenicity, microscopy, electron, neuraminidase
analysis, neutralization tests, poultry diseases immunology, vaccination, viral
vaccines administration and dosage.
Campitelli, L., C. Fabiani, S. Puzelli, A. Fioretti,
E. Foni, A. De Marco, S. Krauss, R.G. Webster, and I. Donatelli (2002). H3N2
influenza viruses from domestic chickens in Italy: an increasing role for
chickens in the ecology of influenza? Journal of General Virology
83(Pt. 2): 413-20. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: In Italy, multiple H3N2 influenza viruses
were isolated from chickens with mild respiratory disease and were shown to
replicate in the respiratory tracts of experimentally infected chickens; this
finding is the first to show that H3N2 influenza viruses can replicate and
cause disease in chickens. H3N2 influenza viruses in pigs on nearby farms
seemed a likely source of the virus; however, antigenic and molecular analyses
revealed that the gene segments of the viruses in chickens were mainly of
Eurasian avian origin and were distinguishable from those isolated from pigs
and wild aquatic birds in Italy. Thus, several different H3 influenza viruses
were circulating in Italy, but we failed to identify the source of the chicken
H3N2 influenza viruses that have disappeared subsequently from Italian poultry.
Until recently, the transmission of influenza viruses (other than the H5 and H7
subtypes) from their reservoir in aquatic birds to chickens was rarely detected
and highly pathogenic and non-pathogenic viruses were considered to be
restricted to poultry species. However, the recent reports of the transmission
of H9N2 and H5N1 influenza viruses to chickens in Hong Kong and, subsequently,
to humans and our findings of the transmission of H3N2 influenza viruses to
domestic chickens in Italy suggest an increased role for chickens as an
intermediate host in the ecology of influenza.
Descriptors: chickens, fowl plague virology, influenza
veterinary, influenza A virus avian pathogenicity, poultry diseases virology,
hemagglutination inhibition tests, hemagglutinin glycoproteins, influenza virus
genetics, influenza virology, avian isolation and purification, avian
physiology, porcine isolation and purification, porcine pathogenicity, Italy,
molecular sequence data, sequence analysis, DNA, swine diseases virology, viral
proteins genetics, virus replication.
Capua, I. and D.J. Alexander (2004). Human health
implications of avian influenza viruses and paramyxoviruses. European
Journal of Clinical Microbiology and Infectious Diseases Official Publication
of the European Society of Clinical Microbiology 23(1): 1-6. ISSN: 0934-9723.
Abstract: Among avian influenza viruses and avian
paramyxoviruses are the aetiological agents of two of the most devastating
diseases of the animal kingdom: (i). the highly pathogenic form of avian
influenza, caused by some viruses of the H5 and H7 subtypes, and (ii).
Newcastle disease, caused by virulent strains of APMV type 1. Mortality rates
due to these agents can exceed 50% in naive bird populations, and, for some
strains of AI, nearly 100%. These viruses may also be responsible for clinical
conditions in humans. The virus responsible for Newcastle disease has been
known to cause conjunctivitis in humans since the 1940s. The conjunctivitis is
self-limiting and does not have any permanent consequences. Until 1997, reports
of human infection with avian influenza viruses were sporadic and frequently
associated with conjunctivitis. Recently, however, avian influenza virus
infections have been associated with fatalities in human beings. These
casualties have highlighted the potential risk that this type of infection
poses to public health. In particular, the pathogenetic mechanisms of highly
pathogenic avian influenza viruses in birds and the possibility of reassortment
between avian and human viruses in the human host represent serious threats to
human health. For this reason, any suspected case should be investigated
thoroughly.
Descriptors: avulavirus isolation and purification,
communicable disease control, disease outbreaks, fowl plague epidemiology,
influenza A virus avian isolation and purification, Newcastle disease
epidemiology, birds, fowl plague prevention and control, Italy epidemiology,
Newcastle disease prevention and control, prognosis, risk assessment, survival
analysis.
Capua, I., F. Mutinelli, M.D. Pozza, I. Donatelli, S.
Puzelli, and F.M. Cancellotti (2002). The 1999-2000 avian influenza (H7N1)
epidemic in Italy: veterinary and human health implications. Acta
Tropica 83(1): 7-11. ISSN:
0001-706X.
NAL
Call Number: 475 AC8
Abstract: From the end of March to the beginning of
December 1999, 199 outbreaks of low pathogenicity avian influenza (LPAI) were
diagnosed in the Veneto and Lombardia regions, which are located in the
northern part of Italy. The virus responsible for the epidemic was
characterized as a type A influenza virus of the H7N1 subtype of low
pathogenicity. On the 17th of December, highly pathogenic avian influenza
(HPAI) was diagnosed in a meat turkey flock in which 100% mortality was
observed in 72 h. The infection spread to the industrial poultry population of
northern Italy including chickens, guinea-fowl, quail, pheasants, ducks and
ostriches for a total of 413 outbreaks. Over 13 million birds were affected by
the epidemic, which caused dramatic economic losses to the Italian poultry
industry with severe social and economic implications. The possibility of H7
virus transmission to humans in close contact with the outbreaks was evaluated
through a serological survey. Seven hundred and fifty nine sera were collected
and tested for the detection of anti-H7 antibodies by means of the
micro-neutralization (MN) and single radial haemolysis (SRH) tests. All samples
resulted negative. A limited number of clinical samples were also collected for
attempted virus isolation with negative results. Current European legislation
considers LPAI and HPAI as two completely distinct diseases, not contemplating
any compulsory eradication policy for LPAI and requiring eradication for HPAI.
Evidence collected during the Italian 1999-2000 epidemic indicates that LPAI
due to viruses of the H7 subtype may mutate to HPAI, and, therefore, LPAI
caused by viruses of the H5 or H7 subtypes must be controlled to avoid the
emergence of HPAI. A reconsideration of the current definition of avian
influenza adopted by the EU, could possibly be an aid to avoiding devastating
epidemics for the poultry industry in Member States.
Descriptors: disease outbreaks, leishmaniasis, visceral
epidemiology, adolescent, adult, age distribution, antibodies, protozoan
isolation and purification, Brazil epidemiology, child, child preschool,
infant, leishmaniasis, visceral immunology, prevalence, seroepidemiologic
studies, skin tests, urban population.
Capua, I. and D.J. Alexander (2002). Avian
influenza and human health. Acta Tropica 83(1): 1-6. ISSN: 0001-706X.
NAL
Call Number: 475 AC8
Abstract: Natural infections with influenza A viruses
have been reported in a variety of animal species including humans, pigs,
horses, sea mammals, mustelids and birds. Occasionally devastating pandemics
occur in humans. Although viruses of relatively few HA and NA subtype
combinations have been isolated from mammalian species, all 15 HA subtypes and
all 9 NA subtypes, in most combinations, have been isolated from birds. In the
20th century the sudden emergence of antigenically different strains
transmissible in humans, termed antigenic shift, has occurred on four
occasions, 1918 (H1N1), 1957 (H2N2), 1968 (H3N2) and 1977 (H1N1), each time
resulting in a pandemic. Genetic analysis of the isolates demonstrated that
'new' strains most certainly emerged after reassortment of genes of viruses of
avian and human origin in a permissive host. The leading theory is that the pig
represents the 'mixing vessel' where this genetic reassortment may occur. In
1996, an H7N7 influenza virus of avian origin was isolated from a woman with a
self-limiting conjunctivitis. During 1997 in Hong Kong, an H5N1 avian influenza
virus was recognised as the cause of death of 6 of 18 infected patients. Genetic
analysis revealed these human isolates of H5N1 subtype to be indistinguishable
from a highly pathogenic avian influenza virus that was endemic in the local
poultry population. More recently, in March 1999, two independent isolations of
influenza virus subtype H9N2 were made from girls aged one to four who
recovered from flu-like illnesses in Hong Kong. Subsequently, five isolations
of H9N2 virus from humans on mainland China in August 1998 were reported. H9N2
viruses were known to be widespread in poultry in China and other Asian
countries. In all these cases there was no evidence of human to human spread
except with the H5N1 infections where there was evidence of very limited
spread. This is in keeping with the finding that all these viruses possessed all
eight genes of avian origin. It may well be that infection of humans with avian
influenza viruses occurs much more frequently than originally assumed, but due
to their limited effect go unrecognised. For the human population as a whole
the main danger of direct infection with avian influenza viruses appears to be
if people infected with an 'avian' virus are infected simultaneously with a
'human' influenza virus. In such circumstances reassortment could occur with
the potential emergence of a virus fully capable of spread in the human
population, but with antigenic characteristics for which the human population
was immunologically naive. Presumably this represents a very rare coincidence,
but one which could result in a true influenza pandemic.
Descriptors: infection, avian influenza, respiratory
system disease, viral disease, self limiting conjunctivitis, eye disease,
genetic analysis genetic techniques, laboratory techniques.
Cauthen, A.N., D.E. Swayne, S. Schultz Cherry, M.L.
Perdue, and D.L. Suarez (2000). Continued circulation in China of highly
pathogenic avian influenza viruses encoding the hemagglutinin gene associated
with the 1997 H5N1 outbreak in poultry and humans. Journal of Virology
74(14): 6592-9. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Since the outbreak in humans of an H5N1 avian
influenza virus in Hong Kong in 1997, poultry entering the live-bird markets of
Hong Kong have been closely monitored for infection with avian influenza. In
March 1999, this monitoring system detected geese that were serologically
positive for H5N1 avian influenza virus, but the birds were marketed before
they could be sampled for virus. However, viral isolates were obtained by
swabbing the cages that housed the geese. These samples, known collectively as
A/Environment/Hong Kong/437/99 (A/Env/HK/437/99), contained four viral
isolates, which were compared to the 1997 H5N1 Hong Kong isolates. Analysis of
A/Env/HK/437/99 viruses revealed that the four isolates are nearly identical
genetically and are most closely related to A/Goose/Guangdong/1/96. These
isolates and the 1997 H5N1 Hong Kong viruses encode common hemagglutinin (H5)
genes that have identical hemagglutinin cleavage sites. Thus, the pathogenicity
of the A/Env/HK/437/99 viruses was compared in chickens and in mice to evaluate
the potential for disease outbreaks in poultry and humans. The A/Env/HK/437/99
isolates were highly pathogenic in chickens but caused a longer mean death time
and had altered cell tropism compared to A/Hong Kong/156/97 (A/HK/156/97). Like
A/HK/156/97, the A/Env/HK/437/99 viruses replicated in mice and remained
localized to the respiratory tract. However, the A/Env/HK/437/99 isolates
caused only mild pathological lesions in these tissues and no clinical signs of
disease or death. As a measure of the immune response to these viruses,
transforming growth factor beta levels were determined in the serum of infected
mice and showed elevated levels for the A/Env/HK/437/99 viruses compared to the
A/HK/156/97 viruses. This study is the first to characterize the
A/Env/HK/437/99 viruses in both avian and mammalian species, evaluating the H5
gene from the 1997 Hong Kong H5N1 isolates in a different genetic background.
Our findings reveal that at least one of the avian influenza virus genes
encoded by the 1997 H5N1 Hong Kong viruses continues to circulate in mainland
China and that this gene is important for pathogenesis in chickens but is not
the sole determinant of pathogenicity in mice. There is evidence that H9N2
viruses, which have internal genes in common with the 1997 H5N1 Hong Kong
isolates, are still circulating in Hong Kong and China as well, providing a
heterogeneous gene pool for viral reassortment. The implications of these
findings for the potential for human disease are discussed.
Descriptors: fowl plague virology, hemagglutinin
glycoproteins, influenza virus genetics, influenza A virus avian genetics,
poultry diseases virology, chickens, China epidemiology, disease outbreaks
veterinary, fowl plague epidemiology, fowl plague pathology, Hong Kong
epidemiology, immunohistochemistry, avian classification, avian pathogenicity,
mice, mice inbred BALB c, molecular sequence data, phylogeny, poultry diseases
epidemiology, poultry diseases pathology, sequence homology, nucleic acid, transforming
growth factor beta blood.
Chan, P.K.S. (2002). Outbreak of avian influenza
A(H5N1) virus infection in Hong Kong in 1997. Clinical Infectious
Diseases 34(Suppl. 2): S58-S64.
ISSN: 1058-4838.
NAL
Call Number: RC111.R4
Abstract: The first outbreak of avian influenza A(H5N1)
virus in humans occurred in Hong Kong in 1997. Infection was confirmed in 18
individuals, 6 of whom died. Infections were acquired by humans directly from
chickens, without the involvement of an intermediate host. The outbreak was
halted by a territory-wide slaughter of more than 1.5 million chickens at the
end of December 1997. The clinical spectrum of H5N1 infection ranges from
asymptomatic infection to fatal pneumonitis and multiple organ failure.
Reactive hemophagocytic syndrome was the most characteristic pathologic finding
and might have contributed to the lymphopenia, liver dysfunction, and abnormal
clotting profiles that were observed among patients with severe infection.
Rapid diagnosis with the use of reverse-transcription polymerase chain reaction
and monoclonal antibody-based immunofluorescent assay were of great clinical
value in the management of the outbreak. The experience of the H5N1 outbreak in
Hong Kong underscores the importance of continuous surveillance of influenza
virus strains in humans and in other animal species.
Descriptors: infection, public health, avian influenza A
virus infection, symptom, viral disease, liver dysfunction, digestive system
disease, lymphopenia, blood and lymphatic disease, immune system disease,
multiple organ failure, disease miscellaneous, pneumonitis, respiratory system
disease, reactive hemophagocytic syndrome, blood and lymphatic disease,
monoclonal antibody based immunofluorescent assay diagnostic method, reverse
transcriptase polymerase chain reaction diagnostic method, polymerase chain
reaction, abnormal clotting profiles disease outbreak mortality.
Choi, Y.K., S.M. Goyal, M.W. Farnham, and H.S. Joo
(2002). Phylogenetic analysis of H1N2 isolates of influenza A virus from pigs
in the United States. Virus Research 87(2): 173-9. ISSN: 0168-1702.
NAL
Call Number: QR375.V6
Abstract: Twenty-four H1N2 influenza A viruses were
newly isolated from pigs in the United States. These isolates originated from
19 farms in 9 different swine producing states between 1999 and 2001. All farms
had clinical histories of respiratory problem and/or abortion. The viral
isolates were characterized genetically to determine the origin of all eight
gene segments. The results showed that all H1N2 isolates were reassortants of
classical swine H1N1 and triple reassortant H3N2 viruses. The neuraminidase
(NA) and PB1 genes of the H1N2 isolates were of human origin, while the
hemagglutinin (HA), nucleoprotein (NP), matrix (M), non-structural (NS), PA and
PB2 polymerase genes were of avian or swine origin. Fifteen of the 24 H1N2
isolates were shown to have a close phylogenic relationship and high amino acid
homology with the first US isolate of H1N2 (A/SW/IN/9K035/99). The remaining
nine isolates had a close phylogenic relationship with classical swine
influenza H1N1 in the HA gene. All other genes including NA, M, NP, NS, PA, PB1
and PB2 showed a close phylogenic relationship with the H1N2 (A/SW/IN/9K035/99)
strain and triple reassortant H3N2 viruses. However, PB1 genes of two isolates
(A/SW/KS/13481-S/00, A/SW/KS/13481-T/00) were originated from avian influenza A
virus lineage. These results suggest that although there are some variations in
the HA genes, the H1N2 viruses prevalent in the US swine population are of a
similar genetic lineage.
Descriptors: influenza A virus, porcine genetics,
antigens, viral, hemagglutinin glycoproteins, influenza virus genetics, porcine
classification, porcine enzymology, porcine isolation and purification,
molecular sequence data, neuraminidase
genetics, phylogeny, swine, United States, variation genetics.
Claas, E.C., A.D. Osterhaus, R. van Beek, J.C. De
Jong, G.F. Rimmelzwaan, D.A. Senne, S. Krauss, K.F. Shortridge, and R.G.
Webster (1998). Human influenza A H5N1 virus related to a highly pathogenic
avian influenza virus. Lancet 351(9101): 472-7. ISSN: 0140-6736.
NAL
Call Number: 448.8 L22
Abstract: BACKGROUND: In May, 1997, a 3-year-old boy in
Hong Kong was admitted to the hospital and subsequently died from influenza
pneumonia, acute respiratory distress syndrome, Reye's syndrome, multiorgan
failure, and disseminated intravascular coagulation. An influenza A H5N1 virus
was isolated from a tracheal aspirate of the boy. Preceding this incident,
avian influenza outbreaks of high mortality were reported from three chicken
farms in Hong Kong, and the virus involved was also found to be of the H5
subtype. METHODS: We carried out an antigenic and molecular comparison of the
influenza A H5N1 virus isolated from the boy with one of the viruses isolated
from outbreaks of avian influenza by haemagglutination-inhibition and
neuraminidase-inhibition assays and nucleotide sequence analysis. FINDINGS:
Differences were observed in the antigenic reactivities of the viruses by the haemagglutination-inhibition
assay. However, nucleotide sequence analysis of all gene segments revealed that
the human virus A/Hong Kong/156/97 was genetically closely related to the avian
A/chicken/Hong Kong/258/97. INTERPRETATION: Although direct contact between the
sick child and affected chickens has not been established, our results suggest
transmission of the virus from infected chickens to the child without another
intermediate mammalian host acting as a "mixing vessel". This event
illustrates the importance of intensive global influenza surveillance.
Descriptors: fowl plague virology, influenza virology,
influenza A virus avian genetics, human genetics, amino acid sequence, base
sequence, chickens virology, child, preschool, disease outbreaks veterinary,
fowl plague epidemiology, Hong Kong epidemiology, influenza epidemiology, avian
isolation and purification, avian pathogenicity, human isolation and
purification, molecular sequence data.
Claas, E.C.J., Y. Kawaoka, J.C. de Jong, N. Masurel,
and R.G. Webster (1994). Infection of children with avian-human reassortant
influenza virus from pigs in Europe. Virology 204(1): 453-457. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Pigs have been proposed to act as the
intermediate hosts in the generation of pandemic human influenza strains by
reassortment of genes from avian and human influenza virus strains. The
circulation of avian-like H1N1 influenza viruses in European pigs since 1979
and the detection of human-avian reassortants in pigs raises the question of
whether these viruses actually have the potential to transmit and cause disease
in humans. We now report the serologic and genetic characterization of two
human influenza A viruses (A/Netherlands/5/93 [H3N2] and A/Netherlands/35/93
[H3N2]) that caused influenza in children in The Netherlands in 1993. The
results show that these viruses are human-avian reassortants that were
generated and currently still are circulating in European swine. This shows the
pivotal role that pigs can play in the generation and transmission of avian
influenza virus genes to humans and their potential to generate a new human
pandemic strain.
Descriptors: swine, Netherlands, intermediate hosts, avian
influenza virus, influenza virus, children, infection, disease transmission,
genes, phylogeny, artiodactyla, biological competition, cell structure,
chromosomes, disease transmission, domestic animals, Europe, evolution, hosts,
influenza virus, livestock, mammals, nucleus, parasitism, pathogenesis,
progeny, suidae, useful animals, viruses,
Western Europe, human influenza virus, pandemics, genetic reassortment,
nucleoprotein genes, structural genes.
Claas, E.C.J. (2000). Pandemic influenza is a
zoonosis, as it requires introduction of avian-like gene segments in the human
population. Veterinary Microbiology 74(1-2): 133-139. ISSN: 0378-1135.
NAL
Call Number: SF601.V44
Abstract: Human influenza viruses manage to cause
epidemics almost every year. The circulating viruses change their surface
glycoproteins by accumulating mutations (antigenic drift) which results in
variant viruses of the same subtype that are able to evade the immune pressure
in the population. Every now and then, a completely new subtype of influenza A
virus is introduced in the human population, which can result in an influenza
pandemic. Pandemic human influenza viruses have been emerging for many
centuries. Based on the genetic information of influenza viruses that have been
isolated in this century, introduction of genes of the avian influenza virus
reservoir obviously is required. Interspecies transmission, via another
mammalian host and reassortment of avian and human influenza viruses are
potential mechanisms for such an introduction. A summary of the cases in which
influenza viruses containing avian-like gene segments were introduced into the
human population is presented. In three cases, such infections resulted in
conjunctivitis. Influenza-like illness and even pneumonia was reported in some
other infections. Finally, a mortality rate of 33% was observed in the avian
influenza A (H5N1) viruses that infected 18 people in Hong Kong in 1997.
Although some of these viruses fulfilled some criteria of pandemic influenza
viruses, they lacked the ability to rapidly spread through the human
population.
Descriptors: molecular genetics, infection, epidemiology,
conjunctivitis, eye disease, influenza virus infection, pandemic, viral
disease, zoonosis, pneumonia, respiratory system disease, antigenic drift
interspecies transmission mortality.
Clements, M.L., S.D. Sears, K. Christina, B.R.
Murphy, and M.H. Snyder (1989). Comparison of the virologic and immunologic
responses of volunteers to live avian-human influenza A H3N2 reassortant virus
vaccines derived from two different avian influenza virus donors. Journal
of Clinical Microbiology 27(1): 219-22.
ISSN: 0095-1137.
NAL
Call Number: QR46.J6
Abstract: We compared the abilities of the six internal
RNA segments of two avian influenza viruses, A/Mallard/Alberta/88/76 (H3N8) and
A/Mallard/NY/6750/78 (H2N2), to confer attenuation on wild-type human influenza
A/Bethesda/1/85 (H3N2) virus in seronegative adult volunteers. Live avian-human
influenza A reassortant virus vaccines derived from either avian virus parent
were comparable in the following properties: safety, infectivity,
immunogenicity, and genetic stability. Since the avian influenza
A/Mallard/Alberta/76 virus offered no clear advantage as a donor virus, we will
conduct our future evaluations on live influenza A virus reassortants derived
from the more extensively characterized avian influenza A/Mallard/NY/78 virus.
Descriptors: antibodies, viral biosynthesis, influenza
prevention and control, influenza A virus avian immunology, human immunology,
influenza vaccine immunology, dose response relationship, immunologic,
electrophoresis, polyacrylamide gel, enzyme linked immunosorbent assay, genes
viral, hemagglutination inhibition tests, avian genetics, avian physiology,
human genetics, human physiology, influenza vaccine adverse effects, vaccines,
attenuated adverse effects, vaccines, attenuated immunology, vaccines,
synthetic adverse effects, vaccines, synthetic immunology, virus replication.
Clements, M.L., M.H. Snyder, A.J. Buckler White, E.L.
Tierney, W.T. London, and B.R. Murphy (1986). Evaluation of avian-human
reassortant influenza A/Washington/897/80 x A/Pintail/119/79 virus in monkeys
and adult volunteers. Journal of Clinical Microbiology 24(1):
47-51. ISSN: 0095-1137.
NAL
Call Number: QR46.J6
Abstract: A reassortant influenza A virus was produced
by mating an avian influenza A/Pintail/Alberta/119/79 (H4N6) virus with
wild-type human influenza A/Washington/897/80 (H3N2) virus. The avian-human
influenza A reassortant virus contained the genes coding for the hemagglutinin
and neuraminidase surface antigens of the human influenza wild-type virus and
the six other RNA segments (internal genes) of the avian influenza A virus
donor. In the lower respiratory tract of squirrel monkeys, this avian-human
influenza reassortant virus, like its avian influenza A parent virus, was
restricted approximately 100-fold in replication compared with the wild-type
human influenza A virus. Despite this restriction of replication, infection of
monkeys with the avian-human influenza A reassortant virus induced resistance
to wild-type human influenza A virus challenge. In comparison with the
wild-type human influenza A virus, the avian-human influenza A reassortant was
also fully attenuated when 10(5.5) to 10(7.5) 50% tissue culture infective
doses were administered to susceptible adult volunteers. Attenuation was
indicated by a more than 300-fold reduction in virus shedding and lack of
reactogenicity. The reassortant virus did not spread to susceptible contacts
and could not be isolated from the blood or stools of infected adults. The 50%
human infectious dose was 10(6.2) 50% tissue culture infective dose, indicating
that this reassortant virus is only slightly less infectious for adults than a
similarly derived avian-human influenza A/Washington/80 X A/Mallard/78
reassortant virus. These findings suggest that the avian influenza A/Pintail/79
virus may be a satisfactory donor of attenuating genes for production of live,
attenuated avian-human influenza A reassortant virus vaccines.
Descriptors: influenza A virus human immunology,
immunology, influenza vaccine immunology, adolescent, adult, genes viral,
influenza immunology, influenza prevention and control, human genetics,
genetics, influenza vaccine adverse effects, saimiri, vaccines, attenuated
adverse effects, vaccines, attenuated immunology, virus replication.
Clements, M.L., E.K. Subbarao, L.F. Fries, R.A.
Karron, W.T. London, and B.R. Murphy (1992). Use of single-gene reassortant
viruses to study the role of avian influenza A virus genes in attenuation of
wild-type human influenza A virus for squirrel monkeys and adult human
volunteers. Journal of Clinical Microbiology 30(3): 655-62. ISSN: 0095-1137.
NAL
Call Number: QR46.J6
Abstract: The transfer of six internal RNA segments
from the avian influenza A/Mallard/New York/6750/78 (H2N2) virus reproducibly
attenuates human influenza A viruses for squirrel monkeys and adult humans. To
identify the avian influenza A virus genes that specify the attenuation and
host range restriction of avian-human (ah) influenza A reassortant viruses
(referred to as ah reassortants), we isolated six single-gene reassortant
viruses (SGRs), each having a single internal RNA segment of the influenza
A/Mallard/New York/6750/78 virus and seven RNA segments from the human
influenza A/Los Angeles/2/87 (H3N2) wild-type virus. To assess the level of
attenuation, we compared each SGR with the A/Los Angeles/2/87 wild-type virus
and a 6-2 gene ah reassortant (having six internal RNA segments from the avian
influenza A virus parent and two genes encoding the hemagglutinin and
neuraminidase glycoproteins from the wild-type human influenza A virus) for the
ability to replicate in seronegative squirrel monkeys and adult human
volunteers. In monkeys and humans, replication of the 6-2 gene ah reassortant
was highly restricted. In humans, the NS, M, PB2, and PB1 SGRs each replicated
significantly less efficiently (P less than 0.05) than the wild-type human
influenza A virus parent, suggesting that each of these genes contributes to
the attenuation phenotype. In monkeys, only the NP, PB2, and possibly the M
genes contributed to the attenuation phenotype. These discordant observations,
particularly with regard to the NP SGR, indicate that not all genetic
determinants of attenuation of influenza A viruses for humans can be identified
during studies of SGRs conducted with monkeys. The PB2 and M SGRs that were
attenuated in humans each exhibited a new phenotype that was not observed for
either parental virus. Thus, it was not possible to determine whether avian
influenza virus PB2 or M gene itself or a specific constellation of avian and
human influenza A virus specified restriction of virus replication in humans.
Descriptors: influenza A virus avian genetics, human
genetics, adult, base sequence, genes viral, human pathogenicity, human
physiology, influenza vaccine isolation and purification, molecular sequence
data, RNA viral genetics, saimiri, transfection, vaccines, attenuated isolation
and purification, virulence genetics, virus replication genetics.
Connor, R.J., Y. Kawaoka, R.G. Webster, and J.C.
Paulson (1994). Receptor specificity in human, avian, and equine H2 and H3
influenza virus isolates. Virology 205(1): 17-23. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The receptor specificity of 56 H2 and H3
influenza virus isolates from various animal species has been determined to
test the relevance of receptor specificity to the ecology of influenza virus.
The results show that the receptor specificity of both H2 and H3 isolates
evaluated for sialic acid linkage specificity and inhibition of
hemagglutination by horse serum correlates with the species of origin, as
postulated earlier for H3 strains based on a limited survey of five human, three
avian, and one equine strain. Elucidation of the amino acid sequence of several
human H2 receptor variants and analysis of known sequences of H2 and H3
isolates revealed that receptor specificity varies in association with an amino
acid change at residues 228 in addition to the change at residue 226 previously
documented to affect receptor specificity of H3 but not H1 isolates. Residues
226 and 228 are leucine and serine in human isolates, which preferentially bind
sialic acid alpha 2,6-galactose beta 1,4-N-acetyl glucosamine (SA alpha
2,6Gal), and glutamine and glycine in avian and equine isolates, which exhibit
specificity for sialic acid alpha-2,3-galactose beta-1,3-N-acetyl galactosamine
(SA alpha 2,3Gal). The results demonstrate that the correlation of receptor
specificity and species of origin is maintained across both H2 and H3 influenza
virus serotypes and provide compelling evidence that influenza virus hosts
exert selective pressure to maintain the receptor specificity characteristics
of strains isolated from that species.
Descriptors: influenza A virus avian metabolism, human
metabolism, metabolism, receptors, virus metabolism, amino acid sequence, amino
acids genetics, carbohydrate sequence, chick embryo, hemagglutinin
glycoproteins, influenza virus, hemagglutinins viral genetics, molecular
sequence data, species specificity, viral envelope proteins genetics.
Cook, R.F., R.J. Avery, and N.J. Dimmock (1980). Complementation
with an avian influenza virus is required for synthesis of M protein of a human
strain in chicken erythocytes. Archives of Virology 65(3-4):
319-24. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: The M protein of avian, but not human,
strains of influenza A viruses is synthesized in infected chicken erythrocytes.
In dual infections an avian strain complemented the human virus and both the
human and avian M proteins were expressed.
Descriptors: erythrocytes microbiology, influenza A virus
avian metabolism, human metabolism, viral proteins biosynthesis, chick embryo,
dactinomycin pharmacology, avian growth and development, human growth and
development.
Cooper, L.A. and K. Subbarao (2000). A simple
restriction fragment length polymorphism-based strategy that can distinguish
the internal genes of human H1N1, H3N2, and H5N1 influenza A viruses. Journal
of Clinical Microbiology 38(7): 2579-83.
ISSN: 0095-1137.
NAL
Call Number: QR46.J6
Abstract: A simple molecular technique for rapid
genotyping was developed to monitor the internal gene composition of currently
circulating influenza A viruses. Sequence information from recent H1N1, H3N2,
and H5N1 human virus isolates was used to identify conserved regions within
each internal gene, and gene-specific PCR primers capable of amplifying all
three virus subtypes were designed. Subtyping was based on subtype-specific
restriction fragment length polymorphism (RFLP) patterns within the amplified
regions. The strategy was tested in a blinded fashion using 10 control viruses
of each subtype (total, 30) and was found to be very effective. Once
standardized, the genotyping method was used to identify the origin of the
internal genes of 51 influenza A viruses isolated from humans in Hong Kong
during and immediately following the 1997-1998 H5N1 outbreak. No avian-human or
H1-H3 reassortants were detected. Less than 2% (6 of 486) of the RFLP analyses
were inconclusive; all were due to point mutations within a restriction site.
The technique was also used to characterize the internal genes of two avian
H9N2 viruses isolated from children in Hong Kong during 1999.
Descriptors: genes viral, influenza virology, influenza A
virus human classification, human genetics, polymorphism, restriction fragment
length, disease outbreaks, Hong Kong, avian classification, avian genetics,
avian isolation and purification, human isolation and purification, reverse
transcriptase polymerase chain reaction.
Cornell University - Department of Population
Medicine & Diagnostic Sciences - Animal Health Diagnostic Center - College
of Veterinary Medicine (2005). Canine Influenza Virus - Detection and
Sampling.
Online: http://www.diaglab.vet.cornell.edu/issues/civ-dect.asp
Abstract: Canine influenza virus is a relatively new
pathogen of dogs. It was first identified in racing greyhounds in 2004 and this
virus appears to have been involved with significant respiratory problems on
the dog tracks throughout the US for the last 2-3 years. The Virology Lab at
Cornell isolated the first influenza virus from an animal that died during one
of these clinical episodes. Evidence of infection of non-greyhounds by
influenza virus has been found in Florida within the past year as part of the
ongoing research efforts by Dr Cynda Crawford at the University of Florida on
respiratory disease in dogs.
Couceiro, J.N., R.D. Machado, and J.R. Chaves (1982).
Influenza A, isolamento e caracerizacao de virus isolados de aves de vida
livre. [Influenza A, isolation and characterization of virus isolated from wild
birds]. Anais De Microbiologia 27:
193-204. ISSN: 0485-1854.
Descriptors: birds microbiology, influenza A virus avian
isolation and purification, antigens, viral analysis, culture media, feces
microbiology, hemagglutination inhibition tests, hemagglutinins viral analysis,
immune sera, avian immunology, virus cultivation.
Davenport, F.M., A.V. Hennessy, and E. Minuse (1968).
The age distribution in humans of hemagglutinating-inhibiting antibodies
reacting with avian strains of influenza A virus. Journal of Immunology
100(3): 581-5. ISSN: 0022-1767.
NAL
Call Number: 448.8 J8232
Descriptors: antibodies analysis, influenza immunology,
influenza A virus avian immunology, adolescent, adult, aged, aging, child,
child preschool, hemagglutination inhibition tests, infant, middle aged,
statistics.
de Boer, G.F., W. Back, and A.D. Osterhaus (1990). An
ELISA for detection of antibodies against influenza A nucleoprotein in humans
and various animal species. Archives of Virology 115(1-2):
47-61. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: A double antibody sandwich blocking ELISA,
using a monoclonal antibody (MAb) against influenza A nucleoprotein (NP) was
developed to detect antibodies against influenza. Collections of serum samples
were obtained from human and various animal species. All influenza A subtypes
induced antibodies against hemagglutinins and NP. A close correlation between
titers of the hemagglutination inhibition (HI) test and the NP-ELISA was seen.
Antibodies against influenza NP were demonstrated in serum samples from humans,
ferrets, swine, horses, chickens, ducks, guinea pigs, mice, and seals. The
serum samples were collected at intervals during prospective epidemiological
studies, from experimental and natural infections, and vaccination studies. The
decline of maternal antibodies was studied in swine and horses. The NP-ELISA
enables rapid serological diagnosis and is suited for influenza A antibody
screening, especially in species which harbor several influenza subtypes. The
HI and neuraminidase inhibition tests, however, must still be used for
subtyping.
Descriptors: antibodies, viral analysis, enzyme linked
immunosorbent assay, influenza A virus immunology, nucleoproteins immunology,
orthomyxoviridae infections immunology, viral core proteins immunology,
ferrets, hemagglutination inhibition tests, horses, avian immunology, human
immunology, porcine immunology, orthomyxoviridae infections veterinary,
poultry, prospective studies, Rodentia, seals, species specificity, specific
pathogen free organisms, swine, vaccination.
de Jong, J.C., E.C. Claas, and A.D. Osterhaus (1998).
Influenza A (H5N1) in Hong Kong: voorbode van een pandemie of alleen een
wetenschappelijk interessant verschijnsel en een nuttige oefening in pandemiologie?
[Influenza A (H5N1) in Hong Kong: forerunner of a pandemic or an only
scientifically interesting phenomenon and a useful exercise in pandemiology?].
Tijdschrift Voor Diergeneeskunde 123(9): 278-82. ISSN: 0040-7453.
NAL
Call Number: 41.8 T431
Abstract: From a three-year old boy in Hong Kong who
died in May 1997 with an extensive influenza pneumonia an influenza A virus has
been isolated which was, first at the National Influenza Centre of the
Netherlands, identified as belonging to subtype H5N1. Presumably the patient
had acquired the infection directly from an outbreak of fowl plague among
chickens. As far as is known this is the first case of the isolation of an
influenza virus belonging to one of the subtypes H4-H15 from a human influenza
patient. At the end of 1997 seventeen more cases of human A (H5N1) influenza
have been detected in Hong Kong, including five fatal cases. Genetic analyses
of seven of these virus isolates did not reveal the occurrence of reassortment
with a human or porcine influenza virus, which could have rendered the virus
potentially pandemic. Man-to-man transmission of the virus has not been
demonstrated but cannot be excluded either. This event has shown that the WHO
surveillance of influenza viruses, although perhaps not perfect, has functioned
well.
Descriptors: influenza virology, influenza A virus avian
isolation and purification, chickens, child preschool, disease outbreaks
veterinary, epidemiologic methods, fowl plague epidemiology, fowl plague
virology, influenza epidemiology, influenza transmission, avian classification,
avian genetics, poultry, poultry
diseases epidemiology, poultry diseases virology, reassortant viruses genetics,
zoonoses.
de Jong, J.C., G.F. Rimmelzwaan, R.A. Fouchier, and
A.D. Osterhaus (2000). Influenza virus: a master of metamorphosis. Journal
of Infection 40(3): 218-28. ISSN:
0163-4453.
Abstract: Novel influenza viruses continuously emerge
in the human population. Three times during the present century, an avian
influenza virus subtype crossed the species barrier, starting a pandemic, and
establishing itself for one to several decades in man. As the 1997 H5N1 event
in Hong Kong indicated, the occurrence of another pandemic in the near future
cannot be excluded. Sufficient vaccine may not be available to ameliorate the
consequences of such an event, because of a shortage of time. During
interpandemic periods, important antigenic drift variants sometimes arise at a
point of time when, with the current state of the technique, production of a correspondingly
adapted vaccine is also impossible. We may be able to solve these problems by
increasing influenza surveillance and by adopting new ways of vaccine
composition, production, formulation, presentation, and delivery. The recently
developed anti-neuraminidase antivirals should only be considered as (valuable)
adjuncts to vaccines.
Descriptors: antigenic variation, influenza epidemiology,
orthomyxoviridae genetics, disease outbreaks, hn protein genetics,
hemagglutinin glycoproteins, influenza virus genetics, influenza mortality,
influenza prevention and control, influenza vaccine therapeutic use,
orthomyxoviridae enzymology, orthomyxoviridae pathogenicity, reassortant
viruses genetics, reassortant viruses pathogenicity, virulence.
de Jong, M.D., V.C. Bach, T.Q. Phan, M.H. Vo, T.T.
Tran, B.H. Nguyen, M. Beld, T.P. Le, H.K. Truong, V.V. Nguyen, T.H. Tran, Q.H.
Do, and J. Farrar (2005). Fatal avian influenza A (H5N1) in a child
presenting with diarrhea followed by coma. New England Journal of
Medicine 352(7): 686-91. ISSN:
1533-4406.
NAL
Call Number: 448.8 N442
Descriptors: coma virology, diarrhea virology,
encephalitis, viral etiology, influenza complications, influenza A virus, avian
influenza genetics, avian influenza isolation and purification, acute disease,
child, preschool child, viral virology, fatal outcome, influenza diagnosis,
influenza virology, lung radiography, seizures virology.
Dea, S., M.A. Elazhary, and R.S. Roy (1980). Les
virus influenza chez l'homme et les animaux. Une revue de la litterature.
[Influenza viruses in man and animals. A literature review (author's transl)].
Canadian Veterinary Journal Revue Veterinaire Canadienne 21(6): 171-8.
ISSN: 0008-5286.
NAL
Call Number: 41.8 R3224
Descriptors: animals, domestic, orthomyxoviridae
infections microbiology, orthomyxoviridae infections veterinary, antigens,
viral analysis, chickens, epitopes, fowl plague microbiology, horse diseases
microbiology, horses, influenza microbiology, influenza A virus avian
immunology, human immunology, porcine immunology, mutation, recombination,
genetic, swine, swine diseases microbiology.
DeLay, P.D., H.L. Casey, and H.S. Tubiash (1967). Comparative
study of fowl plague virus and a virus isolated from man. Public Health
Reports 82(7): 615-20. ISSN:
0094-6214.
NAL
Call Number: 151.65 P96
Descriptors: influenza A virus avian immunology, orthomyxoviridae
infections immunology, viruses immunology, chick embryo, haplorhini,
hemagglutination inhibition tests, hemagglutination tests, neutralization
tests, Newcastle disease immunology, Newcastle disease virus immunology,
poultry, virus diseases immunology, virus diseases pathology.
Dem'ianenko, I.V., Z.I. Rovnova, E.I. Isaeva, and
Z.K. Chuvakova (1989 ). Antigennaia struktura gemaggliutininov virusov
grippa H1N1 (Hsw1N1), vydelennykh ot liudei i utok. [Antigenic structure of
hemagglutinins of influenza H1N1 (Hsw1N1) virus isolated from humans and ducks].
Voprosy Virusologii 34(6): 661-5.
ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: The method of specific adsorption followed by
the use of antisera in HI test and competitive enzyme immunoassay was used to
study the antigenic composition of hemagglutinins (HA) Hsw1 in influenza
viruses isolated in 1982 from humans in Bulgaria and in 1976 in Canada from
ducks as well as their antigenic relationships with HA of Hsw1 variant isolated
from swine and man. Hemagglutinins of Hsw1 strains isolated from man in
Bulgaria and Alma-Ata were found to be similar to HA of A/New Jersey/8/76 virus
in two determinants and with hemagglutinin of the classic virus of swine in
three determinants. The HA of A/duck/Alberta/35/76 virus was similar in three
determinants to HA of A/New Jersey/8/76 virus and in two determinants with
other Hsw1 variants. The similarities and differences in antigenic determinants
of HA in Hsw1 viruses isolated from man and animals attest to their common
origin and different modes of variability.
Descriptors: epitopes analysis, hemagglutinins viral
immunology, influenza A virus avian immunology, human immunology, ducks, enzyme
linked immunosorbent assay, immunosorbent techniques.
Donatelli, I., L. Campitelli, M.R. Castrucci, A.
Ruggieri, L. Sidoli, and J.S. Oxford (1991). Detection of two antigenic
subpopulations of A(H1N1) influenza viruses from pigs: antigenic drift or
interspecies transmission? Journal of Medical Virology 34(4): 248-57. ISSN: 0146-6615.
Abstract: Serological analysis of a group of 63
influenza H1N1 viruses isolated from pigs in Italy in the period 1976-1988
revealed the presence of two distinct antigenic subpopulations: some viruses
possessed a haemagglutinin indistinguishable from that of viruses typically
associated with pigs, i.e., A/New Jersey/8/76 (H1N1), whereas others showed a
close antigenic relatedness with the haemagglutinin of avian-like H1 viruses.
These findings represent further evidence that influenza A viruses from avian
species may be transmitted to mammals. The surface and internal proteins of
some of these viruses were also analyzed biochemically to evaluate the
molecular relatedness among viruses circulating in non-human hosts.
Descriptors: hemagglutinins viral immunology, influenza A
virus avian immunology, porcine immunology, orthomyxoviridae infections
veterinary, swine microbiology, swine diseases microbiology, antibodies,
monoclonal immunology, antigenic variation, electrophoresis, polyacrylamide
gel, avian isolation and purification, porcine isolation and purification,
Italy, orthomyxoviridae infections microbiology, orthomyxoviridae infections
transmission, peptide mapping, species specificity.
Dybing, J.K., S. Schultz Cherry, D.E. Swayne, D.L.
Suarez, and M.L. Perdue (2000). Distinct pathogenesis of hong kong-origin
H5N1 viruses in mice compared to that of other highly pathogenic H5 avian
influenza viruses. Journal of Virology 74(3): 1443-50.
ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: In 1997, an outbreak of virulent H5N1 avian
influenza virus occurred in poultry in Hong Kong (HK) and was linked to a
direct transmission to humans. The factors associated with transmission of
avian influenza virus to mammals are not fully understood, and the potential
risk of other highly virulent avian influenza A viruses infecting and causing
disease in mammals is not known. In this study, two avian and one human
HK-origin H5N1 virus along with four additional highly pathogenic H5 avian
influenza viruses were analyzed for their pathogenicity in 6- to 8-week-old
BALB/c mice. Both the avian and human HK H5 influenza virus isolates caused
severe disease in mice, characterized by induced hypothermia, clinical signs,
rapid weight loss, and 75 to 100% mortality by 6 to 8 days postinfection. Three
of the non-HK-origin isolates caused no detectable clinical signs. One isolate,
A/tk/England/91 (H5N1), induced measurable disease, and all but one of the
animals recovered. Infections resulted in mild to severe lesions in both the
upper and lower respiratory tracts. Most consistently, the viruses caused
necrosis in respiratory epithelium of the nasal cavity, trachea, bronchi, and
bronchioles with accompanying inflammation. The most severe and widespread
lesions were observed in the lungs of HK avian influenza virus-infected mice,
while no lesions or only mild lesions were evident with A/ck/Scotland/59 (H5N1)
and A/ck/Queretaro/95 (H5N2). The A/ck/Italy/97 (H5N2) and the A/tk/England/91
(H5N1) viruses exhibited intermediate pathogenicity, producing mild to moderate
respiratory tract lesions. In addition, infection by the different isolates
could be further distinguished by the mouse immune response. The non-HK-origin
isolates all induced production of increased levels of active transforming
growth factor beta following infection, while the HK-origin isolates did not.
Descriptors: influenza virology, influenza A virus avian
pathogenicity, human pathogenicity, hn protein, Hong Kong,
immunohistochemistry, influenza pathology, avian isolation and purification,
avian physiology, human isolation and purification, human physiology, mice,
mice inbred BALB c, respiratory system pathology, respiratory system virology,
transforming growth factor beta blood, virulence, virus replication.
Easterday, B., W.G. Laver, H.G. Pereira, and G.C.
Schild (1969). Antigenic composition of recombinant virus strains produced
from human and avian influenza A viruses. Journal of General Virology
5(1): 83-91. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Descriptors: antigens analysis, neuraminidase analysis,
orthomyxoviridae analysis, orthomyxoviridae immunology, recombination, genetic,
electrophoresis, hemagglutination inhibition tests, hemagglutinins viral
analysis, hybridization, genetic, immunodiffusion, influenza A virus avian.
Edwards, L.E., D.C. Nguyen, X. Lu, H. Hall, A.
Balish, J.E. Mabry, W. Lim, N.J. Cox, A. Klimov, and J.M. Katz (2004). Antigenic
characteristics of recent avian influenza A H5N1 viruses isolated from humans.
International Congress Series 1263: 109-113.
Abstract: Background: In February 2003, highly
pathogenic avian influenza A H5N1 viruses reemerged in humans. Despite repeated
outbreaks in domestic poultry in Hong Kong since 1999, this was the first
isolation of H5N1 from humans since the outbreak in Hong Kong in 1997, which
resulted in 18 human cases and 6 deaths. Methods: To better understand the
antigenic relationship between the 2003 H5N1 human virus A/Hong Kong/213/03
(HK/213) and other H5 viruses, post-infection ferret sera or post-infection
human sera were tested for reactivity by hemagglutination-inhibition and
microneutralization assays with H5N1 viruses circulating in Hong Kong or
elsewhere in Asia since 1997. Results: The H5N1 virus isolated from a 9-year-old
male in Hong Kong was antigenically distinguishable from recent H5N1 viruses
isolated from wild birds in Hong Kong and from the human 1997 H5N1 viruses,
using post-infection ferret sera. Likewise, sera from this case patient,
collected 22 days post-symptom onset, reacted to high titers with the
homologous HK/213 virus, but gave eightfold lower titers with A/Hong
Kong/156/97, and other H5 viruses. Conclusion: These results suggest that this
recent human H5N1 virus is antigenically distinguishable from current and
previously circulating H5N1 viruses from Asia, including the viruses previously
isolated from humans.
Descriptors: influenza H5N1, antigenicity, serology.
Eiros Bouza, J.M. (2004). Sindrome agudo
respiratorio grave y gripe aviar [Severe acute respiratory syndrome and avian
flu]. Anales De La Real Academia Nacional De Medicina 121(2):
263-88. ISSN: 0034-0634.
Abstract: Severe acute respiratory syndrome (SARS) is a
new disease that caused large ourbreaks in several countries in the first half
of 2003, resulting in infection in more than 8.000 people and more than 900
deaths. The disease originated in southern China and a novel coronavirus (SARS
CoV) has been implicated as the causative organism. We present an overview of
the etiology, clinical presentation and diagnosis, based on the current state
of knowledge derived from published studies and our experience in the National
Microbiology Centre. Influenza is a zoonosis. This appreciation of influenza
ecology facilitated recognition of the H5N1 'bird flu' incident in Hong Kong in
1997 in what was considered to be an incipient pandemic situation, the chicken
being the source of virus for humans and. The current outbreak of avian
influenza in South East Asia has resulted in a small number of human deaths.
These findings highlight the importance of systematic virus surveillance of
domestic poultry in recognizing changes in virus occurrence, host range and
pathogenicity as signals at the avian level that could presage a pandemic.
Descriptors: disease outbreaks, avian influenza
epidemiology, severe acute respiratory syndrome diagnosis, severe acute
respiratory syndrome etiology, severe acute respiratory syndrome virology,
southeastern Asia epidemiology, China epidemiology, diagnosis, avian influenza mortality,
avian influenza virology, middle aged adult.
Englund, L. (1996). The pathogenesis of avian
influenza infection in mink (Mustela vison). In: Research and
Development for Animal Health, Statens Veterinaermedicinska Anstalt:
Uppsala (Sweden), p. 96-97. ISBN: 91-972469-0-5.
Descriptors: minks, viroses, avian influenza virus,
pathogenesis, Carnivora, infectious diseases, influenza virus, mammals,
Mustelidae, orthomyxoviridae, viruses.
Englund, L. (2000). Studies on influenza viruses
H10N4 and H10N7 of avian origin in mink. Veterinary Microbiology
74(1-2): 101-107. ISSN: 0378-1135.
NAL
Call Number: SF601.V44
Abstract: An influenza A virus, A/mink/Sweden/84
(H10N4), was isolated from farmed mink during an outbreak of respiratory
disease, histopathologically characterised by severe interstitial pneumonia.
The virus was shown to be of recent avian origin and closely related to
concomitantly circulating avian influenza virus. Serological investigations
were used to link the isolated virus to the herds involved in the disease
outbreak. Experimental infection of adult mink with the virus isolate from the
disease outbreak reproduced the disease signs and pathological lesions observed
in the field cases. The mink influenza virus also induced an antibody response
and spread between mink by contact. The same pathogenesis in mink was observed
for two avian influenza viruses of the H10N4 subtype, circulating in the avian
population. When mink were infected with the prototype avian H10 influenza
virus, A/chicken/Germany/N/49, H10N7, the animals responded with antibody
production and mild pulmonary lesions but neither disease signs nor contact
infections were observed. Detailed studies, including demonstration of viral
antigen in situ by immunohistochemistry, of the sequential development of
pathological lesions in the mink airways after aerosol exposure to H10N4 or
H10N7 revealed that the infections progress very similarly during the first 24
h, but are distinctly different at later stages. The conclusion drawn is that
A/mink/Sweden/84, but not A/chicken/Germany/N/49, produces a multiple-cycle
replication in mink airways. Since the viral distribution and pathological
lesions are very similar during the initial stages of infection we suggest that
the two viruses differ in their abilities to replicate and spread within the
mink tissues, but that their capacities for viral adherence and entry into mink
epithelial cells are comparable.
Descriptors: animal husbandry, infection, respiratory
system, influenza A virus infection, transmission, viral disease, pneumonia,
interstitial, respiratory system disease, severe, respiratory disease,
respiratory system disease, immunohistochemistry immunohistochemical, immunocytochemical
techniques, analytical method, antibody response viral adherence.
Englund, L. and C. Hard af Segerstad (1998). Two
avian H10 influenza A virus strains with different pathogenicity for mink (Mustela
vison). Archives of Virology 143(4): 653-66. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: We compared two strains of avian influenza A
viruses of subtype H10 by exposing mink to aerosols of A/mink/Sweden/3,900/84
(H10N4) naturally pathogenic for mink, or A/chicken/Germany/N/49, (H10N7).
Lesions in the respiratory tract during the first week after infection were
studied and described. Both virus strains caused inflammatory reactions in the
lungs and antibody production in exposed mink but only mink/84 virus was
reisolated. The lesions caused by mink/84 virus were more severe with higher
area density of pneumonia, lower daily weight gain, and more virus in the
tissues detected by immunohistochemistry. The results indicate that mink/84
(H10N4), but not chicken/49 virus (H10N7), established multiple cycle
replication in infected cells in the mink.
Descriptors: influenza veterinary, influenza A virus avian
pathogenicity, mink virology, antibodies, viral analysis, influenza
physiopathology, influenza virology, lung virology, nasal mucosa virology,
species specificity.
Englund, L., B. Klingeborn, and T. Mejerland (1986). Avian
influenza A virus causing an outbreak of contagious interstitial pneumonia in
mink. Acta Veterinaria Scandinavica 27(4): 497-504. ISSN: 0044-605X.
NAL
Call Number: 41.8 AC87
Descriptors: disease outbreaks veterinary, influenza A
virus avian pathogenicity, mink microbiology, veterinary viral pneumonia viral
pneumonia epidemiology, viral pneumonia microbiology, viral pneumonia
pathology, Sweden.
Enserink, M. (2004). Influenza: girding for
disaster. Looking the pandemic in the eye. Science 306(5695):
392-4. ISSN: 1095-9203.
NAL
Call Number: 470 Sci2
Descriptors: disease outbreaks, influenza epidemiology,
world health, cost of illness, influenza transmission, influenza virology,
avian pathogenicity, influenza A virus, avian physiology, influenza vaccines
administration and dosage, influenza vaccines supply and distribution, models,
biological, orthomyxoviridae pathogenicity, orthomyxoviridae physiology, public
health, reassortant viruses.
Fang, R., W. Min Jou, D. Huylebroeck, R. Devos, and
W. Fiers (1981). Complete structure of A/duck/Ukraine/63 influenza
hemagglutinin gene: animal virus as progenitor of human H3 Hong Kong 1968
influenza hemagglutinin. Cell 25(2): 315-23. ISSN: 0092-8674.
NAL
Call Number: QH573.C42
Descriptors: genes viral, hemagglutinins viral genetics,
influenza A virus avian genetics, influenza A virus human genetics, amino acid
sequence, base sequence, cloning, molecular, ducks microbiology, epitopes,
hemagglutinins viral immunology, influenza A virus avian immunology, influenza
A virus human immunology, mutation.
Fanning, T.G., R.D. Slemons, A.H. Reid, T.A.
Janczewski, J. Dean, and J.K. Taubenberger (2002). 1917 avian influenza
virus sequences suggest that the 1918 pandemic virus did not acquire its
hemagglutinin directly from birds. Journal of Virology 76(15):
7860-2. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Wild waterfowl captured between 1915 and 1919
were tested for influenza A virus RNA. One bird, captured in 1917, was infected
with a virus of the same hemagglutinin (HA) subtype as that of the 1918
pandemic virus. The 1917 HA is more closely related to that of modern avian
viruses than it is to that of the pandemic virus, suggesting (i) that there was
little drift in avian sequences over the past 85 years and (ii) that the 1918
pandemic virus did not acquire its HA directly from a bird.
Descriptors: birds virology, evolution, molecular,
hemagglutinin glycoproteins, influenza virus genetics, influenza history,
influenza A virus avian genetics, influenza A virus human genetics, fowl plague
history, fowl plague virology, hemagglutinin glycoproteins, influenza virus
history, history of medicine, 20th century, influenza epidemiology, influenza
virology, molecular sequence data,
phylogeny, RNA viral genetics, viral history, sequence analysis, DNA.
Feldmann, H., E. Kretzschmar, B. Klingeborn, R. Rott,
H.D. Klenk, and W. Garten (1988). The structure of serotype H10 hemagglutinin
of influenza A virus: comparison of an apathogenic avian and a mammalian strain
pathogenic for mink. Virology 165(2): 428-37. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The primary structure of the hemagglutinin of
the apathogenic avian influenza virus A/chick/Germany/N/49 (H10N7) and of the
serologically related strain A/mink/Sweden/84 (H10N4) pathogenic for mink has
been elucidated by nucleotide sequence analysis, and the carbohydrates attached
to the polypeptide have been determined. The H10 hemagglutinin has 65, 52, 46,
45, and 44% amino acid sequence homology with serotypes H7, H3, H1, H2, and H5,
respectively. H10 and H7 hemagglutinins are also most closely related in their
glycosylation patterns. There is a high sequence homology between both H10
strains supporting the concept that the mink virus has obtained its
hemagglutinin from an avian strain. The sequence homology includes the cleavage
site which consists of a single arginine as is the case with most other
hemagglutinins exhibiting low susceptibility to proteolytic activation. The
similarity in hemagglutinin structure between both H10 strains is discussed in
light of the distinct differences in the pathogenicity of both viruses.
Descriptors: hemagglutinins viral genetics, influenza A
virus genetics, amino acid sequence, base sequence, carbohydrates analysis,
chickens microbiology, glycosylation, hemagglutinins viral analysis, influenza
A virus immunology, mink microbiology, molecular sequence data, sequence
homology, nucleic acid.
Fiszon, B., C. Hannoun, A. Garcia Sastre, E. Villar,
and J.A. Cabezas (1989). Comparison of biological and physical properties of
human and animal A(H1N1) influenza viruses. Research in Virology
140(5): 395-404. ISSN: 0923-2516.
NAL
Call Number: QR355.A44
Abstract: The study of biological properties of
influenza virus strains belonging to the same subtype A(H1N1) and closely
antigenically related, but isolated from different animal species (man, pig and
duck), demonstrated that avian strains were more resistant than those isolated
from mammals to high temperature and low pH, as shown by titration of residual
infectivity in cell cultures (MDCK) and by sialidase assay. The difference in
behaviour could be correlated to biological adaptation of the virus to its
host. Avian body temperature is 40 degrees C and influenza virus, in ducks, is
enterotropic and therefore capable of passing through the low pH values in the
upper digestive tract of the animal. These results do not contradict the
hypothesis of a possible filiation between avian and mammalian
orthomyxoviruses.
Descriptors: influenza A virus physiology, body
temperature, cell line, ducks, hemagglutination tests, hydrogen-ion
concentration, influenza A virus avian enzymology, avian growth and
development, avian physiology, human enzymology, human growth and development,
human physiology, porcine enzymology, porcine growth and development, porcine
physiology, influenza A virus enzymology, influenza A virus growth and
development, neuraminidase analysis, plaque assay, swine, temperature, virus
replication.
Fleck, F. (2004). Avian flu virus could evolve
into dangerous human pathogen, experts fear. Bulletin of the World
Health Organization 82(3): 236-7.
ISSN: 0042-9686.
NAL
Call Number: 449.9 W892B
Descriptors: influenza epidemiology, influenza A virus,
avian pathogenicity, zoonoses, Asia, birds.
Fomsgaard, A., P.C. Grauballe, and S.O. Glismann
(2004). Risiko for en ny influenzapandemi? [Risk of a new influenza
pandemic?]. Ugeskrift for Laeger 166(10): 912-5. ISSN: 0041-5782.
Descriptors: disease outbreaks prevention and control,
influenza epidemiology, influenza A virus classification, influenza A virus
genetics, influenza A virus pathogenicity, zoonoses virology, birds,
communicable disease control, influenza prevention and control, influenza
transmission, avian influenza transmission, poultry, world health, zoonoses
transmission.
Fouchier, R.A., G.F. Rimmelzwaan, T. Kuiken, and A.D.
Osterhaus (2005). Newer respiratory virus infections: human metapneumovirus,
avian influenza virus, and human coronaviruses. Current Opinion in
Infectious Diseases 18(2): 141-6.
ISSN: 0951-7375.
Abstract: PURPOSE OF REVIEW: Recently, several
previously unrecognized respiratory viral pathogens have been identified and
several influenza A virus subtypes, previously known to infect poultry and wild
birds, were transmitted to humans. Here we review the recent literature on
these respiratory viruses. RECENT FINDINGS: Human metapneumovirus has now been
detected worldwide, causing severe respiratory tract illnesses primarily in
very young, elderly and immunocompromised individuals. Animal models and
reverse genetic techniques were designed for human metapneumovirus, and the
first vaccine candidates have been developed. Considerable genetic and
antigenic diversity was observed for human metapneumovirus, but the implication
of this diversity for vaccine development and virus epidemiology requires
further study. Two previously unrecognized human coronaviruses were discovered
in 2004 in The Netherlands and Hong Kong. Their clinical impact and epidemiology
are largely unknown and warrant further investigation. Several influenza A
virus subtypes were transmitted from birds to humans, and these viruses
continue to constitute a pandemic threat. The clinical symptoms associated with
these zoonotic transmissions range from mild respiratory illnesses and
conjunctivitis to pneumonia and acute respiratory distress syndrome, sometimes
resulting in death. More basic research into virus ecology and evolution and
development of effective vaccines and antiviral strategies are required to
limit the impact of influenza A virus zoonoses and the threat of an influenza
pandemic. SUMMARY: Previously unknown and emerging respiratory viruses are an
important threat to human health. Development of virus diagnostic tests,
antiviral strategies, and vaccines for each of these pathogens is crucial to
limit their impact.
Descriptors: coronavirus infections epidemiology,
influenza virology, avian influenza A virus, metapneumovirus, paramyxoviridae
infections epidemiology, respiratory tract infections virology, emerging
communicable diseases, disease outbreaks, influenza epidemiology, risk factors,
paramyxoviridae infections virology, coronavirus infections virology, influenza
epidemiology.
Fouchier, R.A., P.M. Schneeberger, F.W. Rozendaal,
J.M. Broekman, S.A. Kemink, V. Munster, T. Kuiken, G.F. Rimmelzwaan, M.
Schutten, G.J. Van Doornum, G. Koch, A. Bosman, M. Koopmans, and A.D. Osterhaus
(2004). Avian influenza A virus (H7N7) associated with human conjunctivitis
and a fatal case of acute respiratory distress syndrome. Proceedings of
the National Academy of Sciences of the United States of America 101(5):
1356-61. ISSN: 0027-8424.
NAL
Call Number: 500 N21P
Abstract: Highly pathogenic avian influenza A viruses
of subtypes H5 and H7 are the causative agents of fowl plague in poultry.
Influenza A viruses of subtype H5N1 also caused severe respiratory disease in
humans in Hong Kong in 1997 and 2003, including at least seven fatal cases,
posing a serious human pandemic threat. Between the end of February and the end
of May 2003, a fowl plague outbreak occurred in The Netherlands. A highly
pathogenic avian influenza A virus of subtype H7N7, closely related to low
pathogenic virus isolates obtained from wild ducks, was isolated from chickens.
The same virus was detected subsequently in 86 humans who handled affected
poultry and in three of their family members. Of these 89 patients, 78
presented with conjunctivitis, 5 presented with conjunctivitis and
influenza-like illness, 2 presented with influenza-like illness, and 4 did not
fit the case definitions. Influenza-like illnesses were generally mild, but a
fatal case of pneumonia in combination with acute respiratory distress syndrome
occurred also. Most virus isolates obtained from humans, including probable
secondary cases, had not accumulated significant mutations. However, the virus
isolated from the fatal case displayed 14 amino acid substitutions, some of
which may be associated with enhanced disease in this case. Because H7N7 viruses
have caused disease in mammals, including horses, seals, and humans, on several
occasions in the past, they may be unusual in their zoonotic potential and,
thus, form a pandemic threat to humans.
Descriptors: conjunctivitis etiology, fowl plague epidemiology,
influenza A virus avian isolation and purification, respiratory distress
syndrome, adult etiology, amino acid sequence, birds, disease outbreaks, fatal
outcome, fowl plague virology, hemagglutinin glycoproteins, influenza virus
chemistry, influenza A virus avian classification, middle aged, molecular
sequence data, Netherlands epidemiology, respiratory distress syndrome, adult
pathology.
Fukumi, H., K. Nerome, M. Nakayama, and M. Ishida
(1977). Serological and virological investigations fo orthomyxovirus in
birds in South-East Asian area. Developments in Biological
Standardization 39: 475-60. ISSN:
0301-5149.
NAL
Call Number: QR180.3.D4
Abstract: We have previously reported that some species
of migrating ducks (pintail, mallard, widgeon and falcated teal) possess in
their sera antibodies against H antigens of human or avian influenza viruses.
Such findings have also been reported from other workers, and the appearance of
new types of influenza viruses accompanied by outbreaks of new influenza pandemics,
or circulation of influenza virus antigens in animals, birds and humans have
been discussed on the basis of such findings. Recently a number of
orthomyxoviruses have been isolated from wild birds such as myna, banded
parakeets, etc. imported from India and some areas of South-East Asia. Some of
them have H antigens not recognized previously, and some are found to have more
or less common reactions with human H3 antigen, and consequently antigens Hav 7
and Heq 2, which are known to show cross-reaction with H3. The significance of
such a fact in connection with the appearance of a new influenza pandemic is
discussed.
Descriptors: antibodies, viral, birds microbiology,
influenza A virus avian immunology, Asia, Southeastern, ducks, hemagglutinins
viral, influenza A virus avian isolation and purification, Japan, neuraminidase
immunology.
Gandolfi, P. (2004). Influenza aviaria ed epidemia
nei Paesi del sud-est asiatico. [Avian influenza and the epidemic in the
countries of South East Asia]. Rivista Di Avicoltura 73(3):
26-32. ISSN: 1722-6945.
NAL
Call Number: 47.8 R523
Descriptors: avian influenza virus, disease control,
epidemic, poultry, zoonoses, South East Asia.
Gao, P., S. Watanabe, T. Ito, H. Goto, K. Wells, M.
McGregor, A.J. Cooley, and Y. Kawaoka (1999). Biological heterogeneity,
including systemic replication in mice, of H5N1 influenza A virus isolates from
humans in Hong Kong. Journal of Virology 73(4): 3184-9. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: An H5N1 avian influenza A virus was
transmitted to humans in Hong Kong in 1997. Although the virus causes systemic
infection and is highly lethal in chickens because of the susceptibility of the
hemagglutinin to furin and PC6 proteases, it is not known whether it also
causes systemic infection in humans. The clinical outcomes of infection in Hong
Kong residents ranged widely, from mild respiratory disease to multiple organ
failure leading to death. Therefore, to understand the pathogenesis of
influenza due to these H5N1 isolates, we investigated their virulence in mice.
The results identified two distinct groups of viruses: group 1, for which the
dose lethal for 50% of mice (MLD50) was between 0.3 and 11 PFU, and group 2,
for which the MLD50 was more than 10(3) PFU. One day after intranasal
inoculation of mice with 100 PFU of group 1 viruses, the virus titer in lungs
was 10(7) PFU/g or 3 log units higher than that for group 2 viruses. Both types
of viruses had replicated to high titers (>10(6) PFU/g) in the lungs by day
3 and maintained these titers through day 6. More importantly, only the group 1
viruses caused systemic infection, replicating in nonrespiratory organs,
including the brain. Immunohistochemical analysis demonstrated the replication
of a group 1 virus in brain neurons and glial cells and in cardiac myofibers.
Phylogenetic analysis of all viral genes showed that both groups of Hong Kong
H5N1 viruses had formed a lineage distinct from those of other viruses and that
genetic reassortment between H5N1 and H1 or H3 human viruses had not occurred.
Since mice and humans harbor both the furin and the PC6 proteases, we suggest
that the virulence mechanism responsible for the lethality of influenza viruses
in birds also operates in mammalian hosts. The failure of some H5N1 viruses to
produce systemic infection in our model indicates that multiple,
still-to-be-identified, factors contribute to the severity of H5N1 infection in
mammals. In addition, the ability of these viruses to produce systemic infection
in mice and the clear differences in pathogenicity among the isolates studied
here indicate that this system provides a useful model for studying the
pathogenesis of avian influenza virus infection in mammals.
Descriptors: genes viral, influenza virology, influenza A
virus physiology, variation genetics, Hong Kong epidemiology,
immunohistochemistry, influenza epidemiology, mice, phylogeny, virus
replication genetics.
Geisler, B., W. Seidel, B. Herrmann, and L. Dohner
(1986). Differences of nucleoproteins of human and avian influenza A virus
strains shown by polyacrylamide gel electrophoresis and by the peptide mapping
technique. Archives of Virology 90(3-4): 289-99. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Electrophoretic mobility differences in
polyacrylamide gels were detected between (35S)-methionine-labelled
nucleoproteins (NPs) induced in monolayer cells by 15 human and 4 avian
reference strains of influenza viruses. The (35S)-methionine-labelled tryptic
peptides of nucleoproteins of these strains were also analyzed by peptide
mapping technique. Based on several detectable hydrophilic peptides the NPs
could be arranged in 7 clearly differentiable groups. After radioiodination of
NPs from 4 human and 3 avian reference strains the tryptic peptide patterns
showed one clear difference between human and avian strains.
Descriptors: influenza A virus analysis, nucleoproteins
analysis, viral proteins analysis, electrophoresis, polyacrylamide gel,
influenza A virus avian analysis, influenza A virus avian genetics, influenza A
virus human analysis, influenza A virus human genetics, influenza A virus
genetics, peptide fragments analysis, variation genetics.
Geraci, J.R., D.J. St Aubin, I.K. Barker, V.S.
Hinshaw, R.G. Webster, and H.L. Ruhnke (1984). Susceptibility of grey (Halichoerus
grypus) and harp (Phoca groenlandica) seals to the influenza virus
and mycoplasma of epizootic pneumonia of harbor seals (Phoca vitulina).
Canadian Journal of Fisheries and Aquatic Sciences 41(1): 151-156. ISSN: 0706-652X.
NAL
Call Number: 442.9 C16J
Descriptors: influenza virus, experimental infection,
surveys, pneumonia, mycoplasmosis, Halichoerus grypus, Phoca
groenlandica, Phoca vitulina.
Gerber, A., C. Sauter, and J. Lindenmann (1973). Fowl
plague virus adapted to human epithelial tumor cells and human myeloblasts in
vitro. I. Characteristics and replication in monolayer cultures. Archiv
Fur Die Gesamte Virusforschung 40(1): 137-51. ISSN: 0003-9012.
NAL
Call Number: 448.3 Ar23
Descriptors: influenza A virus avian growth and
development, virus cultivation, virus replication, bone marrow microbiology,
bone marrow cells, carcinoma, bronchogenic, cell line, chick embryo, clone
cells, cytological techniques, cytopathogenic effect, viral, diploidy,
epithelial cells, epithelium microbiology, fibroblasts microbiology, HeLa
cells, hemagglutination inhibition tests, leukemia, myelocytic, acute, plaque
assay.
Gerber, A., C. Sauter, and J. Lindenmann (1973). Fowl
plague virus adapted to human epithelial tumor cells and human myeloblasts in
vitro. II. Replication in human leukemic myoloblast cultures. Archiv Fur
Die Gesamte Virusforschung 40(3): 255-64.
ISSN: 0003-9012.
NAL
Call Number: 448.3 Ar23
Descriptors: bone marrow microbiology, bone marrow cells,
influenza A virus avian growth and development, leukemia, myelocytic, acute
microbiology, virus replication, adult, aged, cultured cells, hemadsorption,
influenza A virus avian pathogenicity, middle aged, virulence, virus
cultivation.
Ghendon, Y., A. Klimov, O. Blagoveshenskaya, and D.
Genkina (1979). Investigation of recombinants of human influenza and fowl
plague viruses. Journal of General Virology 43(1): 183-91. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: Recombinants of human influenza type A
viruses, A/Krasnodar/101/1959 (H2N2) or A/Habarovsk/15/1976 (H3N2), and fowl
plague virus (FPV), strain Weybridge (Hav1Neq1) were obtained. The genome of
the recombinant obtained by recombination of influenza A/Habarovsk/15/1976
virus and FPV contained the genes 4 (HA) and 6 (NA) derived from the influenza
A/Habarovsk virus and all the other genes [1, 2, 3, 5 (NP), 7 (M), 8 (NS)] from
FPV. The genome of the recombinant of A/Krasnodar/101/1959 virus and FPV
contained the genes 2, 4 (HA) and 6 (NA) derived from influenza A/Krasnodar
virus and all the other genes [1, 3, 5, (NP), 7 (M), 8 (NS)] from FPV. The
recombinants, like FPV, gave high virus yields in chick embryos and could
multiply at high temperatures (40 and 42 degrees C), but, like human influenza
viruses, were non-pathogenic for chickens and did not replicate in chick embryo
fibroblast culture, but did replicate in a human conjunctiva cell line, clone
1-5C-4. The virion transcriptase of the recombinants, in a number of properties
determined in vitro, was similar to FPV transcriptase but not to the human
influenza virus enzyme.
Descriptors: influenza A virus avian genetics, influenza A
virus human genetics, recombination, genetic, chick embryo, influenza A virus
avian analysis, influenza A virus human analysis, peptides analysis, RNA viral
analysis, viral proteins analysis, virus replication.
Ginzburg, V.P., E.E. Rosina, O.K. Sharova, and Y.Z.
Ghendon (1982). The replication of influenza A viruses in organ cultures of
human nasal polyps. Archives of Virology 74(4): 293-8. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Organ cultures of human nasal polyps were
shown to support the replication of five out of seven human influenza A viruses
and three out of six avian strains with varying degrees of efficiency. The
ability to replicate was independent of the antigenic formula of the virus. The
structure of nasal polyps closely resembled that of normal nasal mucosa and
infection with influenza A virus resulted in histological changes analogous to
those seen in natural infections. This system provides an in vitro method for
more detailed studies of influenza A virus and possibly other respiratory virus
infections of man.
Descriptors: influenza microbiology, influenza A virus
physiology, nasal polyps microbiology, virus replication, influenza A virus
avian physiology, influenza A virus human physiology, organ culture, species
specificity.
Ginzburg, V.P., E.E. Rozina, O.K. Sharova, and Y.U.Z.
Ghendon (1985). Reproduction of human and animal influenza viruses in human
nasal polyp organ cultures. Acta Virologica 29(5): 424-7. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: Human influenza virus strains were easily
grown and passaged in human nasal polyp organ cultures causing marked damage of
the epithelium. Unlike to human strains, the animal influenza virus strain
could be propagated for no longer than 2 or 3 passages and even the 1st passage
failed to cause significant morphological changes of the epithelium cells.
Descriptors: influenza A virus avian growth and
development, influenza A virus human growth and development, influenza A virus
growth and development, nasal polyps microbiology, DNA replication, deer,
influenza A virus genetics, nasal polyps pathology, organ culture, species
specificity, virus replication.
Gourreau, J.M., C. Kaiser, M. Valette, A.R. Douglas,
J. Labie, and M. Aymard (1994). Isolation of two H1N2 influenza viruses from
swine in France. Archives of Virology 135(3-4): 365-82. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Samples collected in 1987 and 1988 in
Brittany from influenza-infected swine made it possible to isolate and
antigenically characterize two H1N2 recombinant viruses (Sw/France/5027/87 and
Sw/France/5550/88). The former virus was cloned and reinoculated to swine to
allow reproduction of the disease and reisolation of a strain similar to the
original one. The serodiagnostic tests carried out on both the original sera
and those from the experimentally infected animals confirmed that the virus was
actually type Sw/H1N2.
Descriptors: influenza A virus, porcine isolation and
purification, swine virology, antibodies, monoclonal, antibody formation,
antigens, viral analysis, birds, cloning, molecular, France, influenza
immunology, influenza A virus avian classification, influenza A virus avian
isolation and purification, influenza A virus human classification, influenza A
virus human isolation and purification, influenza A virus, porcine genetics, influenza A virus, porcine immunology,
variation genetics.
Govorkova, E.A., V.M. Kibardin, A.A. Kizina, G.M.
Nazarova, and I.U.A. Smirnov (1991). Vzaimosviazi virusov grippa A(H2)
cheloveka i ptits, opredeliaemye matematicheskoi obrabotkoi dannykh ob
antigennoi strukture gemagglutinina. [The interrelations of the human and avian
influenza viruses A(H2) determined by the mathematical processing of data on
the antigenic structure of their hemagglutinin]. Voprosy Virusologii
36(6): 463-7. ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Mathematical methods were used to analyse the
data on the antigenic specificity of H2 subtype hemagglutinin of human and
avian influenza A viruses. This approach allowed the evaluation of possible
evolutional relationships in this little-studied group of viruses. Influenza A
(H2) viruses isolated from birds in the USA were found to represent a
sufficiently isolated group, whereas European avian strains
(A/duck/Germany/1215/73, A/pintail duck/Primor'e/695/76, A/duck/Marseilles/46/76)
were close to "human" viruses. The A/Leningrad/1468/65, A/laughing
gull/New Jersey/75/85, and A/pintail duck/Alberta/2728/77 strains represent
marked antigenic variants apparently rather far gone as a result of
hemagglutinin drift.
Descriptors: antigens, viral immunology, hemagglutinins
viral immunology, influenza A virus avian immunology, influenza A virus human
immunology, algorithms, antigenic variation immunology, antigens, viral
classification, cluster analysis, ducks microbiology, evolution, hemagglutinins
viral classification, influenza A virus avian classification, influenza A virus
human classification.
Govorkova, E.A. and Y.U.A. Smirnov (1997). Cross-protection
of mice immunized with different influenza A (H2) strains and challenged with
viruses of the same HA subtype. Acta Virologica 41(5): 251-7. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: Cross-protection of mice immunized with
inactivated preparations of human and avian influenza A (H2) viruses was
determined after lethal infection with mouse-adapted (MA) variants of human
A/Jap x Bell/57 (H2N1) and avian A/NJers/78 (H2N3) viruses. The MA variants
differed from the original strains by acquired virulence for mice and changes
in the HA antigenicity. These studies indicated that mice vaccinated with human
influenza A (H2) viruses were satisfactorily protected against challenge with
A/Jap x Bell/57-MA variant; the survival rate was in the range of 61%-88.9%.
Immunization of mice with the same viral preparations provided lower levels of
protection against challenge with A/NJers/78-MA variant. Vaccination of mice
with the avian influenza A (H2) viruses induced better protection than with
human strains against challenge with both MA variants. Challenge with A/NJers/78-MA
variant revealed that 76.2%-95.2% of animals were protected when vaccinated
with avian influenza virus strains isolated before 1980, and that the
protection reached only 52.4%-60.0% in animals vaccinated with strains isolated
in 1980-1985. The present study revealed that cross-protection experiments in a
mouse model could provide necessary information for the development of
appropriate influenza A (H2) virus vaccines with a potential for these viruses
to reappear in a human population.
Descriptors: influenza prevention and control, influenza A
virus avian immunology, influenza A virus human immunology, influenza vaccine
immunology, cross reactions, disease models, animal, influenza mortality,
influenza A virus avian classification, influenza A virus avian pathogenicity,
influenza A virus human classification, influenza A virus human pathogenicity,
mice, vaccination, vaccines, attenuated immunology.
Guan, Y., J.S.M. Peiris, A.S. Lipatov, T.M. Ellis,
K.C. Dyrting, S. Krauss, L.J. Zhang, R.G. Webster, and K.F. Shortridge (2002). Emergence
of multiple genotypes of H5N1 avian influenza viruses in Hong Kong SAR. Proceedings
of the National Academy of Sciences of the United States of America 99(13):
8950-8955. ISSN: 0027-8424.
NAL
Call Number: 500 N21P
Abstract: Although A/Hong Kong/156/97 (H5N1/97)-like
viruses associated with the "bird flu" incident in Hong Kong SAR have
not been detected since the slaughter of poultry in 1997, its putative
precursors continue to persist in the region. One of these, Goose/Guangdong/1/96
(H5N1 Gs/Gd)-like viruses, reassorted with other avian viruses to generate
multiple genotypes of H5N1 viruses that crossed to chickens and other
terrestrial poultry from its reservoir in geese. Whereas none of these recent
reassortants had acquired the gene constellation of H5N1/97, these events
provide insight into how such a virus may have been generated. The recent H5N1
reassortants readily infect and kill chicken and quail after experimental
infection, and some were associated with significant mortality of chickens
within the poultry retail markets in Hong Kong. Some genotypes are lethal for
mice after intra-nasal inoculation and spread to the brain. On this occasion,
the early detection of H5N1 viruses in the retail, live poultry markets led to
preemptive intervention before the occurrence of human disease, but these newly
emerging, highly pathogenic H5N1 viruses provide cause for pandemic concern.
Descriptors: avian influenza virus, genotypes, genes,
viral hemagglutinins, sialidase, nucleotide sequences, phylogenetics, strains,
isolation, abattoirs, chickens, geese, ducks, pheasants, pathogenicity,
experimental infections, mice, quails, hemagglutination inhibition test, amino
acid sequences, Hong Kong, molecular sequence data, gene reassortants.
Guan, Y., J.S.M. Peiris, L.L.M. Poon, K.C. Dyrting,
T.M. Ellis, L. Sims, R.G. Webster, and K.F. Shortridge (2003). Reassortants
of H5N1 influenza viruses recently isolated from aquatic poultry in Hong Kong
SAR. Avian Diseases 47(Special Issue): 911-913. ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: The H5N1 virus (H5N1/97) that caused the bird
flu incident in Hong Kong in 1997 has not been isolated since the poultry
slaughter in late 1997. But the donor of its H5 hemagglutinin gene,
Goose/Guangdong/1/96-like (Gs/Gd/96-like) virus, established a distinct lineage
and continued to circulate in geese in the area. In 2000, a virus from the
Goose/Guangdong/1/96 lineage was isolated for the first time from domestic
ducks. Subsequently, it has undergone reassortment, and these novel
reassortants now appear to have replaced Gs/Gd/96-like viruses from its
reservoir in geese and from ducks. The internal gene constellation is also
different from H5N1/97, but these variants have the potential for further
reassortment events that may allow the interspecies transmission of the virus.
Descriptors: epidemiology, infection, avian influenza,
infectious disease, respiratory system disease, viral disease, interspecies
viral transmission, viral lineage, viral reservoir.
Guan, Y., M. Peiris, K.F. Kong, K.C. Dyrting, T.M.
Ellis, T. Sit, L.J. Zhang, and K.F. Shortridge (2002). H5N1 influenza
viruses isolated from geese in Southeastern China: evidence for genetic
reassortment and interspecies transmission to ducks. Virology
292(1): 16-23. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The H5N1 viruses (H5N1/97) associated with
the "bird-flu" incident in the Hong Kong SAR have not been isolated
since the slaughter of poultry in December 1997 brought that outbreak to an
end. Recent evidence points to this virus as having arisen through a
reassortment of a number of precursor avian viruses and a virus related to
Goose/Guangdong/1/96 (H5N1) (Gs/Gd/96) was the likely donor of the H5 hemagglutinin.
We characterize the Goose/Guangdong/1/96-like viruses isolated from geese and
ducks imported into Hong Kong in the year 2000. Antigenically and genetically,
these recent H5N1 viruses fall into two groups, one mainly associated with
geese, and the other, recently transmitted to ducks. Further, viruses isolated
from a goose and a duck in December 2000 have acquired NS, PA, M, and PB2 genes
from the aquatic avian influenza gene pool through reassortment. For pandemic
preparedness, it is important to monitor whether these reassortant viruses have
the capacity for interspecies transmission to terrestrial poultry or mammals.
Descriptors: ducks virology, fowl plague transmission,
geese virology, influenza A virus avian genetics, poultry diseases transmission,
China, evolution, molecular, fowl plague virology, influenza A virus avian
isolation and purification, molecular sequence data, phylogeny, poultry
diseases virology, recombination, genetic, sequence analysis, DNA.
Guan, Y., L.L. Poon, C.Y. Cheung, T.M. Ellis, W. Lim,
A.S. Lipatov, K.H. Chan, K.M. Sturm Ramirez, C.L. Cheung, Y.H. Leung, K.Y.
Yuen, R.G. Webster, and J.S. Peiris (2004). H5N1 influenza: a protean
pandemic threat. Proceedings of the National Academy of Sciences of the
United States of America 101(21): 8156-61.
ISSN: 0027-8424.
NAL
Call Number: 500 N21P
Abstract: Infection with avian influenza A virus of the
H5N1 subtype (isolates A/HK/212/03 and A/HK/213/03) was fatal to one of two
members of a family in southern China in 2003. This incident was preceded by
lethal outbreaks of H5N1 influenza in waterfowl, which are the natural hosts of
these viruses and, therefore, normally have asymptomatic infection. The
hemagglutinin genes of the A/HK/212/03-like viruses isolated from humans and waterfowl
share the lineage of the H5N1 viruses that caused the first known cases of
human disease in Hong Kong in 1997, but their internal protein genes originated
elsewhere. The hemagglutinin of the recent human isolates has undergone
significant antigenic drift. Like the 1997 human H5N1 isolates, the 2003 human
H5N1 isolates induced the overproduction of proinflammatory cytokines by
primary human macrophages in vitro, whereas the precursor H5N1 viruses and
other H5N1 reassortants isolated in 2001 did not. The acquisition by the
viruses of characteristics that enhance virulence in humans and waterfowl and
their potential for wider distribution by infected migrating birds are causes
for renewed pandemic concern.
Descriptors: influenza epidemiology, influenza virology,
birds virology, cytokines biosynthesis, cytokines immunology, hemagglutination
inhibition tests, Hong Kong, inflammation mediators immunology, influenza
transmission, influenza veterinary, influenza A virus, avian classification,
avian genetics, avian immunology, avian pathogenicity, macrophages immunology,
macrophages metabolism, mice, molecular sequence data, organ specificity,
phylogeny, reassortant viruses immunology, reassortant viruses pathogenicity,
time factors, virulence.
Guan, Y., K.F. Shortridge, S. Krauss, P.S. Chin, K.C.
Dyrting, T.M. Ellis, R.G. Webster, and M. Peiris (2000). H9N2 influenza
viruses possessing H5N1-like internal genomes continue to circulate in poultry
in southeastern China. Journal of Virology 74(20): 9372-80. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: The transmission of H9N2 influenza viruses to
humans and the realization that the A/Hong Kong/156/97-like (H5N1) (abbreviated
HK/156/97) genome complex may be present in H9N2 viruses in southeastern China
necessitated a study of the distribution and characterization of H9N2 viruses
in poultry in the Hong Kong SAR in 1999. Serological studies indicated that
H9N2 influenza viruses had infected a high proportion of chickens and other
land-based birds (pigeon, pheasant, quail, guinea fowl, and chukka) from
southeastern China. Two lineages of H9N2 influenza viruses present in the
live-poultry markets were represented by A/Quail/Hong Kong/G1/97
(Qa/HK/G1/97)-like and A/Duck/Hong Kong/Y280/97 (Dk/HK/Y280/97)-like viruses.
Up to 16% of cages of quail in the poultry markets contained Qa/HK/G1/97-like
viruses, while about 5% of cages of other land-based birds were infected with
Dk/HK/Y280/97-like viruses. No reassortant between the two H9N2 virus lineages
was detected despite their cocirculation in the poultry markets. Reassortant
viruses represented by A/Chicken/Hong Kong/G9/97 (H9N2) were the major H9N2
influenza viruses circulating in the Hong Kong markets in 1997 but have not
been detected since the chicken slaughter in 1997. The Qa/HK/G1/97-like viruses
were frequently isolated from quail, while Dk/HK/Y280/97-like viruses were
predominately associated with chickens. The Qa/HK/G1/97-like viruses were
evolving relatively rapidly, especially in their PB2, HA, NP, and NA genes,
suggesting that they are in the process of adapting to a new host. Experimental
studies showed that both H9N2 lineages were primarily spread by the aerosol
route and that neither quail nor chickens showed evidence of disease. The high
prevalence of quail infected with Qa/HK/G1/97-like virus that contains six gene
segments genetically highly related to HK/156/97 (H5N1) virus emphasizes the
need for surveillance of mammals including humans.
Descriptors: genome, viral, influenza A virus avian isolation
and purification, poultry virology, China, hemagglutination inhibition tests,
influenza A virus avian genetics, phylogeny, temperature, virus replication.
Guan, Y., K.F. Shortridge, S. Krauss, P.H. Li, Y.
Kawaoka, and R.G. Webster (1996). Emergence of avian H1N1 influenza viruses
in pigs in China. Journal of Virology 70(11): 8041-8046. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Avian influenza A viruses from Asia are
recognized as the source of genes that reassorted with human viral genes to
generate the Asian/57 (H2N2) and Hong Kong/68 (H3N2) pandemic strains earlier
in this century. Here we report the genetic analysis of avian influenza A H1N1
viruses recently isolated from pigs in southern China, a host suspected to
generate new pandemic strains through gene reassortment events. Each of the
eight gene segments was of avian origin. Phylogenetic analysis indicates that
these genes form an Asian sublineage of the Eurasian avian lineage, suggesting
that these viruses are an independent introduction into pigs in Asia. The
presence of avian influenza viruses in pigs in China places them in an optimal
position for transmission to humans and may serve as an early warning of the
emergence of the next human influenza virus pandemic.
Descriptors: Hunan, Jiangxi, Guizhou, Guangdong, swine,
avian influenza virus, nucleotide sequence, genes, agglutinins, swine influenza
virus, influenza virus, genotypes, mutation, animal viruses, proteins,
nucleoproteins, Asia, cell structure, China, chromosomes, domestic animals,
East Asia, genetics, genomes, influenza virus, livestock, nucleus,
orthomyxoviridae, proteins, suidae, useful animals, viruses, nonstructural
proteins, isolation, phylogenetics, structural genes, viral hemagglutinins,
influenza virus A, matrix proteins.
Guan, Y., K.F. Shortridge, S. Krauss, and R.G.
Webster (1999). Molecular characterization of H9N2 influenza viruses: were
they the donors of the "internal" genes of H5N1 viruses in Hong Kong?
Proceedings of the National Academy of Sciences of the United States of
America 96(16): 9363-7. ISSN:
0027-8424.
NAL
Call Number: 500 N21P
Abstract: The origin of the H5N1 influenza viruses that
killed six of eighteen infected humans in 1997 and were highly pathogenic in
chickens has not been resolved. These H5N1 viruses transmitted directly to
humans from infected poultry. In the poultry markets in Hong Kong, both H5N1
and H9N2 influenza viruses were cocirculating, raising the possibility of
genetic reassortment. Here we analyze the antigenic and genetic features of
H9N2 influenza viruses with different epidemiological backgrounds. The results
suggest that the H9N2 influenza viruses of domestic ducks have become
established in the domestic poultry of Asia. Phylogenetic and antigenic
analyses of the H9N2 viruses isolated from Hong Kong markets suggest three
distinct sublineages. Among the chicken H9N2 viruses, six of the gene segments
were apparently derived from an earlier chicken H9N2 virus isolated in China,
whereas the PB1 and PB2 genes are closely related to those of the H5N1 viruses
and a quail H9N2 virus-A/quail/Hong Kong/G1/97 (Qa/HK/G1/97)-suggesting that
many of the 1997 chicken H9 isolates in the markets were reassortants. The
similarity of the internal genes of Qa/HK/G1/97 virus to those of the H5N1
influenza viruses suggests that the quail virus may have been the internal gene
donor. Our findings indicate that the human and poultry H5N1 influenza viruses
in Hong Kong in 1997 were reassortants that obtained internal gene segments
from Qa/HK/G1/97. However, we cannot be certain whether the replicate complex
of H5N1 originated from Qa/HK/G1/97 or whether the reverse transfer occurred;
the available evidence supports the former proposal.
Descriptors: genes viral, influenza epidemiology, influenza
veterinary, influenza A virus avian classification, influenza A virus avian
genetics, influenza A virus human classification, influenza A virus human
genetics, poultry diseases epidemiology, chick embryo, chickens, coturnix,
ducks, feces virology, Hong Kong epidemiology, influenza virology, influenza A
virus avian pathogenicity, molecular sequence data, phylogeny, pigeons, poultry
diseases virology.
Guo, Y., J. Li, and X. Cheng (1999). [Discovery of
men infected by avian influenza A (H9N2) virus]. Zhonghua Shi Yan He Lin
Chuang Bing Du Xue Za Zhi Zhonghua Shiyan He Linchuang Bingduxue Zazhi [Chinese
Journal of Experimental and Clinical Virology]. 13(2): 105-8. ISSN: 1003-9279.
Abstract: OBJECTIVE: To understand whether the avian
influenza A(H9N2) virus can infect men or not. METHODS: Seroepidemiological
surveys for avian (H9N2) virus in human, chickens and pigs were conducted. The
specimens for viral isolation were taken from throat of patients with influenza
like disease, as well as from chickens, then the specimens were inoculated into
embryonated chicken eggs. Afterward, the idsolates were identified with HI and
NI tests. Meanwhile, the patients who would be studied individually were found
to carry H9N2 virus. RESULTS: Approximately 19% of human had antibody to H9N2
virus with HI titers > or = 20, 5 strains of influenza A (H9N2) virus were
isolated from the patients. CONCLUSION: Avian influenza A(H9N2) virus can
infect men.
Descriptors: antibodies, viral blood, influenza virology,
influenza A virus avian pathogenicity, China epidemiology, influenza
epidemiology, influenza A virus avian classification, influenza A virus avian
isolation and purification, seroepidemiologic studies.
Guo, Y., M. Wang, Y. Kawaoka, O. Gorman, T. Ito, T.
Saito, and R.G. Webster (1992). Characterization of a new avian-like
influenza A virus from horses in China. Virology 188(1):
245-55. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: In March 1989 a severe outbreak of
respiratory disease occurred in horses in the Jilin and Heilongjiang provinces
of Northeast China that caused up to 20% mortality in some herds. An influenza
virus of the H3N8 subtype was isolated from the infected animals and was
antigenically and molecularly distinguishable from the equine 2 (H3N8) viruses
currently circulating in the world. The reference strain A/Equine/Jilin/1/89
(H3N8) was most closely related to avian H3N8 influenza viruses. Sequence
comparisons of the entire hemagglutinin (HA), nucleoprotein (NP), neuraminidase
(NA), matrix (M), and NS genes along with partial sequences of the three
polymerase (PB1, PB2, PA) genes suggest that six of the eight gene segments
(PA, HA, NP, NA, M, NS) are closely related to avian influenza viruses. Since
direct sequence analysis can only provide a crude measure of relationship,
phylogenetic analysis was done on the sequence information. Phylogenetic
analyses of the entire HA, NP, M, and NS genes and of partial sequences of PB1,
PB2, and PA indicated that these genes are of recent avian origin. The NP gene
segment is closely related to the gene segment found in the newly described H14
subtype isolated from ducks in the USSR. The A/Equine/Jilin/1/89 (H3N8)
influenza virus failed to replicate in ducks, but did replicate and cause
disease in mice on initial inoculation and on subsequent passaging caused 100%
mortality. In ferrets, the virus caused severe influenza symptoms. A second
outbreak of influenza in horses in Northeast China occurred in April 1990 in
the Heilongjiang province with 48% morbidity and no mortality. The viruses
isolated from this outbreak were antigenically indistinguishable from those in
the 1989 outbreak and it is probable that the reduced mortality was due to the
immune status of of the horses in the region. No influenza was detected in horses
in Northern China in the spring, summer, or fall of 1991 and no influenza has
been detected in horses in adjacent areas. Our analysis suggests that this new
equine influenza virus in horses in Northeast China is the latest influenza
virus in mammals to emerge from the avian gene pool in nature and that it may
have spread to horses without reassortment. The appearance of this new equine
virus in China emphasizes the potential for whole avian influenza viruses to
successfully enter mammalian hosts and serves as a model and a warning for the
appearance of new pandemic influenza viruses in humans.(ABSTRACT TRUNCATED AT
250 WORDS)
Descriptors: horse diseases microbiology, influenza A
virus isolation and purification, orthomyxoviridae infections veterinary,
antigens, viral genetics, antigens, viral immunology, base composition, chick
embryo, China epidemiology, cloning, molecular, genes viral, horse diseases
epidemiology, horses, influenza A virus avian immunology, influenza A virus
genetics, influenza A virus immunology, influenza A virus pathogenicity,
orthomyxoviridae infections epidemiology, orthomyxoviridae infections
microbiology, phylogeny, species specificity, virus replication.
Guo, Y., M. Wang, G.S. Zheng, W.K. Li, Y. Kawaoka,
and R.G. Webster (1995). Seroepidemiological and molecular evidence for the
presence of two H3N8 equine influenza viruses in China in 1993-94. Journal
of General Virology 76(Pt. 8): 2009-14.
ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: In May 1993, a severe epidemic of respiratory
disease began in horses in Inner Mongolia and spread throughout horses in
China. The disease affected mules and donkeys as well as horses but did not
spread to other species, including humans. The severity of the disease raised
the question of whether the outbreak might have been caused by the new
avian-like influenza viruses detected in horses in China in 1989 or by current
variants ofA/equine/Miami/1/63 (H3N8) (equine-2) or by a reassortant between
these viruses. Antigenic and sequence analysis established that all gene
segments of the influenza virus causing the epidemic were of recent equine-2
origin and that the virus was not a reassortant. Serological analysis of
post-infection horse sera provided evidence for the continued circulation of
the A/Equine/Jilin/1/89 (Eq/Jilin) (H3N8) avian-like viruses in horses in
Heilongjiang province with original antigenic sin-like responses. It is
noteworthy that prior infection with the avian-like Eq/Jilin strain did not
afford cross-protection against a current equine-2 strain. Serological evidence
for the continued circulation of the avian-like H3N8 influenza virus in horses
indicates that this virus has probably established itself in horses in Asia.
Descriptors: horse diseases epidemiology, influenza
veterinary, influenza A virus genetics, antibodies, viral blood, antigens,
viral immunology, base sequence, China epidemiology, disease outbreaks
veterinary, genome, viral, horse
diseases virology, horses, influenza epidemiology, influenza virology,
influenza A virus classification, influenza A virus immunology, molecular
sequence data, phylogeny, sequence analysis, DNA, sequence homology, nucleic
acid, seroepidemiologic studies, serotyping.
Guo, Y.J., S. Krauss, D.A. Senne, I.P. Mo, K.S. Lo,
X.P. Xiong, M. Norwood, K.F. Shortridge, R.G. Webster, and Y. Guan (2000). Characterization
of the pathogenicity of members of the newly established H9N2 influenza virus
lineages in Asia. Virology 267(2): 279-88. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The reported transmission of avian H9N2
influenza viruses to humans and the isolation of these viruses from Hong Kong
poultry markets lend urgency to studies of their ecology and pathogenicity. We
found that H9N2 viruses from North America differ from those of Asia. The North
American viruses, which infect primarily domestic turkeys, replicated poorly in
inoculated chickens. Phylogenetic analysis of the hemagglutinin and nucleoprotein
genes indicated that the Asian H9N2 influenza viruses could be divided into
three sublineages. Initial biological characterization of at least one virus
from each lineage was done in animals. Early isolates of one lineage
(A/Chicken/Beijing/1/94, H9N2) caused as high as 80% mortality rates in
inoculated chickens, whereas all other strains were nonpathogenic. Sequence
analysis showed that some isolates, including the pathogenic isolate, had one
additional basic amino acid (A-R/K-S-S-R-) at the hemagglutinin cleavage site.
Later isolates of the same lineage (A/Chicken/Hong Kong/G9/97, H9N2) that
contains the PB1 and PB2 genes similar to Hong Kong/97 H5N1 viruses replicated
in chickens, ducks, mice, and pigs but were pathogenic only in mice. A/Quail/Hong
Kong/G1/97 (H9N2), from a second lineage that possesses the replicative complex
similar to Hong Kong/97 H5N1 virus, replicated in chickens and ducks without
producing disease signs, was pathogenic in mice, and spread to the brain
without adaptation. Examples of the third Asian H9N2 sublineage
(A/Chicken/Korea/323/96, Duck/Hong Kong/Y439/97) replicated in chickens, ducks,
and mice without producing disease signs. The available evidence supports the
notion of differences in pathogenicity of H9N2 viruses in the different
lineages and suggests that viruses possessing genome segments similar to 1997
H5N1-like viruses are potentially pathogenic in mammals. Copyright 2000
Academic Press.
Descriptors: influenza A virus avian genetics, influenza A
virus avian pathogenicity, binding sites genetics, chickens virology, DNA
complementary chemistry, DNA complementary genetics, glycosylation,
hemagglutinins viral genetics, hemagglutinins viral metabolism, Hong Kong
epidemiology, mice, mice inbred BALB c virology, molecular sequence data,
phylogeny, poultry diseases epidemiology, RNA viral genetics, reverse
transcriptase polymerase chain reaction, sequence analysis, DNA, virulence
genetics, virus replication.
Ha, Y., D.J. Stevens, J.J. Skehel, and D.C. Wiley
(2002). H5 avian and H9 swine influenza virus haemagglutinin structures:
possible origin of influenza subtypes. EMBO Journal 21(5):
865-75. ISSN: 0261-4189.
NAL
Call Number: QH506.E46
Abstract: There are 15 subtypes of influenza A virus
(H1-H15), all of which are found in avian species. Three caused pandemics in
the last century: H1 in 1918 (and 1977), H2 in 1957 and H3 in 1968. In 1997, an
H5 avian virus and in 1999 an H9 virus caused outbreaks of respiratory disease
in Hong Kong. We have determined the three-dimensional structures of the
haemagglutinins (HAs) from H5 avian and H9 swine viruses closely related to the
viruses isolated from humans in Hong Kong. We have compared them with known
structures of the H3 HA from the virus that caused the 1968 H3 pandemic and of
the HA--esterase--fusion (HEF) glycoprotein from an influenza C virus.
Structure and sequence comparisons suggest that HA subtypes may have originated
by diversification of properties that affected the metastability of HAs
required for their membrane fusion activities in viral infection.
Descriptors: hemagglutinin glycoproteins, influenza virus
chemistry, influenza A virus avian chemistry, porcine chemistry,
orthomyxoviridae classification, amino acid motifs, amino acid sequence, amino
acid substitution, crystallography,
x-ray, evolution, molecular, hemagglutinin glycoproteins, influenza virus
genetics, hemagglutinin glycoproteins, influenza virus physiology, hydrogen-ion
concentration, avian classification, influenza A virus avian genetics, avian
physiology, porcine classification, porcine genetics, porcine physiology,
membrane fusion, models, molecular, molecular sequence data, protein
conformation, protein structure, secondary, rotation, sequence alignment,
sequence homology, amino acid, structure activity relationship.
Ha, Y., D.J. Stevens, J.J. Skehel, and D.C. Wiley
(2003). X-ray structure of the hemagglutinin of a potential H3 avian
progenitor of the 1968 Hong Kong pandemic influenza virus. Virology
309(2): 209-218. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: We have determined the structure of the HA of
an avian influenza virus, A/duck/Ukraine/63, a member of the same antigenic
subtype, H3, as the virus that caused the 1968 Hong Kong influenza pandemic,
and a possible progenitor of the pandemic virus. We find that structurally
significant differences between the avian and the human HAs are restricted to
the receptor-binding site particularly the substitutions Q226L and G228S that
cause the site to open and residues within it to rearrange, including the
conserved residues, Y98, W153, and H183. We have also analyzed complexes formed
by the HA with sialopentasaccharides in which the terminal sialic acid is in
either alpha2,3- or alpha2,6-linkage to galactose. Comparing the structures of
complexes in which an alpha2,3-linked receptor analog is bound to the H3 avian
HA or to an H5 avian HA leads to the suggestion that all avian influenza HAs
bind to their preferred alpha2,3-linked receptors similarly, with the analog in
a trans conformation about the glycosidic linkage. We find that alpha2,6-linked
analogs are bound by both human and avian HAs in a cis conformation, and that
the incompatibility of an alpha2,6-linked receptor with the
alpha2,3-linkage-specific H3 avian HA-binding site is partially resolved by a
small change in the position and orientation of the sialic acid. We discuss our
results in relation to the mechanism of transfer of influenza viruses between
species.
Descriptors: biochemistry and molecular biophysics, virology,
1968 Hong Kong influenza pandemic.
Haller, O. (1975). A mouse hepatotropic variant of
influenza virus. Archives of Virology 49(2-3): 99-116. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: A hepatotropic variant of avian influenza
virus A/Turkey/England 63 (Hav 1, Nav 3) was selected by serial passages in
mouse liver. Adaptation to this organ was established after 13 in vivo passages
and was found to improve during further passages as shown by increasing rates
of replication in livers of ICR mice. The mutant virus finally selected was
stable and differed from the original virus mainly in lethality upon
intraperitoneal injection in mice, in its ability to grow to high titers in
livers of susceptible animals and in plaque morphology in chick embryo
fibroblasts. No differences were detected in hemagglutination inhibition and
neutralization by standard mouse antisera. Pathogenicity for the liver was
independent of the route of inoculation, included other laboratory animals
sensitive to influenza virus and could be inhibited by amantadine. Fatal
hepatitis in 50 per cent of susceptible mice by the intraperitoneal route
required from 10 to 20 EID50-. Pathological changes consisted of severe
necrosis of liver parenchyma accompanied by release of F antigen into the serum
and were apparently due to virus replication in hepatic cells as evidenced by
immunofluorescence. The main implications of this animal model for studies on
experimental hepatitis and on myxovirus-host interactions in an organ not usually
associated with influenza are discussed.
Descriptors: adaptation, physiological, hepatitis A
microbiology, liver microbiology, mutation, orthomyxoviridae growth and
development, amantadine therapeutic use, antigens, viral, disease models,
animal, guinea pigs, hamsters, hepatitis A pathology, hepatitis A prevention
and control, liver immunology, liver pathology, mice, mice inbred strains,
orthomyxoviridae immunology, orthomyxoviridae pathogenicity, rats, virus
replication.
Haller, O. (1974). Myxovirus-Hepatitis: Ein
Modell. [A model of myxovirus hepatitis (infection of mice with avian influenza
virus)]. Pathologia Et Microbiologia 40(3-4.)
NAL
Call Number: 448.8 Sch9
Descriptors: hepatitis, disease models, avian influenza
virus, mice.
Hassler, D., T.F. Schwarz, and P. Kimmig (2003). Gefluegelpest:
eine potenzielle Gefahr auch fuer Menschen.
[Avian influenza: Potential risk for humans.]. DMW Deutsche
Medizinische Wochenschrift 128(27): 1467.
ISSN: 0012-0472.
NAL
Call Number: 448.8 D48
Descriptors: human medicine, infection, veterinary
medicine, avian influenza, drug therapy, pathology, respiratory system disease,
transmission, viral disease, coinfection, gene transfer, potential risk,
prevention, recombination, zoonosis.
Hatta, M., P. Gao, P. Halfmann, and Y. Kawaoka
(2001). Molecular basis for high virulence of Hong Kong H5N1 influenza A
viruses. Science 293(5536): 1840-2.
ISSN: 0036-8075.
NAL
Call Number: 470 Sci2
Abstract: In 1997, an H5N1 influenza A virus was
transmitted from birds to humans in Hong Kong, killing 6 of the 18 people
infected. When mice were infected with the human isolates, two virulence groups
became apparent. Using reverse genetics, we showed that a mutation at position
627 in the PB2 protein influenced the outcome of infection in mice. Moreover,
high cleavability of the hemagglutinin glycoprotein was an essential
requirement for lethal infection.
Descriptors: influenza epidemiology, influenza virology,
influenza A virus genetics, influenza A virus pathogenicity, amino acid
sequence, birds virology, DNA, recombinant genetics, hemagglutinin
glycoproteins, influenza virus chemistry, hemagglutinin glycoproteins,
influenza virus genetics, hemagglutinin glycoproteins, influenza virus
metabolism, Hong Kong epidemiology, influenza mortality, influenza transmission
, influenza A virus avian genetics, avian pathogenicity, avian physiology,
human genetics, human pathogenicity, human physiology, influenza A virus
physiology, lung virology, mice, mutation, missense genetics, reassortant
viruses genetics, reassortant viruses pathogenicity, reassortant viruses
physiology, viral proteins chemistry, viral proteins genetics, viral proteins
metabolism.
Hatta, M., P. Halfmann, K. Wells, and Y. Kawaoka
(2002). Human influenza a viral genes responsible for the restriction of its
replication in duck intestine. Virology 295(2): 250-5. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: ducks virology, genes viral, influenza A
virus human physiology, intestines virology,
viral proteins genetics, virus replication, cell line, DNA,
complementary, avian genetics, avian metabolism, human genetics, human
pathogenicity, RNA viral metabolism, recombination, genetic, transcription,
genetic, viral proteins metabolism.
Hatta, M. and Y. Kawaoka (2002). The continued
pandemic threat posed by avian influenza viruses in Hong Kong. Trends in
Microbiology 10(7): 340-4. ISSN:
0966-842X.
NAL
Call Number: QR1.T74
Abstract: In 1997, a highly pathogenic avian H5N1
influenza virus was transmitted directly from live commercial poultry to humans
in Hong Kong. Of the 18 people infected, six died. The molecular basis for the
high virulence of this virus in mice was found to involve an amino acid change
in the PB2 protein. To eliminate the source of the pathogenic virus, all birds
in the Hong Kong markets were slaughtered. In 1999, another avian influenza
virus of H9N2 subtype was transmitted to two children in Hong Kong. In
2000-2002, H5N1 avian viruses reappeared in the poultry markets of Hong Kong,
although they have not infected humans. Continued circulation of H5N1 and other
avian viruses in Hong Kong raises the possibility of future human influenza
outbreaks. Moreover, the acquisition of properties of human viruses by the
avian viruses currently circulating in southeast China might result in a
pandemic.
Descriptors: communicable diseases, emerging virology,
disease outbreaks, fowl plague virology, communicable diseases, emerging
epidemiology, disease reservoirs, fowl plague epidemiology, Hong Kong
epidemiology, influenza A virus avian genetics, avian pathogenicity, avian
physiology, mice, virulence.
Hinshaw, V.S., D.J. Alexander, M. Aymard, P.A.
Bachmann, B.C. Easterday, C. Hannoun, H. Kida, M. Lipkind, J.S. MacKenzie, K.
Nerome, and et al. (1984). Antigenic comparisons of swine-influenza-like
H1N1 isolates from pigs, birds and humans: an international collaborative
study. Bulletin of the World Health Organization 62(6): 871-8.
ISSN: 0042-9686.
NAL
Call Number: 449.9 W892B
Descriptors: antigens, viral analysis, influenza A virus,
porcine immunology, influenza A virus immunology, antibodies, monoclonal
immunology, hemagglutination inhibition tests, hemagglutination tests, immune
sera, avian immunology, influenza A virus human immunology, porcine isolation
and purification.
Hinshaw, V.S., W.J. Bean, J. Geraci, P. Fiorelli, G.
Early, and R.G. Webster (1986). Characterization of two influenza A viruses
from a pilot whale. Journal of Virology 58(2): 655-6. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Influenza A viruses of the H13N2 and H13N9
subtypes were isolated from the lung and hilar node of a pilot whale.
Serological, molecular, and biological analyses indicate that the whale
isolates are closely related to the H13 influenza viruses from gulls.
Descriptors: cetacea microbiology, influenza A virus
isolation and purification, whales microbiology, antigens, viral immunology,
ferrets microbiology, hemagglutinins viral immunology, influenza A virus avian
analysis, influenza A virus analysis, influenza A virus immunology, influenza A
virus physiology, lung microbiology, lymph nodes microbiology, neuraminidase
immunology, nucleic acid hybridization, RNA viral analysis, virus replication.
Hinshaw, V.S., W.J. Bean, R.G. Webster, J.E. Rehg, P.
Fiorelli, G. Early, J.R. Geraci, and D.J. St. Aubin (1984). Are seals
frequently infected with avian influenza viruses? Journal of Virology
51(3): 863-5. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Influenza A virus isolates of the H4N5
subtype (which has previously been detected only in birds) were recovered from
harbor seals dying of viral pneumonia on the New England coast from June 1982
through March 1983. When these isolates were compared with other mammalian and
avian viruses in serological assays and RNA-RNA competitive hybridization, it
was found that the seal viruses were most closely related antigenically and
genetically to recent avian virus strains and were readily distinguishable from
mammalian viruses, including H7N7 isolates recovered from seals in 1980. Unlike
any previous isolates from mammals, these recent seal viruses replicate in the
intestinal tracts of ducks, a characteristic of avian viruses. The association
of avian viruses with influenza outbreaks in seals suggests that transmission
of avian viruses to seals is occurring in nature. Potentially, this may be an
example of the adaptation of avian viruses to mammals, which would represent an
intermediate step in the evolution of new mammalian strains.
Descriptors: animal diseases microbiology, fowl plague
veterinary, influenza A virus avian pathogenicity, pinnipedia microbiology,
seals microbiology, animal diseases mortality, fowl plague microbiology, fowl
plague mortality, avian isolation and purification.
Hinshaw, V.S., R.G. Webster, B.C. Easterday, and
W.J.J. Bean (1981). Replication of avian influenza A viruses in mammals.
Infection and Immunity 34(2): 354-61.
ISSN: 0019-9567.
NAL
Call Number: QR1.I57
Abstract: The recent appearance of an avian influenza A
virus in seals suggests that viruses are transmitted from birds to mammals in
nature. To examine this possibility, avian viruses of different antigenic
subtypes were evaluated for their ability to replicate in three mammals-pigs,
ferrets, and cats. In each of these mammals, avian strains replicated to high
titers in the respiratory tract (10(5) to 10(7) 50% egg infective doses per ml
of nasal wash), with peak titers at 2 to 4 days post-inoculation, similar to the
pattern of human and other mammalian viruses in these animals. Most avian
strains were recovered for 5 to 9 days post-inoculation. One avian H1N1 virus
initially replicated poorly in pigs, but was adapted to this host and even
transmitted to other pigs. Replication of the avian viruses occurred in the
respiratory tracts of mammals, whereas, in birds, they replicate in the
intestinal tract as well. The infected mammals had no significant disease signs
and produced low levels of humoral antibodies; however, challenge experiments
in ferrets indicated that they were immune. These studies suggest that
influenza A viruses currently circulating in avian species represent a source
of viruses capable of infecting mammals, thereby contributing to the influenza
A antigenic pool from which new pandemic strains may originate.
Descriptors: Carnivora microbiology, cats microbiology,
ferrets microbiology, influenza A virus avian growth and development, swine
microbiology, adaptation, physiological, antibodies, viral biosynthesis,
antigens, viral analysis, avian immunology, human growth and development,
porcine growth and development, respiratory system microbiology, virus
replication.
Hinshaw, V.S., R.G. Webster, C.W. Naeve, and B.R.
Murphy (1983). Altered tissue tropism of human-avian reassortant influenza
viruses. Virology 128(1): 260-3.
ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Avian influenza viruses replicate to high
titers in the cells lining the intestinal tract of birds; however, human
strains do not. A series of reassortant viruses with all six internal genes
from an avian strain and one or both genes for the surface antigens from a
human strain failed to transit and infect the intestinal tracts of ducks.
However, these reassortants did replicate in the bursa of ducks after rectal
inoculation. These studies provide the first evidence that the hemagglutinin
and neuraminidase are critical for the enterotropism of avian viruses but are
not essential for replication in other avian tissues.
Descriptors: hemagglutinins viral, influenza A virus avian
physiology, human physiology, intestines microbiology, neuraminidase
physiology, bursa of fabricius microbiology, ducks microbiology, genes viral,
avian genetics, human genetics, recombination, genetic, virus replication.
Hiromoto, Y., T. Saito, S. Lindstrom, and K. Nerome
(2000). Characterization of low virulent strains of highly pathogenic A/Hong
Kong/156/97 (H5N1) virus in mice after passage in embryonated hens' eggs. Virology
272(2): 429-37. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: influenza A virus avian pathogenicity, ovum
virology, cell line, chick embryo, clone cells, dogs, fowl plague mortality,
avian growth and development, avian isolation and purification, mice, organ
specificity, sequence analysis, DNA, sequence analysis, protein, serial
passage, tropism, virulence, virus replication.
Hiti, A.L., A.R. Davis, and D.P. Nayak (1981). Complete
sequence analysis shows that the hemagglutinins of the H0 and H2 subtypes of
human influenza virus are closely related. Virology 111(1):
113-24. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: genes viral, hemagglutinins viral genetics,
influenza A virus human immunology, amino acid sequence, base sequence, DNA,
viral, avian immunology, human classification, human genetics.
Hoffmann, E., J. Stech, I. Leneva, S. Krauss, C.
Scholtissek, P.S. Chin, M. Peiris, K.F. Shortridge, and R.G. Webster (2000). Characterization
of the influenza A virus gene pool in avian species in southern China: was H6N1
a derivative or a precursor of H5N1? Journal of Virology 74(14):
6309-15. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: In 1997, an H5N1 influenza virus outbreak
occurred in chickens in Hong Kong, and the virus was transmitted directly to
humans. Because there is limited information about the avian influenza virus
reservoir in that region, we genetically characterized virus strains isolated
in Hong Kong during the 1997 outbreak. We sequenced the gene segments of a
heterogeneous group of viruses of seven different serotypes (H3N8, H4N8, H6N1,
H6N9, H11N1, H11N9, and H11N8) isolated from various bird species. The
phylogenetic relationships divided these viruses into several subgroups. An
H6N1 virus isolated from teal (A/teal/Hong Kong/W312/97 [H6N1]) showed very
high (>98%) nucleotide homology to the human influenza virus A/Hong
Kong/156/97 (H5N1) in the six internal genes. The N1 neuraminidase sequence
showed 97% nucleotide homology to that of the human H5N1 virus, and the N1 protein
of both viruses had the same 19-amino-acid deletion in the stalk region. The
deduced hemagglutinin amino acid sequence of the H6N1 virus was most similar to
that of A/shearwater/Australia/1/72 (H6N5). The H6N1 virus is the first known
isolate with seven H5N1-like segments and may have been the donor of the
neuraminidase and the internal genes of the H5N1 viruses. The high homology
between the internal genes of H9N2, H6N1, and the H5N1 isolates indicates that
these subtypes are able to exchange their internal genes and are therefore a
potential source of new pathogenic influenza virus strains. Our analysis
suggests that surveillance for influenza A viruses should be conducted for wild
aquatic birds as well as for poultry, pigs, and humans and that H6 isolates should
be further characterized.
Descriptors: genome, viral, influenza A virus avian
genetics, birds, China, fowl plague, hemagglutinin glycoproteins, influenza
virus genetics, avian classification, avian isolation and purification, avian
pathogenicity, human classification, human genetics, human isolation and
purification, human pathogenicity, mice, mice inbred BALB c, neuraminidase
genetics, phylogeny, polymerase chain reaction, sequence analysis, DNA.
Horimoto, T. and Y. Kawaoka (2001). Pandemic
threat posed by avian influenza A viruses. Clinical Microbiology Reviews
14(1): 129-49. ISSN: 0893-8512.
NAL
Call Number: QR67.C54
Abstract: Influenza pandemics, defined as global
outbreaks of the disease due to viruses with new antigenic subtypes, have exacted
high death tolls from human populations. The last two pandemics were caused by
hybrid viruses, or reassortants, that harbored a combination of avian and human
viral genes. Avian influenza viruses are therefore key contributors to the
emergence of human influenza pandemics. In 1997, an H5N1 influenza virus was
directly transmitted from birds in live poultry markets in Hong Kong to humans.
Eighteen people were infected in this outbreak, six of whom died. This avian
virus exhibited high virulence in both avian and mammalian species, causing
systemic infection in both chickens and mice. Subsequently, another avian virus
with the H9N2 subtype was directly transmitted from birds to humans in Hong
Kong. Interestingly, the genes encoding the internal proteins of the H9N2 virus
are genetically highly related to those of the H5N1 virus, suggesting a unique
property of these gene products. The identification of avian viruses in humans
underscores the potential of these and similar strains to produce devastating influenza
outbreaks in major population centers. Although highly pathogenic avian
influenza viruses had been identified before the 1997 outbreak in Hong Kong,
their devastating effects had been confined to poultry. With the Hong Kong
outbreak, it became clear that the virulence potential of these viruses
extended to humans.
Descriptors: disease outbreaks prevention and control,
disease outbreaks veterinary, fowl plague epidemiology, influenza epidemiology,
influenza A virus avian pathogenicity, adaptation, physiological, disease
vectors, fowl plague transmission, Hong Kong epidemiology, influenza virology,
avian classification, Mexico epidemiology, Pennsylvania epidemiology, poultry,
viral proteins, virulence.
Inkster, M.D., V.S. Hinshaw, and I.T. Schulze (1993).
The hemagglutinins of duck and human H1 influenza viruses differ in sequence
conservation and in glycosylation. Journal of Virology 67(12):
7436-43. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: We determined the deduced amino acid sequences
of two H1 duck influenza A virus hemagglutinins (HAs) and found that the
consensus sequence of the HA, determined directly from virus recovered from the
intestinal tract, remains unchanged through many generations of growth in MDCK
cells and chicken embryos. These two duck viruses differ from each other by 5
amino acids and from A/Dk/Alberta/35/1976 (F. J. Austin, Y. Kawaoka, and R. G.
Webster, J. Gen. Virol. 71:2471-2474, 1990) by 9 and 12 amino acids, most of
which are in the HA1 subunit. They are antigenically similar to each other but
different from the Alberta virus. We compared these H1 duck HAs with the HAs of
human isolates to identify structural properties of this viral glycoprotein
that are associated with host range. By comparison to the human H1 HAs, the
duck virus HA sequences are highly conserved as judged by the small fraction of
nucleotide differences between strains which result in amino acid
substitutions. However, the most striking difference between these duck and
human HAs is in the number and distribution of glycosylation sites. Whereas
duck and swine viruses have four and five conserved glycosylation sites per HA1
subunit, none of which are on the tip of the HA, all human viruses have at
least four additional sites, two or more of which are on the tip of the HA.
These findings stress the role of glycosylation in the control of host range
and suggest that oligosaccharides on the tip of the HA are important to the
survival of H1 viruses in humans but not in ducks or swine.
Descriptors: consensus sequence genetics, ducks
microbiology, hemagglutinins viral genetics, influenza A virus avian genetics,
human genetics, amino acid sequence, antigens, viral genetics, antigens, viral
immunology, cultured cells, consensus sequence immunology, feces microbiology,
glycosylation, hemagglutinin glycoproteins, influenza virus, hemagglutinins
viral immunology, avian immunology, human immunology, models, molecular,
molecular sequence data, protein processing, post translational, regulatory
sequences, nucleic acid genetics, selection genetics, sequence homology, amino
acid, variation genetics.
Isaeva, E.I., T.S. Belkina, Z.I. Rovnova, P.N.
Kosiakov, and I.A.M. Selivanov (1982). Antigennye determinanty virusov
grippa cheloveka v sostave grippoznykh virusov, vydelennykh ot zhivotnykh.
[Antigenic determinants of human influenza viruses among the influenza viruses
isolated from animals]. Voprosy Virusologii 27(6): 681-6. ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Comparative studies of the antigenic
properties of hemagglutinin (HA) of animal and human viruses revealed both
similarities between them and complete differences in the composition of
antigenic determinants. Avian influenza viruses A/chicken/Kamchatka/12/71, A/pintail/Primorie/730/76,
and A/bat/Alma-Ata/73/77 were completely identical with human strains of
influenza virus. Influenza A/horse/Miami/63 contains one antigenic determinant
H3.1.HA of A/tern/Turkmenia/18/73 (Hav7) viruses has a peculiar set of
antigens. Apart from two antigenic determinants H3.1 and H3.3 inherent in human
virus strains, HA of A/tern/Turkmenia/18/73 virus contains an antigenic
determinant the population of antibodies to which shows no relation to HA of
subtypes Hav2-Hav9.
Descriptors: epitopes isolation and purification,
influenza A virus human immunology, orthomyxoviridae immunology, complement
fixation tests, epitopes analysis, hemagglutination inhibition tests,
hemagglutinins viral analysis, hemagglutinins viral isolation and purification,
immunoelectrophoresis, orthomyxoviridae isolation and purification.
Israel, A. (1980). Genotypic and phenotypic
characterization of a mammalian cell-adapted mutant of fowl plague virus (FPV).
Journal of General Virology 51(Pt. 1): 33-44. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: A mammalian cell-adapted mutant of the Dobson
strain of fowl plague virus (FPV-B) was characterized. Genetic analyses of
recombinants between a ts mutant of this virus and either the non-adapted
Dobson strain or the Rostock strain of FPV showed that the gene coding for the
P3 protein of the adapted Dobson strain was sufficient to enable any
recombinant to grow in L cells. The abortive cycle of wild-type Dobson strain
(FPV+) was compared to the productive cycle of the mutant. By using 100
p.f.u./cell, no quantitative difference could be detected in infected L cells
between polypeptides and cRNAs induced by FPV+ and FPV-B. However, the
maturation of virions at the plasma membrane did not proceed correctly. At a lower
m.o.i. the amounts of virus polypeptides decreased with the m.o.i. This
decrease was not the same for all polypeptides and cRNA segments: HA, M and NA
and their mRNAs decreased to a greater extent than the others. These results
are discussed in relation to a possible biological activity of polypeptide P3.
Descriptors: genes viral, influenza A virus avian
genetics, virus replication, avian growth and development, avian metabolism, L
cells cell line, mice, mutation, RNA viral biosynthesis, recombination,
genetic, viral proteins biosynthesis.
Itamura, S. (2004). [SARS, pandemic influenza,
avian influenza: quest for missing link]. Tanpakushitsu Kakusan Koso;
Protein, Nucleic Acid, Enzyme 49(6): 772-80. ISSN: 0039-9450.
NAL
Call Number: QD431.T3
Descriptors: influenza A virus, avian pathogenicity, SARS
virus pathogenicity, severe acute respiratory syndrome virology, Asia
epidemiology, disease outbreaks, avian influenza epidemiology, avian influenza
transmission, avian influenza virology, poultry diseases epidemiology, poultry
diseases transmission, poultry diseases virology, severe acute respiratory
syndrome epidemiology, severe acute respiratory syndrome transmission,
virulence, zoonoses epidemiology, zoonoses transmission.
Ito, T. (1999). Host range and pathogenicity of
avian influenza virus: Animal surveilance of Hong Kong H5 virus. Journal
of the Japanese Society of Poultry Diseases 35(1): 1-8. ISSN: 0285-709X.
Descriptors: chickens, avian influenza virus, Newcastle
disease virus, host parasite relations,
Hong Kong, Asia, birds, domestic animals, East Asia, Galliformes,
influenza virus, livestock, orthomyxoviridae, paramyxoviridae, parasitism,
poultry, useful animals, viruses.
Ito, T., J.N. Couceiro, S. Kelm, L.G. Baum, S.
Krauss, M.R. Castrucci, I. Donatelli, H. Kida, J.C. Paulson, R.G. Webster, and
Y. Kawaoka (1998). Molecular basis for the generation in pigs of influenza A
viruses with pandemic potential. Journal of Virology 72(9):
7367-73. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract:
Genetic and biologic observations
suggest that pigs may serve as "mixing vessels" for the generation of
human-avian influenza A virus reassortants, similar to those responsible for
the 1957 and 1968 pandemics. Here we demonstrate a structural basis for this
hypothesis. Cell surface receptors for both human and avian influenza viruses
were identified in the pig trachea, providing a milieu conducive to viral
replication and genetic reassortment. Surprisingly, with continued replication,
some avian-like swine viruses acquired the ability to recognize human virus
receptors, raising the possibility of their direct transmission to human
populations. These findings help to explain the emergence of pandemic influenza
viruses and support the need for continued surveillance of swine for viruses
carrying avian virus genes.
Descriptors: hemagglutinin glycoproteins, influenza virus
chemistry, influenza A virus avian metabolism, human metabolism, receptors,
virus chemistry, adaptation, biological, amino acid sequence, amino acids,
binding sites, ducks, hemagglutinin glycoproteins, influenza virus metabolism,
avian classification, avian physiology, human classification, human physiology,
molecular sequence data, phylogeny, receptors, virus metabolism, sequence
homology, amino acid, swine, trachea virology.
Ito, T. (2003). Avian influenza and human health.
Japanese Poultry Science 40(J2): J83-J88. ISSN: 0029-0254.
NAL
Call Number: 41.8 V6446
Abstract: An H5N1 avian influenza A virus was directly
transmitted from birds to humans in 1997-1998 in Hong Kong, infecting 18
humans, 6 of whom died. Epidemiological studies indicate that there has been no
human-to-human transmission of the virus, suggesting that human cases in Hong
Kong originated from independent transmission of the virus from birds. The H5N1
viruses isolated from humans have still displayed avian virus-like receptor
specificity. This property is consistent with the fact that the virus did not
establish within human populations. Subsequently, in March of 1999, another
avian virus with the H9N2 subtype was isolated from two persons in Hong Kong.
This virus also did not have the capacity for human-to-human spread. However,
this case suggests that all subtypes of avian viruses (except H1 and H3
viruses) could be novel human influenza viruses with pandemic potential. It
also supports the contention that intensive monitoring of bird populations
should be an integral part of control policies for new human pandemic of
influenza.
Descriptors: epidemiology, infection, avian influenza,
epidemiology, infectious disease, respiratory system disease, transmission,
viral disease, viral transmission.
Jameson, J., J. Cruz, M. Terajima, and F.A. Ennis
(1999). Human CD8+ and CD4+ T lymphocyte memory to influenza A viruses of
swine and avian species. Journal of Immunology 162(12):
7578-83. ISSN: 0022-1767.
NAL
Call Number: 448.8 J8232
Abstract: Recently, an avian influenza A virus (A/Hong
Kong/156/97, H5N1) was isolated from a young child who had a fatal influenza
illness. All eight RNA segments were of avian origin. The H5 hemagglutinin is
not recognized by neutralizing Abs present in humans as a result of infection
with the human H1, H2, or H3 subtypes of influenza A viruses. Subsequently,
five other deaths and several more human infections in Hong Kong were
associated with this avian-derived virus. We investigated whether influenza
A-specific human CD8+ and CD4+ T lymphocytes would recognize epitopes on
influenza A virus strains derived from swine or avian species, including the
1997 H5N1 Hong Kong virus strains. Our results demonstrate that adults living
in an urban area of the U.S. possess influenza A cross-serotype reactive CD8+
and CD4+ CTL that recognize multiple epitopes on influenza A viruses of other
species. Bulk culture cytotoxicity was demonstrated against avian and human
influenza A viruses. Enzyme-linked immunospot assays detected precursor CTL
specific for both human CTL epitopes and the corresponding A/HK/97 viral
sequences. We hypothesize that these cross-reactive CTL might provide partial
protection to humans against novel influenza A virus strains introduced into
humans from other species.
Descriptors: cd4 positive T lymphocytes immunology, CD4
positive T lymphocytes virology, CD8 positive T lymphocytes immunology, CD8
positive T lymphocytes virology, influenza A virus avian immunology, porcine
immunology, cell line, chickens, cytotoxicity, immunologic genetics, ducks,
enzyme linked immunosorbent assay, avian genetics, porcine genetics,
leukocytes, mononuclear immunology, leukocytes, mononuclear virology, peptides
genetics, peptides immunology, point mutation, stem cells immunology, stem
cells virology, swine.
Jemmi, T., J. Danuser, and C. Griot (2000). Zoonosen
als Risiko im Umgang mit Tieren und tierischen Produkten. [Zoonoses as a risk
when associating with livestock or animal products]. Schweizer Archiv
Fur Tierheilkunde 142(12): 665-71.
ISSN: 0036-7281.
NAL
Call Number: 41.8 Sch9
Abstract: The risk of zoonotic disease transmission
when handling livestock or animal products is substantial. In industrialized
countries, the classical zoonotic diseases such as tuberculosis or brucellosis
are no longer in the foreground. Latent zoonoses such as salmonellosis and
campylobacteriosis can cause serious disease in humans and have become a major
public health problem during the past years. Since animals infected with these
pathogens show only mild transient disease or no clinical signs at all, new
concepts in the entire production line ("stable to table") are
necessary in order to avoid human infection. Two emerging viruses with zoonotic
potential--avian influenza virus and Nipah virus--have been found in Asia in
1997 and 1999. Both diseases had a major impact on disease control and public
health in the countries of origin. In order to cope threats from infectious
diseases, in particular those of public health relevance, a combined effort
among all institutions involved will be necessary. The proposed "European
Center for Infectious Diseases" and the "Swiss Center for Zoonotic
Diseases" could be a potential approach in order to achieve this goal.
Descriptors: public health, infection, veterinary
medicine, Campylobacteriosis, bacterial disease, Salmonellosis, animal product
handling, livestock handling, meat inspection, foodborne zoonosis, food
contamination prevention and control, food microbiology, meat microbiology,
meat products microbiology, zoonoses transmission, animal husbandry, European
Union, food handling, risk factors.
Jennings, L. (2004). Avian influenza: a public
health risk for New Zealand. New Zealand Medical Journal 117(1192):
U843. ISSN: 1175-8716.
NAL
Call Number: R99.N4
Descriptors: influenza, avian epidemiology, public health,
communicable disease control methods, disease outbreaks statistics and
numerical data, influenza A virus isolation and purification, avian influenza
transmission, avian influenza virology, New Zealand epidemiology, poultry, risk
factors, world health, zoonoses epidemiology, zoonoses transmission, zoonoses
virology.
Jerabek, J. (2002). Chripka - ptaci, prasata,
verejne zdravi. [Influenza - birds, swine, public health]. Veterinarstvi
(Czech Republic) 52(3): 150-152.
ISSN: 0506-8231.
NAL
Call Number: 41.8 V6439
Abstract: This review article deals with influenza as a
zoonosis. The pathogenicity of viruses, clinical symptoms, diagnosis and
methods of transmission of the disease between different animal species and man
are presented.
Descriptors: avian influenza virus, swine influenza virus,
zoonoses, viroses, disease transmission, diagnosis, symptoms, ELISA, Europe,
Asia, North America, America, immunoenzyme techniques, immunological
techniques, infectious diseases, pathogenesis.
Joffe, H. and N.Y. Lee (2004). Social
representation of a food risk: the Hong Kong avian bird flu epidemic. Journal
of Health Psychology 9(4): 517-33.
ISSN: 1359-1053.
Abstract: The paper explores the social representation
of the 2001 Hong Kong avian bird flu epidemic from the perspective of local
women. Fifty women were asked to describe their first thoughts about the flu,
and these were subsequently explored. Thematic analysis of the semi-structured
interviews revealed that the first thoughts were characterized by: (a) the
origin of the epidemic, (b) anchors for it, (c) emotions about it, and (d)
images of it. Aspersion concerning the lack of hygiene of Mainland Chinese
chicken rearers and chicken sellers in Hong Kong dominated the interviews.
Other environmental factors were also stressed, as was regulation leniency and
a drive to profit. Comparisons between old traditions and newer practices
formed a central feature. The findings are discussed in terms of their
continuity with western risk findings as well as their specific cultural
nuances.
Descriptors: bird diseases epidemiology, food, social
behavior, adult, bird diseases virology, culture, disease outbreaks, health
behavior, Hong Kong epidemiology, hygiene, influenza A virus, avian isolation
and purification, middle aged, questionnaires.
John, T.J. (2004). Avian influenza: expect the
best but prepare for the worst. Indian Journal of Medical Research
119(2): iii-iv. ISSN: 0971-5916.
Descriptors: birds virology, disease outbreaks prevention
and control, influenza A virus, avian genetics, avian influenza transmission,
India, avian influenza pathogenicity, avian influenza diagnosis.
Jou, W.M., M. Verhoeyen, R. Devos, E. Saman, R. Fang,
D. Huylebroeck, W. Fiers, G. Threlfall, C. Barber, N. Carey, and S. Emtage
(1980). Complete structure of the hemagglutinin gene from the human
influenza A/Victoria/3/75 (H3N2) strain as determined from cloned DNA. Cell
19(3): 683-96. ISSN: 0092-8674.
NAL
Call Number: QH573.C42
Abstract: The complete sequence of a hemagglutinin (HA)
gene of a recent human influenza A strain, A/Victoria/3/75, is 1768 nucleotides
long and contains the information for 567 amino acids. It codes for a signal
peptide of 16 amino acids, the HA1 chain of the mature hemagglutinin of 329
amino acids, a connecting region between HA1 and HA2 consisting of a single
arginine residue and the HA2 portion of 221 amiino acids. The sequence is
compared with the hemagglutinin of two members of other subtypes, the human H2
strain A/Jap/305/57 and the avian Hav1 strain A/FPV/Rostock/34, and with one of
the same H3 subtype, A/Memphis/3/72. To align the HA1 chain of different major
subtypes several deletions/insertions of single amino acids must be invoked,
but two more extensive differences are found at both ends, one leading to an
extension of the amino terminal sequence of HA1 and the other (four residues)
occurring in the region processed away between HA1 and HA2. Comparison of the
HA1 of two H3 strains suggests that drift probably depends on single base
mutations, some of which change antigenic determinants. The HA2 region, which
apparently is not involved in the immune response, is highly conserved even
between different subtypes, and single base substitutions account for all the
observed diversity. A hydrophobic segment of 24 residues is present in the same
position close to the carboxyl terminus of HA2 in both Victoria and FPV, and
presumably functions in implantation into the lipid bilayer. The many conserved
features not only in HA2 but also in HA1 suggest a rather rigid architecture
for the whole hemagglutinin molecule.
Descriptors: genes viral, hemagglutinins viral genetics,
influenza A virus human genetics, RNA viral genetics, amino acid sequence, base
sequence, carbohydrates analysis, cloning, molecular, codon, DNA, viral
genetics, epitopes, hemagglutinins viral analysis, avian genetics.
Kaiser, J. (2004). Influenza: girding for
disaster. Facing down pandemic flu, the world's defenses are weak. Science
306(5695): 394-7. ISSN: 1095-9203.
NAL
Call Number: 470 Sci2
Descriptors: antiviral agents therapeutic use, disease
outbreaks prevention and control, influenza prevention and control, influenza
vaccines supply and distribution, world health, adjuvants, immunologic,
antiviral agents supply and distribution, clinical trials, developed countries,
developing countries, influenza epidemiology, influenza A virus, avian
immunology, avian pathogenicity, orthomyxoviridae immunology, orthomyxoviridae
pathogenicity, patents, United States, vaccines, synthetic.
Kanegae, Y., S. Sugita, K.F. Shortridge, Y. Yoshioka,
and K. Nerome (1994). Origin and evolutionary pathways of the H1
hemagglutinin gene of avian, swine and human influenza viruses: cocirculation
of two distinct lineages of swine virus. Archives of Virology
134(1-2): 17-28. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: The nucleotide sequences of the HA1 domain of
the H1 hemagglutinin genes of A/duck/Hong Kong/36/76, A/duck/Hong Kong/196/77,
A/sw/North Ireland/38, A/sw/Cambridge/39 and A/Yamagata/120/86 viruses were
determined, and their evolutionary relationships were compared with those of
previously sequenced hemagglutinin (H1) genes from avian, swine and human
influenza viruses. A pairwise comparison of the nucleotide sequences revealed
that the genes can be segregated into three groups, the avian, swine and human
virus groups. With the exception of two swine strains isolated in the 1930s, a
high degree of nucleotide sequence homology exists within the group. Two
phylogenetic trees constructed from the substitutions at the synonymous site and
the third codon position showed that the H1 hemagglutinin genes can be divided
into three host-specific lineages. Examination of 21 hemagglutinin genes from
the human and swine viruses revealed that two distinct lineages are present in
the swine population. The swine strains, sw/North Ireland/38 and
sw/Cambridge/39, are clearly on the human lineage, suggesting that they
originate from a human A/WSN/33-like variant. However, the classic swine
strain, sw/Iowa/15/30, and the contemporary human viruses are not direct
descendants of the 1918 human pandemic strain, but did diverge from a common
ancestral virus around 1905. Furthermore, previous to this the above mammalian
viruses diverged from the lineage containing the avian viruses at about 1880.
Descriptors: evolution, hemagglutinins viral genetics,
influenza A virus avian genetics, human genetics, porcine genetics, amino acid
sequence, chick embryo, genes viral, hemagglutinin glycoproteins, influenza
virus, avian classification, human classification, porcine classification,
molecular sequence data, phylogeny, sequence homology, amino acid.
Kaplan, M.M. (1980). Some epidemiological and
virological relationships between human and animal influenza. Comparative
Immunology, Microbiology and Infectious Diseases 3(1-2): 19-24. ISSN: 0147-9571.
NAL
Call Number: QR180.C62
Descriptors: disease reservoirs, influenza microbiology,
influenza A virus genetics, orthomyxoviridae infections veterinary, genes
viral, horses microbiology, influenza A virus avian, influenza A virus,
porcine, orthomyxoviridae infections microbiology, orthomyxoviridae infections
transmission, recombination, genetic.
Karasin, A.I., I.H. Brown, S. Carman, and C.W. Olsen
(2000). Isolation and characterization of H4N6 avian influenza viruses from
pigs with pneumonia in Canada. Journal of Virology 74(19): 9322-7. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: In October 1999, H4N6 influenza A viruses
were isolated from pigs with pneumonia on a commercial swine farm in Canada.
Phylogenetic analyses of the sequences of all eight viral RNA segments
demonstrated that these are wholly avian influenza viruses of the North
American lineage. To our knowledge, this is the first report of interspecies
transmission of an avian H4 influenza virus to domestic pigs under natural
conditions.
Descriptors: influenza A virus avian isolation and
purification, pneumonia, viral virology, swine diseases virology, Canada
epidemiology, influenza A virus avian genetics, molecular sequence data,
phylogeny, pneumonia, viral epidemiology, swine, swine diseases epidemiology.
Karasin, A.I., C.W. Olsen, I.H. Brown, S. Carman, M.
Stalker, and G. Josephson (2000). H4N6 influenza virus isolated from pigs in
Ontario. Canadian Veterinary Journal Revue Veterinaire Canadienne 41(12): 938-9.
ISSN: 0008-5286.
NAL
Call Number: 41.8 R3224
Descriptors: influenza A virus avian isolation and
purification, swine diseases virology, antigens, viral analysis, enzyme linked
immunosorbent assay veterinary, incidence, avian immunology, Ontario
epidemiology, swine, swine diseases epidemiology, swine diseases immunology.
Karasin, A.I., M.M. Schutten, L.A. Cooper, C.B.
Smith, K. Subbarao, G.A. Anderson, S. Carman, and C.W. Olsen (2000). Genetic
characterization of H3N2 influenza viruses isolated from pigs in North America,
1977-1999: evidence for wholly human and reassortant virus genotypes. Virus
Research 68(1): 71-85. ISSN:
0168-1702.
NAL
Call Number: QR375.V6
Abstract: Since 1998, H3N2 viruses have caused epizootics
of respiratory disease in pigs throughout the major swine production regions of
the U.S. These outbreaks are remarkable because swine influenza in North
America had previously been caused almost exclusively by H1N1 viruses. We
sequenced the full-length protein coding regions of all eight RNA segments from
four H3N2 viruses that we isolated from pigs in the Midwestern U.S. between
March 1998 and March 1999, as well as from H3N2 viruses recovered from a piglet
in Canada in January 1997 and from a pig in Colorado in 1977. Phylogenetic
analyses demonstrated that the 1977 Colorado and 1997 Ontario isolates are
wholly human influenza viruses. However, the viruses isolated since 1998 from
pigs in the Midwestern U.S. are reassortant viruses containing hemagglutinin,
neuraminidase and PB1 polymerase genes from human influenza viruses, matrix,
non-structural and nucleoprotein genes from classical swine viruses, and PA and
PB2 polymerase genes from avian viruses. The HA proteins of the Midwestern
reassortant swine viruses can be differentiated from those of the 1995 lineage
of human H3 viruses by 12 amino acid mutations in HA1. In contrast, the
Sw/ONT/97 virus, which did not spread from pig-to-pig, lacks 11 of these
changes.
Descriptors: influenza A virus avian genetics, human
genetics, porcine classification, porcine genetics, reassortant viruses
genetics, genotype, influenza veterinary, influenza virology, molecular
sequence data, North America, phylogeny, swine, swine diseases virology.
Katz, J.M. (2003). The impact of avian influenza
viruses on public health. Avian Diseases 47(Special Issue):
914-920. ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: In the late 1990s, H5N1 and H9N2 avian
influenza viruses caused respiratory infections in humans in Hong Kong.
Exposure to domestic poultry in live-bird markets was significantly associated
with human H5N1 disease. Seroepidemiologic studies conducted among contacts of
H5N1-infected persons determined that human-to-human transmission of the avian
H5N1 viruses occurred but was rare. The relatively high rates of H5 and H9
antibody seroprevalence among Hong Kong poultry workers in 1997 highlight the
potential for avian viruses to transmit to humans, particularly those with
occupational exposure. Such transmission increases the likelihood of
reassortment between a currently circulating human virus and an avian virus and
thus the creation of a strain with pandemic potential.
Descriptors: epidemiology, immune system, infection,
respiratory infection, infectious disease, respiratory system disease, antibody
seroprevalence, live bird markets, pandemic, potential public health, viral
transmission.
Katz, J.M., W. Lim, C.B. Bridges, T. Rowe, J. Hu
Primmer, X. Lu, R.A. Abernathy, M. Clarke, L. Conn, H. Kwong, M. Lee, G. Au,
Y.Y. Ho, K.H. Mak, N.J. Cox, and K. Fukuda (1999). Antibody response in
individuals infected with avian influenza A (H5N1) viruses and detection of
anti-H5 antibody among household and social contacts. Journal of
Infectious Diseases 180(6): 1763-70.
ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Abstract: The first documented outbreak of human
respiratory disease caused by avian influenza A (H5N1) viruses occurred in Hong
Kong in 1997. The kinetics of the antibody response to the avian virus in H5N1-infected
persons was similar to that of a primary response to human influenza A viruses;
serum neutralizing antibody was detected, in general, >/=14 days after
symptom onset. Cohort studies were conducted to assess the risk of
human-to-human transmission of the virus. By use of a combination of serologic
assays, 6 of 51 household contacts, 1 of 26 tour group members, and none of 47
coworkers exposed to H5N1-infected persons were positive for H5 antibody. One
H5 antibody-positive household contact, with no history of poultry exposure,
provided evidence that human-to-human transmission of the avian virus may have
occurred through close physical contact with H5N1-infected patients. In
contrast, social exposure to case patients was not associated with H5N1 infection.
Descriptors: antibodies, viral blood, hemagglutinin
glycoproteins, influenza virus immunology, influenza immunology, influenza
transmission, influenza A virus avian immunology, adolescent, adult, child,
child, preschool, cohort studies, family health, infant, influenza virology,
avian isolation and purification, interpersonal relations, middle aged,
neutralization tests, poultry virology.
Katz, J.M., X. Lu, A.M. Frace, T. Morken, S.R. Zaki,
and T.M. Tumpey (2000). Pathogenesis of and immunity to avian influenza A H5
viruses. Biomedicine and Pharmacotherapy Biomedecine and
Pharmacotherapie 54(4): 178-87.
ISSN: 0753-3322.
NAL
Call Number: R41.B52
Abstract: In 1997 in Hong Kong, 18 human cases of respiratory
illness were caused by an avian influenza A H5N1 virus. Although avian
influenza viruses had not previously been known to cause respiratory illness in
humans, the H5N1 viruses caused severe illness and death, primarily in
individuals aged > 12 years. The introduction of H5N1 viruses into humans
raised concerns about the potential of these viruses to cause a pandemic. We
have used the BALB/c mouse to better understand the pathogenesis of and
immunity to the H5N1 viruses in a mammalian model. Previously, we demonstrated
that H5N1 viruses isolated from humans replicated efficiently in the lungs of
mice without prior adaptation to this host. Two general phenotypes of
pathogenicity of H5N1 viruses, based on high and low lethality for mice, were
observed. We now demonstrate that in addition to a lethal outcome, H5N1 viruses
with a high pathogenicity phenotype exhibit additional features that include
rapid and uncontrolled replication in the lungs of infected mice, dissemination
and replication of the virus in other organs, and depletion of peripheral blood
leukocytes. The BALB/c mouse model was also used to better understand the
parameters of protective immunity to the H5N1 viruses. Prior infection with
H5N1 viruses of low pathogenicity or an antigenically related non-pathogenic
H5N3 virus protected mice from death by infection with a highly pathogenic
HK/483 virus. Serum hemagglutination-inhibition antibody titers of 40 or
greater were associated with protection of mice from death. Immunization of
mice with baculovirus-expressed recombinant H5 hemagglutinin protein or a
previously defined HS-specific synthetic peptide induced MHC class II
restricted CTL activity. Mice that had CTL activity but no serum
hemagglutination-inhibition antibody were not protected from a lethal challenge
with H5N1 virus. These results suggest that antibody is required for protection
of mice against lethal challenge with H5N1 viruses of the high pathogenicity
phenotype.
Descriptors: influenza A virus avian immunology, avian
pathogenicity, antibodies, viral blood, antigens, viral analysis, immunization,
influenza virology, influenza vaccine immunology, mice, mice inbred BALB c, T
lymphocytes, cytotoxic immunology, virus replication.
Katz, J.M., X. Lu, T.M. Tumpey, C.B. Smith, M.W. Shaw,
and K. Subbarao (2000). Molecular correlates of influenza A H5N1 virus
pathogenesis in mice. Journal of Virology 74(22): 10807-10. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Highly pathogenic avian influenza A H5N1
viruses caused an outbreak of human respiratory illness in Hong Kong. Of 15
human H5N1 isolates characterized, nine displayed a high-, five a low-, and one
an intermediate-pathogenicity phenotype in the BALB/c mouse model. Sequence
analysis determined that five specific amino acids in four proteins correlated
with pathogenicity in mice. Alone or in combination, these specific residues
are the likely determinants of virulence of human H5N1 influenza viruses in
this model.
Descriptors: influenza virology, influenza A virus avian
genetics, avian pathogenicity, adolescent, adult, child, preschool, disease
models, animal, infant, influenza physiopathology, avian classification, mice,
mice inbred BALB c, middle aged, molecular sequence data, phenotype, sequence
analysis, DNA, viral proteins genetics, virulence.
Kaverin, N.V., I.A. Rudneva, Y.A. Smirnov, and N.N.
Finskaya (1988). Human-avian influenza virus reassortants: effect of
reassortment pattern on multi-cycle reproduction in MDCK cells. Archives
of Virology 103(1-2): 117-26. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Human-avian influenza reassortants possessing
the HA gene of the avian parent virus were tested for their ability to
replicate in MDCK cells at 37 degrees C and 31 degrees C. Both avian parent
viruses, A/Duck/Ukraine/1/63 (H3N8) and A/Duck/Hoshimin/014/78 (H5N3) induced
an efficient multi-cycle infection at 37 degrees C, but replicated poorly at 31
degrees C, whereas the human parent virus, MDCK-adapted variant of A/USSR/90/77
(H1N1) strain, replicated efficiently at both temperatures. The reassortant
clone possessing the HA gene of A/Duck/Ukraine/1/63 virus and the other 7 genes
of A/USSR/90/77 virus replicated at both temperatures almost as efficiently as
the human parent virus. Among the reassortants between A/Duck/Hoshimin/014/78
and A/USSR/90/77, the clones possessing the HA and NA genes of the avian
strain, or the HA, NA, NP, and NS genes of the avian strain, and the other
genes of the human parent virus, replicated poorly at both temperatures, especially
at 31 degrees C, whereas the reassortant possessing the HA, NA, and M genes of
the avian virus replicated at both temperatures fairly efficiently. The results
are discussed in connection with the limitations imposed by different genes
upon avian influenza viruses' ability to replicate in mammalian cells.
Descriptors: genes viral, hemagglutinins viral physiology,
influenza A virus avian pathogenicity, human pathogenicity, virus replication,
birds microbiology, chick embryo, hemagglutinins viral biosynthesis,
hemagglutinins viral genetics, avian genetics, human genetics, RNA viral
analysis, temperature, transfection, viral proteins biosynthesis.
Kaverin, N.V., Y.A. Smirnov, E.A. Govorkova, I.A.
Rudneva, A.K. Gitelman, A.S. Lipatov, N.L. Varich, S.S. Yamnikova, N.V.
Makarova, R.G. Webster, and D.K. Lvov (2000). Cross-protection and
reassortment studies with avian H2 influenza viruses. Archives of
Virology 145(6): 1059-66. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: In order to assess the degree of immune
cross-protection among avian H2 influenza virus strains, mice were immunised
with beta-propiolactone-inactivated virus preparations and infected
intranasally with mouse-adapted variant of A/Black Duck/New Jersey/1580/78
(H2N3) strain. The experiments with 11 avian H2 strains revealed that both
Eurasian and American H2 avian influenza viruses exhibit either high or
moderate degree of cross-protection. The grouping of the strains in accordance
with their cross-protection efficiency does not coincide with H2 phylogenetic
branches. Several reassortant clones were obtained with the use of A/Pintail
Duck/Primorie/695/76 (H2N3) strain and high-yield X-67 reassortant as parent
viruses, among them a high-yield H2N3 reassortant. Taking into account the data
on cross-protection among avian H2 strains, the high-yield H2N3 reassortant may
be regarded as a prototype strain to be used for the preparation of killed
vaccines in the case of a new appearance of avian H2 haemagglutinin in
circulation in humans.
Descriptors: influenza prevention and control, influenza A
virus avian genetics, avian immunology, influenza vaccine immunology,
reassortant viruses immunology, chick embryo, cross reactions, immunization,
influenza immunology, avian pathogenicity, mice, reassortant viruses genetics,
vaccines, attenuated immunology.
Kaverin, N.V. and Y.A. Smirnov (2003). An
interspecies transmission of influenza A viruses and pandemics. Voprosy
Virusologii 48(3): 4-10. ISSN:
0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Molecular and genetic data are summarized on
the origin of influenza A virus pandemic variants. Conceptual modifications of
the reassortment theory of the origin of pandemic strains are discussed in
connection with the appearance of new H5 and H9 avian influenza viruses, which
caused the respiratory infection in man and which are presently in the focus of
attention as possible agents of future pandemic.
Descriptors: epidemiology, infection, respiratory system,
veterinary medicine, influenza A, respiratory system disease, viral disease,
pandemic, strain origins, reassortment theory.
Kawaoka, Y. (1991). Difference in replication and
pathogenicity of influenza A viruses in chickens and mice. Journal of
Veterinary Medical Science the Japanese Society of Veterinary Science
53(1): 125-6. ISSN: 0916-7250.
NAL
Call Number: SF604.J342
Descriptors: chickens microbiology, influenza A virus
avian physiology, porcine physiology, influenza A virus physiology, mice
microbiology, cloaca microbiology, avian pathogenicity, porcine pathogenicity,
influenza A virus pathogenicity, orthomyxoviridae infections microbiology,
orthomyxoviridae infections veterinary, poultry diseases microbiology, rodent
diseases microbiology, trachea microbiology, virus replication.
Kawaoka, Y., E. Bordwell, and R.G. Webster (1987). Intestinal
replication of influenza A viruses in two mammalian species. Brief report. Archives
of Virology 93(3-4): 303-8. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: The sites of replication of influenza A
viruses in ferrets and pigs were studied. The majority of the swine, equine,
and avian influenza A viruses tested were recovered from the intestinal tract
of ferrets as well as from the respiratory tract; most of the human influenza
viruses studied were recovered only from the respiratory tract. In contrast
with ferrets, only Hong Kong/1/68 (H 3 N 2) influenza virus was recovered from
the intestinal tract of pigs. Despite the large biological variability found in
ferrets and in pigs, the results do establish that the majority of influenza
viruses have the potential to replicate in the intestinal tissues of some
mammals. Additionally, the study suggests that there are differences among the
influenza A viruses in tissue tropism in different mammals. Both viral and host
genetic factors determine the tissue tropism of influenza viruses in mammals.
Descriptors: influenza A virus physiology, intestines
microbiology, virus replication, ferrets, avian physiology, human physiology,
porcine physiology, swine.
Kawaoka, Y., S. Krauss, and R.G. Webster (1989). Avian-to-human
transmission of the PB1 gene of influenza A viruses in the 1957 and 1968
pandemics. Journal of Virology 63(11): 4603-8. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: We determined the origin and evolutionary
pathways of the PB1 genes of influenza A viruses responsible for the 1957 and
1968 human pandemics and obtained information on the variable or conserved
region of the PB1 protein. The evolutionary tree constructed from nucleotide
sequences suggested the following: (i) the PB1 gene of the 1957 human pandemic
strain, A/Singapore/1/57 (H2N2), was probably introduced from avian species and
was maintained in humans until 1968; (ii) in the 1968 pandemic strain,
A/NT/60/68 (H3N2), the PB1 gene was not derived from the previously circulating
virus in humans but probably from another avian virus; and (iii) a current
human H3N2 virus inherited the PB1 gene from an A/NT/60/68-like virus.
Nucleotide sequence analysis also showed that the avian PB1 gene was introduced
into pigs. Hence, transmission of the PB1 gene from avian to mammalian species
is a relatively frequent event. Comparative analysis of deduced amino acid
sequences disclosed highly conserved regions in PB1 proteins, which may be key
structures required for PB1 activities.
Descriptors: evolution, genes, structural, viral,
influenza transmission, influenza A virus avian genetics, human genetics, viral
proteins genetics, amino acid sequence, cloning, molecular, influenza
epidemiology, porcine genetics, molecular sequence data, sequence homology,
nucleic acid, species specificity, swine.
Kaye, D. and C.R. Pringle (2005). Avian influenza
viruses and their implication for human health. Clinical Infectious
Diseases 40(1): 108-12. ISSN:
1537-6591.
NAL
Call Number: RC111.R4
Abstract: Widespread outbreaks of avian influenza in
domestic fowl throughout eastern Asia have reawakened concern that avian
influenza viruses may again cross species barriers to infect the human population
and thereby initiate a new influenza pandemic. Simultaneous infection of humans
(or swine) by avian influenza viruses in the presence of human influenza
viruses could theoretically generate novel influenza viruses with pandemic
potential as a result of reassortment of genome subunits between avian and
mammalian influenza viruses. These hybrid viruses would have the potential to
express surface antigens from avian viruses to which the human population has
no preexisting immunity. This article reviews current knowledge of the routes
of transmission of avian influenza A viruses to humans, places the risk of
appearance of a new pandemic influenza virus in perspective, and describes the
recently observed epidemiology and clinical syndromes of avian influenza in
humans.
Descriptors: influenza A virus, viral diseases, zoonoses,
birds, human, avian influenza virus.
Keawcharoen, J., K. Oraveerakul, T. Kuiken, R.A.
Fouchier, A. Amonsin, S. Payungporn, S. Noppornpanth, S. Wattanodorn, A.
Theambooniers, R. Tantilertcharoen, R. Pattanarangsan, N. Arya, P. Ratanakorn,
D.M. Osterhaus, and Y. Poovorawan (2004). Avian influenza H5N1 in tigers and
leopards. Emerging Infectious Diseases 10(12): 2189-91. ISSN: 1080-6040.
NAL
Call Number: RA648.5.E46
Abstract: Influenza virus is not known to affect wild
felids. We demonstrate that avian influenza A (H5N1) virus caused severe
pneumonia in tigers and leopards that fed on infected poultry carcasses. This
finding extends the host range of influenza virus and has implications for
influenza virus epidemiology and wildlife conservation.
Descriptors: zoo animals virology, influenza veterinary,
influenza A virus, avian pathogenicity, Panthera virology, chickens virology,
food microbiology, influenza virology, avian genetics, lung virology, meat
virology, phylogeny, tigers virology, variation genetics.
Kelly, D.C. and N.J. Dimmock (1974). Fowl plaque
virus replication in mammalian cell-avian erythrocyte heterokaryons: studies
concerning the actinomycin D and ultra-violet light sensitive phase in
influenza virus replication. Virology 61(1): 210-22. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: cell nucleus microbiology, dactinomycin
pharmacology, influenza A virus avian growth and development, ultraviolet rays,
virus replication drug effects, virus replication radiation effects, antigens,
viral analysis, autoradiography, cell fusion, cell line, cell nucleus
immunology, cultured cells cytology, chick embryo, chickens, erythrocytes
cytology, fluorescent antibody technique, hamsters, hemagglutinins viral, avian
immunology, avian metabolism, kidney, l cells cell line, mice, neuraminidase
biosynthesis, nucleoproteins biosynthesis, radiation effects, viral proteins
biosynthesis.
Kemink, S.A., R.A. Fouchier, F.W. Rozendaal, J.M.
Broekman, M. Koopmans, A.D. Osterhaus, and P.M. Schneeberger (2004 ). Een
fatale infectie door aviair influenza-A (H7N7)-virus en aanpassing van het
preventiebeleid. [A fatal infection due to avian influenza-A (H7N7) virus and
adjustment of the preventive measures]. Nederlands Tijdschrift Voor
Geneeskunde 148(44): 2190-4. ISSN:
0028-2162.
Abstract: In February 2003, the highly pathogenic avian
influenza-A virus, subtype H7N7, was the causative agent of a large outbreak of
fowl plague in the Netherlands. Two days after visiting a poultry farm that was
infected by fowl plague, a 57-year-old male veterinarian developed malaise,
headache and fever. After 8 days he was admitted to hospital with signs of
pneumonia. Five days later, his condition deteriorated alarmingly. Despite
extensive pharmacotherapy he died 4 days later of acute pneumonia. Influenza-A
virus, subtype H7N7, was identified by means of reverse transcriptase/PCR in
broncho-alveolar washings that had been obtained earlier; routine virus culture
yielded the isolate A/Nederland/219/03, which differs by 14 amino-acid
substitutions from the first isolate in a chicken (A/kip/Nederland/1/03).
Partly as a result of this case, the preventive measures were then adjusted;
people who came into contact with infected poultry were given increased
possibilities for vaccination and the administration of oseltamivir.
Descriptors: influenza A virus, avian isolation and
purification, avian influenza transmission, occupational diseases prevention
and control, poultry diseases transmission, zoonoses, disease outbreaks, fatal
outcome, avian influenza pathogenicity, avian influenza epidemiology, avian
influenza prevention and control, avian influenza virology, middle aged,
Netherlands epidemiology, occupational diseases virology, poultry, poultry
diseases epidemiology, veterinarians.
Kida, H. (1997). [Ecology of influenza viruses in
animals and the mechanism of emergence of new pandemic strains]. Nippon
Rinsho Japanese Journal of Clinical Medicine 55(10): 2521-6. ISSN: 0047-1852.
Abstract: Ecological studies on influenza viruses
revealed that the hemagglutinin genes are introduced into new pandemic strains
from viruses circulating in migratory ducks through domestic ducks and pigs in
southern China. Experimental infection of pigs with 38 avian influenza virus
strains with H1-H13 hemagglutinins showed that at least one strain of each HA
subtype replicated in the upper respiratory tract of pigs. Co-infection of pigs
with a swine virus and with an avian virus generated reassortant viruses. The
results indicate that avian viruses of any subtype can contribute genes in the
generation of reassortants. Virological surveillance revealed that influenza
viruses in waterfowl reservoir are perpetuated year-by-year in the frozen lake
water while ducks are absent.
Descriptors: influenza veterinary, bird diseases
transmission, birds, horse diseases transmission, horses, influenza transmission, swine, swine
diseases transmission, zoonoses.
Kida, H., T. Ito, J. Yasuda, Y. Shimizu, C. Itakura,
K.F. Shortridge, Y. Kawaoka, and R.G. Webster (1994). Potential for
transmission of avian influenza viruses to pigs. Journal of General
Virology 75(9): 2183-2188. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: Pandemic strains of influenza A virus arise
by genetic reassortment between avian and human viruses. Pigs have been
suggested to generate such reassortants as intermediate hosts. In order for
pigs to serve as 'mixing vessels' in genetic reassortment events, they must be
susceptible to both human and avian influenza viruses. The ability of avian
influenza viruses to replicate in pigs, however, has not been examined
comprehensively. In this study, we assessed the growth potential of 42 strains
of influenza virus in pigs. Of these, 38 were avian strains, including 27 with
non-human-type haemagglutinins (HA; H4 to H13). At least one strain of each HA
subtype replicated in the respiratory tract of pigs for 5 to 7 days to a level
equivalent to that of swine and human viruses. These results indicate that
avian influenza viruses with or without non-human-type HAs can be transmitted
to pigs, thus raising the possibility of introduction of their genes into
humans. Sera from pigs infected with avian viruses showed high titres of
antibodies in ELISA and neutralization tests, but did not inhibit
haemagglutination of homologous viruses, cautioning against the use of
haemagglutination-inhibition tests to identify pigs infected with avian
influenza viruses. Co-infection of pigs with a swine virus and with an avian
virus unable to replicate in this animal generated reassortant viruses, whose
polymerase and HA genes were entirely of avian origin, that could be passaged
in pigs. This finding indicates that even avian viruses that do not replicate
in pigs can contribute genes in the generation of reassortants.
Descriptors: evolution and adaptation, genetics, immune
system, infection, microbiology, vector biology, veterinary medicine, ELISA
antibody hemagglutination inhibiting antibody mixing vessel neutralizing
antibody pandemic strain origin reassortant virus generation swine virus avian
virus co infection virus replication.
Klimov, A., Y. Ghendon, H. Zavadova, J. Broucek, and
T. Medvedeva (1983). High reproduction capacity of recombinants between H3N2
human influenza and fowl plague viruses is due to the gene coding for M
proteins. Acta Virologica 27(5): 434-8. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: Recombinants between H3N2 human influenza
viruses (A/Victoria/3/75 and A/Bangkok/1/79, low-yielding parents in chick
embryos) and fowl plague virus (FPV, a high-yielding parent in chick embryos)
have been obtained. The high reproductive capacity of recombinants in chick
embryos has been shown to be due to the gene coding for M proteins.
Descriptors: genes viral, influenza A virus avian
genetics, human genetics, recombination, genetic, viral proteins genetics,
virus replication, chick embryo, avian physiology, human physiology, viral
matrix proteins.
Klingeborn, B., L. Englund, R. Rott, N. Juntti, and
G. Rockborn (1985). An avian influenza A virus killing a mammalian
species--the mink. Brief report. Archives of Virology 86(3-4):
347-51. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: During October of 1984 an influenza epidemic
occurred on mink farms in the coastal region of South Sweden. Six strains of an
influenza A virus were isolated. All six isolates were of the H 10 subtype in
combination with N4. The H 10 subtype in combination with various N subtypes
was hitherto only known to occur in avian strains, the prototype being the
A/chicken/Germany/N/49 (H 10N7) virus.
Descriptors: disease outbreaks veterinary, influenza
veterinary, influenza A virus avian pathogenicity, mink, influenza
epidemiology.
Kodihalli, S., H. Goto, D.L. Kobasa, S. Krauss, Y.
Kawaoka, and R.G. Webster (1999). DNA vaccine encoding hemagglutinin
provides protective immunity against H5N1 influenza virus infection in mice.
Journal of Virology 73(3): 2094-8.
ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: In Hong Kong in 1997, a highly lethal H5N1
avian influenza virus was apparently transmitted directly from chickens to
humans with no intermediate mammalian host and caused 18 confirmed infections
and six deaths. Strategies must be developed to deal with this virus if it
should reappear, and prospective vaccines must be developed to anticipate a
future pandemic. We have determined that unadapted H5N1 viruses are pathogenic
in mice, which provides a well-defined mammalian system for immunological
studies of lethal avian influenza virus infection. We report that a DNA vaccine
encoding hemagglutinin from the index human influenza isolate A/HK/156/97
provides immunity against H5N1 infection of mice. This immunity was induced
against both the homologous A/HK/156/97 (H5N1) virus, which has no
glycosylation site at residue 154, and chicken isolate A/Ck/HK/258/97 (H5N1),
which does have a glycosylation site at residue 154. The mouse model system
should allow rapid evaluation of the vaccine's protective efficacy in a
mammalian host. In our previous study using an avian model, DNA encoding
hemagglutinin conferred protection against challenge with antigenic variants
that differed from the primary antigen by 11 to 13% in the HA1 region. However,
in our current study we found that a DNA vaccine encoding the hemagglutinin
from A/Ty/Ir/1/83 (H5N8), which differs from A/HK/156/97 (H5N1) by 12% in HA1,
prevented death but not H5N1 infection in mice. Therefore, a DNA vaccine made
with a heterologous H5 strain did not prevent infection by H5N1 avian influenza
viruses in mice but was useful in preventing death.
Descriptors: hemagglutinin glycoproteins, influenza virus
immunology, influenza prevention and control, influenza A virus avian
immunology, influenza vaccine immunology, vaccines, DNA immunology, antibodies,
viral blood, hemagglutinin glycoproteins, influenza virus genetics,
immunization, mice, mice inbred BALB c.
Kodihalli, S., D.L. Kobasa, and R.G. Webster (2000). Strategies
for inducing protection against avian influenza A virus subtypes with DNA
vaccines. Vaccine 18(23): 2592-9.
ISSN: 0264-410X.
NAL
Call Number: QR189.V32
Abstract: The cross-species transfer of a H5N1
influenza virus from birds to humans, and the systemic spread of this virus in
mice, has accelerated the efforts to devise protective strategies against
lethal influenza viruses. DNA vaccination with the highly conserved
nucleoprotein gene appears to provide cross protection against influenza A
viruses in murine models. Whether such vaccines would protect human hosts
against different influenza A viruses, including strains with pandemic
potential, is unclear. Our aim in this study is to evaluate the ability of a
combination DNA vaccine consisting of two plasmids encoding the HA genes from
two different subtypes and a DNA vaccine encoding the viral nucleoprotein gene
from a H5 virus to induce protection against highly lethal infection caused by
H5 and H7 influenza viruses in chickens. Chickens given a single dose of
plasmids expressing H5 and H7 hemagglutinins protected the birds from infection
by either subtype. However, birds immunized with nucleoprotein DNA and
challenged with either A/Ck/Vic/1/85(H7N7) or A/Ty/Ir/1/83 (H5N8) showed
definite signs of infection, suggesting inadequate immunity against viral
infection. Fifty percent of the nucleoprotein DNA immunized birds survived
infection by influenza A/Ty/Ir/1/83 (H5N8) virus (virus of same subtype) while
42% survived infection by influenza A/Ck/Vic/1/85/(H7N7) virus (virus of a
different subtype). These studies demonstrate that immunization with DNA
encoding a type-specific gene may not be effective against either homologous or
heterologous strains of virus, particularly if the challenge virus causes a
highly lethal infection. However, the combination of HA subtype vaccines are
effective against lethal infection caused by viruses expressing any of the HA
subtypes used in the combination preparation.
Descriptors: chickens immunology, hemagglutinin
glycoproteins, influenza virus immunology, influenza veterinary, influenza A
virus avian immunology, influenza vaccine immunology, nucleoproteins, poultry
diseases prevention and control, vaccination veterinary, vaccines, DNA
immunology, viral core proteins immunology, cos cells, Cercopithecus
aethiops, evaluation studies, hemagglutinin glycoproteins, influenza virus
genetics, influenza immunology, influenza prevention and control, influenza
transmission, avian genetics, mice, plasmids immunology, poultry diseases
immunology, recombinant fusion proteins immunology, species specificity,
transfection, viral core proteins genetics, zoonoses.
Koopmans, M., B. Wilbrink, M. Conyn, G. Natrop, H.
van der Nat, H. Vennema, A. Meijer, J. van Steenbergen, R. Fouchier, A.
Osterhaus, and A. Bosman (2004). Transmission of H7N7 avian influenza A
virus to human beings during a large outbreak in commercial poultry farms in
the Netherlands. Lancet 363(9409): 587-93. ISSN: 1474-547X.
NAL
Call Number: 448.8 L22
Abstract: BACKGROUND: An outbreak of highly pathogenic
avian influenza A virus subtype H7N7 started at the end of February, 2003, in
commercial poultry farms in the Netherlands. Although the risk of transmission
of these viruses to humans was initially thought to be low, an outbreak
investigation was launched to assess the extent of transmission of influenza A
virus subtype H7N7 from chickens to humans. METHODS: All workers in poultry
farms, poultry farmers, and their families were asked to report signs of conjunctivitis
or influenza-like illness. People with complaints were tested for influenza
virus type A subtype H7 (A/H7) infection and completed a health questionnaire
about type of symptoms, duration of illness, and possible exposures to infected
poultry. FINDINGS: 453 people had health complaints--349 reported
conjunctivitis, 90 had influenza-like illness, and 67 had other complaints. We
detected A/H7 in conjunctival samples from 78 (26.4%) people with
conjunctivitis only, in five (9.4%) with influenza-like illness and
conjunctivitis, in two (5.4%) with influenza-like illness only, and in four
(6%) who reported other symptoms. Most positive samples had been collected
within 5 days of symptom onset. A/H7 infection was confirmed in three contacts
(of 83 tested), one of whom developed influenza-like illness. Six people had
influenza A/H3N2 infection. After 19 people had been diagnosed with the
infection, all workers received mandatory influenza virus vaccination and
prophylactic treatment with oseltamivir. More than half (56%) of A/H7
infections reported here arose before the vaccination and treatment programme.
INTERPRETATION: We noted an unexpectedly high number of transmissions of avian
influenza A virus subtype H7N7 to people directly involved in handling infected
poultry, and we noted evidence for person-to-person transmission. Our data
emphasise the importance of adequate surveillance, outbreak preparedness, and
pandemic planning.
Descriptors: avian influenza A virus, transmission,
humans, outbreak, poultry farms, sub type H7N7.
Kosiakov, P.N., V.S. Pankratov, and Z.I. Rovnova
(1979). Antigeny gemaggliutininov virusov grippa, vydelennykh ot cheloveka i
ptits. [Hemagglutinin antigens of influenza viruses isolated from man and
birds]. Voprosy Virusologii (3): 242-7. ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Immunological analysis has shown
hemagglutinins of avian viruses like hemagglutinins of human viruses to have a
complex antigenic composition. Three antigenic determinants were discovered in hemagglutinin
of A/Chicken/12/71 virus previously designated H3 and in hemagglutinin of
A/Tern/18/73 virus previously designated Hav7. The H3 determinant and the
second determinant are identical in avian and A/Hong Kong/1/68 human viruses.
In addition, hemagglutinins of avian viruses have a determinant specific for
each virus which is lacking in human influenza virus hemagglutinin.
Descriptors: antigens, viral isolation and purification,
birds microbiology, hemagglutinins viral isolation and purification, influenza
A virus avian immunology, human immunology, adsorption, chick embryo,
complement fixation tests, epitopes, hemagglutination inhibition tests.
Krichevets, S.G., N.L. Varich, I.A. Rudneva, and N.V.
Kaverin (1999). Relationship between antigenic characteristics of human and
avian influenza virus NP protein and strain variations of amino acid sequences.
Voprosy Virusologii 44(4): 158-162.
ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Human and avian influenza A strains with a
known amino acid sequence of NP protein were studied in
radioimmunoprecipitation test with a panel of anti-NP monoclonal antibodies.
Two of 7 MAbs (315 and IVE8) reacted with variable epitopes. One of the epitopes
was present only in human strains, while the other in both human and avian
strains, but absent in gull strains and in one human strain, A/Puerto Rico/8/34
(H1N1). The variations recognized by antibodies 315 and IVE8 correlated with
amino acid substitutes in positions 16 and 353, respectively.
Descriptors: biochemistry and molecular biophysics,
infection, amino acid substitution molecular variability.
Kroes, A.C., W.J. Spaan, and E.C. Claas (2004). Van
vogelpest tot influenzapandemie; reden tot voorzorgen. [From fowl plague to
influenza pandemic; a reason for taking precautions]. Nederlands
Tijdschrift Voor Geneeskunde 148(10): 458-63. ISSN: 0028-2162.
Abstract: Throughout Eastern Asia, there is currently
an epidemic of fowl plague or highly pathogenic avian influenza, on an
unprecedented scale. The prospects for rapid containment are poor. The
causative virus, influenza A of the H5N1 subtype, is of limited infectivity for
humans. If infection occurs, however, then the consequences are serious and
even fatal in a majority of cases. In view of the receptor specificity of avian
influenza viruses, this may be related to individually increased
susceptibility, which does not lead to further spread. However, it is known
that influenza A viruses can readily adapt to replication in the human host by
the acquisition of specific gene segments or even by mutations of the avian
virus. The extreme scale of human contact with influenza virus of the H5N1
subtype at present engenders fear that there is a high risk of such adaptation
and a subsequent pandemic spread. Adequate precautions are necessary, not only
in terms of an acceleration of vaccine production but primarily in arranging
for sufficient availability of the new antiviral drugs.
Descriptors: disease outbreaks, influenza A virus, avian
pathogenicity, human pathogenicity, avian influenza transmission, zoonoses,
chickens, avian genetics, human genetics.
Ku, A.S.W. and L.T.W. Chan (1999). The first case
of H5N1 avian influenza infection in a human with complications of adult
respiratory distress syndrome and Reye's syndrome. Journal of
Paediatrics and Child Health 35(2): 207-209. ISSN: 1034-4810.
Abstract: Avian influenza virus was not known to cause
systemic infection in humans before. We report a 3-year-old boy with good past
health who developed pneumonia caused by H5N1 avian influenza A virus (A/Hong
Kong/156/97). The virus was isolated from a tracheal aspirate. There were
complications of Reye's syndrome, adult respiratory distress syndrome, and
multiple organ system failure. He had a history of receiving aspirin. His adult
respiratory distress syndrome did not respond to endotracheal surfactant
replacement therapy. He died 6 days after admission. Clinicians should be alert
to the importance of a new human influenza strain.
Descriptors: infection, pediatrics, pulmonary medicine,
adult respiratory distress syndrome, respiratory system disease, pneumonia,
respiratory system disease, H5N1 avian influenza infection, first case,
respiratory system disease, viral disease, Reye's syndrome, digestive system
disease, nervous system disease, endotracheal surfactant replacement therapy
therapeutic method, case study.
Kul'kova, L.V. and V.Z. Soloukhin (1979). Reproduktsiia
virusa istinnoi chumy ptits v organizme komarov Aedes aegypti.
[Classical fowl plague virus reproduction in the body of Aedes aegypti
mosquitoes]. Voprosy Virusologii (6): 652-4. ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: The results of the studies on fowl plague
virus (FPV, Rostok strain) reproduction in Aedes aegypti mosquitoes are
presented. The virus-containing allantoic fluid was inoculated intrathoracally
in volumes of 0.1 and 0.2 microliter. The virus was isolated in chick embryos
and could be detected at 5--14 days after inoculation. After inoculation of 0.1
microliter of virus it could be detected in doses of 0.5, 2.0, 1.75 Ig2 ID50,
after inoculation of 0.2 microliter--in doses of 5, 1.5, and 0.5 Ig2 ID50.
Descriptors: Aedes microbiology, influenza A virus
avian physiology, time factors, virus replication.
Kurtz, J., R.J. Manvell, and J. Banks (1996). Avian
influenza virus isolated from a woman with conjunctivitis. Lancet
348(9031): 901-902.
NAL
Call Number: 448.8 L22
Descriptors: viroses, women, conjunctivitis, mankind,
zoonoses, avian influenza virus, eye diseases, infectious diseases, influenza
virus, mankind, organic diseases, orthomyxoviridae, viruses, influenza.
L'vov, D.K., R.I.A. Podcherniaeva, R. Webster, M.V.
Ronina, and T.V. Pysina (1979). Poluchenie rekombinantov, antigenno
identichynykh tsirkuliruiushchim v prirode shtammam virusa grippa. [Production
of recombinants antigenically identical to influenza virus strains circulating
in nature]. Voprosy Virusologii (5): 493-7. ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Recombination of a human influenza virus with
an avian influenza virus produced a H2Nav2 recombinant with the antigenic
properties analogous to those of avian influenza virus (H2Nav2) isolated from
wild ducks in the Far East, USSR. Recombination of two avian influenza viruses
yielded a recombinant H2N2, an antigenic analogues of influenza
A/Singapore/1/57 (H2N2) virus which had started an epidemic of influenza in
1957.
Descriptors: antigens, viral genetics, influenza A virus
genetics, recombination, genetic, animals, wild, crosses, genetic, ducks
microbiology, hemagglutination inhibition tests, influenza A virus human
genetics, neuraminidase antagonists and inhibitors.
L'vov, D.K., A.N. Slepushkin, S.S. Iamnikova, and
E.I. Burtseva (1998). Gripp ostaetsia nepredskazuemoi infektsiei. [Influenza
remains an unpredictable infection]. Voprosy Virusologii 43(3):
141-4. ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Influenza virus A (H5N1) was isolated from
the tracheal swab of a 3-year-old boy who died from influenza with the Raye
syndrome in Hong Kong in May, 1997. Up to the present time, influenza viruses
with hemagglutinin H5 were known to circulate only among birds. They caused a
variety of diseases: from asymptomatic to epizootic with 100% mortality,
particularly among chickens. The main difference between virulent and avirulent
strains is as follows: virulent viruses are isolated from all tissues of an
infected bird. A (H5) virus hemagglutinin, transformed into a virulent variant,
becomes sensitive to cleavage by proteases of mammalian and avian cells.
Intensive epidemiological surveillance of influenza in Hong Kong started by the
WHO and Department of Public Health of Hong Kong in August-September, 1997,
resulted in detection of 17 more cases with Influenza A (H5N1) in
November-December 1997. all of the occurred before December 28, 1997 and were
detected in hospitals and health centers of Hong Kong. Nine patients were children
aged under 5 years. Six patients died as a result of complications (pneumonia)
and exacerbations of concomitant chronic diseases. Virological and logical
studies showed that the main route of infection transmission was from birds to
humans. Human to human transmission is probable. Study of 7 influenza A (H5N1)
viruses isolated from patients showed that they contained all 8 RNA gene
segments of avian virus. There are no reports about new cases of influenza A
(H5N1) in humans in January 1998, and we can hope that the outbreak of
Influenza A (H5N1) in Hong Kong caused by avian virus will not develop into a
new influenza pandemic, although an unfavorable course of events is probable.
Descriptors: influenza virology, influenza A virus avian
pathogenicity, chickens virology, Hong Kong epidemiology, influenza
epidemiology, influenza physiopathology, avian genetics, RNA, viral, virulence.
Lang, G., A. Gagnon, and J.R. Geraci (1981). Isolation
of an influenza A virus from seals. Archives of Virology 68(3-4): 189-95. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Influenza A virus of serotype Hav1 Neq1 (H7N7
by the 1980 revised influenza typing system proposed by WHO experts) was
repeatedly isolated from lung and brain tissues taken from harbor seals (Phoca
vitulina) found suffering from pneumonia on Cape Cod Peninsula (U.S.A.) in
the winter of 1979-1980. The seal isolates, although of a serotype identical to
some fowl plaque virus strains, were harmless to chickens and turkeys in
transmission experiments. An earlier human infection by a Hav1 Neq1 influenza
virus and the serologic relatedness of this avian serotype with the equine 1
serotype are cited in support of the view that influenza viruses with these
antigenic characteristics seem to have a facility to pass from birds to
mammals.
Descriptors: influenza microbiology, influenza A virus
avian isolation and purification, Pinnipedia microbiology, pneumonia, viral
microbiology, seals microbiology, antigens, viral immunology, brain
microbiology, epitopes, avian immunology, lung microbiology.
Langlois, I. (2005). Viral diseases of ferrets.
Veterinary Clinics of North America. Exotic Animal Practice 8(1):
139-60. ISSN: 1094-9194.
NAL
Call Number: SF997.5.E95E97
Abstract: Distemper and rabies vaccination are highly
recommended because of the almost invariable fatal outcome of these conditions.
Vaccination should constitute an important part of a ferret's preventative
medicine program. With the current and anticipated development and licensing of
new vaccines, practitioners are invited to gain awareness of the latest vaccine
information. Establishment of a practice vaccination protocol with regards to
the site of administration of rabies and distemper vaccines is paramount to
document any future abnormal tissue reactions. Influenza is the most common
zoonotic disease that is seen in ferrets. Although it generally is benign in
most ferrets, veterinarians must take this condition seriously. The
characteristic continuous antigenic variation of this virus may lead to more
virulent strains; the recent emergence of avian influenza virus outbreaks; and
the increased susceptibility of elderly, young, and immunosuppressed
individuals.
Descriptors: ferrets virology, virus diseases veterinary,
viruses isolation and purification, virus diseases diagnosis, virus diseases
pathology, virus diseases prevention and control, viruses pathogenicity,
diagnosis differential, virology.
Lashley, F.R. (2004). Emerging infectious
diseases: vulnerabilities, contributing factors and approaches. Expert
Review of Anti Infective Therapy 2(2): 299-316. ISSN: 1478-7210.
Abstract: We live in an ever more connected global
village linked through international travel, politics, economics, culture and
human-human and human-animal interactions. The realization that the concept of
globalization includes global exposure to disease-causing agents that were
formerly confined to small, remote areas and that infectious disease outbreaks
can have political, economic and social roots and effects is becoming more
apparent. Novel infectious disease microbes continue to be discovered because
they are new or newly recognized, have expanded their geographic range, have
been shown to cause a new disease spectrum, have jumped the species barrier
from animals to humans, have become resistant to antimicrobial agents, have
increased in incidence or have become more virulent. These emerging infectious
disease microbes may have the potential for use as agents of bioterrorism.
Factors involved in the emergence of infectious diseases are complex and
interrelated and involve all classifications of organisms transmitted in a
variety of ways. In 2003, outbreaks of interest included severe acute
respiratory syndrome, monkeypox and avian influenza. Information from the human
genome project applied to microbial organisms and their hosts will provide new
opportunities for detection, diagnosis, treatment, prevention, control and
prognosis. New technology related not only to genetics but also to satellite
and monitoring systems will play a role in weather, climate and the approach to
environmental manipulations that influence factors contributing to infectious
disease emergence and control. Approaches to combating emerging infectious
diseases include many disciplines, such as animal studies, epidemiology,
immunology, ecology, environmental studies, microbiology, pharmacology, other
sciences, health, medicine, public health, nursing, cultural, political and
social studies, all of which must work together. Appropriate financial support
of the public health infrastructure including surveillance, prevention,
communication, adherence techniques and the like will be needed to support
efforts to address emerging infectious disease threats.
Descriptors: communicable diseases, emerging economics,
prevention and control, emerging transmission, climate, demography, disease
susceptibility, disease transmission prevention and control, industry,
politics, social conditions, economics, technology, travel, weather.
Laver, G. and E. Garman (2002). Pandemic
influenza: its origin and control. Microbes and Infection Institut
Pasteur 4(13): 1309-16. ISSN:
1286-4579.
NAL
Call Number: QR180.M53
Abstract: A "new" influenza virus will appear
at some time in the future. This virus will arise by natural processes, which
we do not fully understand, or it might be created by some bioterrorist. The
world's population will have no immunity to the new virus, which will spread
like wild-fire, causing much misery, economic disruption and many deaths. Vaccines
will take time to develop and the only means of control, at least in the early
stages of the epidemic, are anti-viral drugs, of which the neuraminidase
inhibitors currently seem the most effective.
Descriptors: disease outbreaks prevention and control,
influenza epidemiology, influenza prevention and control, antiviral agents
therapeutic use, birds, chickens, China epidemiology, drug resistance, viral,
influenza drug therapy, influenza virology, influenza A virus avian
classification, avian physiology, models, molecular, neuraminidase physiology,
orthomyxoviridae genetics, orthomyxoviridae immunology.
Laver, G. and E. Garman (2001). Virology. The
origin and control of pandemic influenza. Science 293(5536):
1776-7. ISSN: 0036-8075.
NAL
Call Number: 470 Sci2
Descriptors: chickens virology, influenza epidemiology,
influenza prevention and control, influenza A virus enzymology, influenza A
virus pathogenicity, antiviral agents therapeutic use, drug industry methods,
drug resistance, microbial, enzyme inhibitors therapeutic use, hn protein
chemistry, hn protein genetics, hn protein metabolism, Hong Kong epidemiology,
influenza diagnosis, influenza drug therapy, influenza A virus avian
enzymology, avian genetics, avian immunology, avian pathogenicity, human
enzymology, human genetics, human immunology, human pathogenicity, influenza A
virus genetics, influenza A virus immunology, influenza vaccine biosynthesis,
influenza vaccine economics, influenza vaccine immunology, models, molecular,
mutation genetics, neuraminidase antagonists and inhibitors, neuraminidase
chemistry, neuraminidase genetics, neuraminidase metabolism, protein
conformation, RNA viral analysis, viral genetics, reassortant viruses
enzymology, reassortant viruses genetics, reassortant viruses immunology,
reassortant viruses pathogenicity, sialic acids therapeutic use.
Lazzari, S. and K. Stohr (2004). Avian influenza
and influenza pandemics. Bulletin of the World Health Organization
82(4): 242. ISSN: 0042-9686.
NAL
Call Number: 449.9 W892B
Descriptors: disease outbreaks prevention and control,
influenza epidemiology, influenza A virus, avian pathogenicity, influenza
prevention and control, influenza transmission, influenza virology, avian
influenza epidemiology, avian influenza transmission, avian influenza virology,
sentinel surveillance, world health, zoonoses virology.
Lee, P.J. and L.R. Krilov (2005). When animal
viruses attack: SARS and avian influenza. Pediatric Annals 34(1):
42-52. ISSN: 0090-4481.
NAL
Call Number: RJ1.P35
Abstract: SARS and avian influenza have many common
features. They both arose in Asia and originated from animal viruses. They both
have the potential to become pandemics because human beings lack antibodies to
the animal-derived antigens present on the viral surface and rapid
dissemination can occur from the relative ease and availability of high speed
and far-reaching transportation methods. Pediatricians, in particular, should
remain alert about the possibility of pandemic illnesses in their patients. Annual
rates of influenza in children may be 1.5 to 3 times those in the adult
population, and infection rates during a community epidemic may exceed 40% in
preschool-aged children and 30% in school-aged children. Infected children also
play a central role in disseminating influenza, as they are the major point of
entry for the virus into the household, from which adults spread disease into
the community. Of course, children younger than 24 months also are at high risk
for complications from influenza. A 1999 Centers for Disease Control and
Prevention projection of an influenza pandemic in the US paints a grim picture:
89,000 to 207,000 deaths, 314,000 to 734,000 hospitalizations, 18 million to 42
million outpatient visits, and 20 million to 47 million additional illnesses,
at a cost to society of at least dollars 71.3 billion to dollars 166.5 billion.
High-risk patients (15% of the population) would account for approximately 84%
of all deaths. Although SARS has been kind to the pediatric population so far,
there are no guarantees that future outbreaks would be as sparing. To aid
readers in remaining up-to-date with SARS and avian influenza, some useful
websites are listed in the Sidebar. Two masters of suspense, Alfred Hitchcock
and Stephen King, may have been closer to the truth than they ever would have
believed. Both birds and a super flu could bring about the end of civilization
as we know it. But all is not lost--to paraphrase Thomas Jefferson, the price
of health is eternal vigilance. Although we may not be able to prevent future
pandemics, mankind has the ability to recognize new diseases and outbreaks as
they occur, to study these infections and find ways to contain and treat them,
and to implement the necessary measures to defeat them.
Descriptors: avian influenza prevention and control,
severe acute respiratory syndrome prevention and control, adult, child,
antiviral agents therapeutic use, disease outbreaks prevention and control,
disease vectors, avian influenza diagnosis, avian influenza epidemiology, avian
influenza transmission, pediatrics methods, population surverillance methods,
severe acute respiratory syndrome diagnosis, severe acute respiratory syndrome
epidemiology, severe acute respiratory syndrome transmission, world health,
SARS.
Leneva, I.A., O. Goloubeva, R.J. Fenton, M. Tisdale,
and R.G. Webster (2001). Efficacy of zanamivir against avian influenza A
viruses that possess genes encoding H5N1 internal proteins and are pathogenic
in mammals. Antimicrobial Agents and Chemotherapy 45(4): 1216-24. ISSN: 0066-4804.
NAL
Call Number: RM265.A5132
Abstract: In 1997, an avian H5N1 influenza virus,
A/Hong Kong/156/97 (A/HK/156/97), caused six deaths in Hong Kong, and in 1999,
an avian H9N2 influenza virus infected two children in Hong Kong. These viruses
and a third avian virus [A/Teal/HK/W312/97 (H6N1)] have six highly related
genes encoding internal proteins. Additionally, A/Chicken/HK/G9/97 (H9N2) virus
has PB1 and PB2 genes that are highly related to those of A/HK/156/97 (H5N1),
A/Teal/HK/W312/97 (H6N1), and A/Quail/HK/G1/97 (H9N2) viruses. Because of their
similarities with the H5N1 virus, these H6N1 and H9N2 viruses may have the
potential for interspecies transmission. We demonstrate that these H6N1 and
H9N2 viruses are pathogenic in mice but that their pathogenicities are less
than that of A/HK/156/97 (H5N1). Unadapted virus replicated in lungs, but only
A/HK/156/97 (H5N1) was found in the brain. After three passages (P3) in mouse
lungs, the pathogenicity of the viruses increased, with both A/Teal/HK/W312/97
(H6N1) (P3) and A/Quail/HK/G1/97 (H9N2) (P3) viruses being found in the brain.
The neuraminidase inhibitor Zanamivir inhibited viral replication in
Madin-Darby canine kidney cells in virus yield assays (50% effective
concentration, 8.5 to 14.0 microM) and inhibited viral neuraminidase activity
(50% inhibitory concentration, 5 to 10 nM). Twice daily intranasal
administration of Zanamivir (50 and 100 mg/kg of body weight) completely
protected infected mice from death. At a dose of 10 mg/kg, Zanamivir completely
protected mice from infection with H9N2 viruses and increased the mean survival
day and the number of survivors infected with H6N1 and H5N1 viruses. Zanamivir,
at all doses tested, significantly reduced the virus titers in the lungs and
completely blocked the spread of virus to the brain. Thus, Zanamivir is
efficacious in treating avian influenza viruses that can be transmitted to
mammals.
Descriptors: antiviral agents therapeutic use, enzyme
inhibitors therapeutic use, influenza drug therapy, influenza A virus avian
drug effects, neuraminidase antagonists and inhibitors, sialic acids
therapeutic use, administration, intranasal, antiviral agents administration
and dosage, antiviral agents pharmacology, brain virology, cell line, dogs,
enzyme inhibitors administration and dosage, enzyme inhibitors pharmacology,
genes viral, influenza virology, avian genetics, avian pathogenicity, kinetics,
lung virology, mice, mice inbred BALB c, microbial sensitivity tests, sialic
acids administration and dosage, sialic acids pharmacology, species
specificity, virus replication drug effects.
Leneva, I.A., N. Roberts, E.A. Govorkova, O.G.
Goloubeva, and R.G. Webster (2000). The neuraminidase inhibitor GS4104
(oseltamivir phosphate) is efficacious against A/Hong Kong/156/97 (H5N1) and
A/Hong Kong/1074/99 (H9N2) influenza viruses. Antiviral Research
48(2): 101-15. ISSN: 0166-3542.
NAL
Call Number: QR355.A5
Abstract: In 1997, an H5N1 avian influenza A/Hong
Kong/156/97 virus transmitted directly to humans and killed six of the 18
people infected. In 1999, another avian A/Hong/1074/99 (H9N2) virus caused
influenza in two children. In such cases in which vaccines are unavailable,
antiviral drugs are crucial for prophylaxis and therapy. Here we demonstrate
the efficacy of the neuraminidase inhibitor GS4104 (oseltamivir phosphate)
against these H5N1 and H9N2 viruses. GS4071 (the active metabolite of
oseltamivir) inhibited viral replication in MDCK cells (EC(50) values, 7.5-12
microM) and neuraminidase activity (IC(50) values, 7.0-15 nM). When orally
administered at doses of 1 and 10 mg/kg per day, GS4104 prevented death of mice
infected with A/Hong Kong/156/97 (H5N1), mouse-adapted A/Quail/Hong Kong/G1/97
(H9N2), or human A/Hong Kong/1074/99 (H9N2) viruses and reduced virus titers in
the lungs and prevented the spread of virus to the brain of mice infected with
A/Hong Kong/156/97 (H5N1) and mouse-adapted A/Quail/Hong Kong/G1/97 (H9N2)
viruses. When therapy was delayed until 36 h after exposure to the H5N1 virus,
GS4104 was still effective and significantly increased the number of survivors
as compared with control. Oral administration of GS4104 (0.1 mg/kg per day) in
combination with rimantadine (1 mg/kg per day) reduced the number of deaths of
mice infected with 100 MLD(50) of H9N2 virus and prevented the deaths of mice
infected with 5 MLD(50) of virus. Thus, GS4104 is efficacious in treating
infections caused by H5N1 and H9N2 influenza viruses in mice.
Descriptors: acetamides pharmacology, antiviral agents
pharmacology, influenza drug therapy, influenza A virus avian drug effects,
human drug effects, neuraminidase antagonists and inhibitors, acetamides
therapeutic use, antiviral agents therapeutic use, brain virology, cell line,
dogs, enzyme inhibitors pharmacology, enzyme inhibitors therapeutic use,
influenza virology, avian enzymology, avian pathogenicity, human enzymology,
human pathogenicity, kidney, lung virology, mice, mice inbred BALB c,
neuraminidase metabolism, rimantadine therapeutic use, virus replication drug
effects.
Lesník, F., N. Ucekaj, O. Ondrasovicová, and V.
Bajová (2003). A highly virulent avian influenza virus in Europe. Slovenský
Veterinársky Casopis 28(3): 31-32.
ISSN: 1335-0099.
Descriptors: disease control, mutations, virulence, avian
influenza virus, ducks, Europe.
Letonturier, P. (2004). Quand les virus attaquent.
[When viruses attack]. Presse Medicale Paris, France 1983 33(6):
428. ISSN: 0755-4982.
Descriptors: disease outbreaks, influenza A virus, avian
influenza, avian influenza epidemiology, avian influenza transmission,
zoonoses, poultry, risk factors.
Li, S., M.L. Perdue, and E. Patzer (2002). Seed
viruses containing novel avian HA and NA antigens for prevention against
potential influenza pandemic. Developments in Biologicals 110:
135-41. ISSN: 1424-6074.
NAL
Call Number: QR180.3.D4
Abstract: An influenza pandemic could arise
unexpectedly with rapid spread across the world. The efficiency of production
of a vaccine and the ability to administer it widely will be among the most
important factors in the ability to protect public health. The current process
for producing inactivated or live attenuated influenza vaccines requires six to
nine months. That reduces considerably the likelihood that the vaccine will be
available during the first wave of the pandemic. Therefore, a key element of
preparedness is to optimize the production process and to reduce the vaccine
development time. During the 1997 H5N1 outbreak in Hong Kong, seed viruses were
prepared for production of inactivated and live-attenuated vaccines. We used
the cold-adapted A/Ann Arbor/6/60 as the donor virus to generate live
attenuated vaccines containing genetically modified HA and NA genes from H5N1
influenza viruses. These reassortants were shown to be safe and protective in
animal models. This study indicates that production of live attenuated avian
influenza vaccines is feasible and that development of a library of reassortants
containing different subtype HA and NA genes may reduce the vaccine preparation
time for future influenza pandemics.
Descriptors: antigens, viral immunology, influenza
prevention and control, influenza A virus avian immunology, influenza epidemiology,
influenza vaccine administration and dosage.
Li, S.Q., M. Orlich, and R. Rott (1990). Generation
of seal influenza virus variants pathogenic for chickens, because of
hemagglutinin cleavage site changes. Journal of Virology 64(7):
3297-303. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Influenza virus A/seal/Mass/1/80 (H7N7) was
adapted to grow in MDCK cells and chicken embryo cells (CEC) in the absence of
exogenous protease. The biological properties of the virus variants obtained
coincided with intracellular activation of the hemagglutinin (HA) by
posttranslational proteolytic cleavage and depended on the cell type used for
adaptation. MDCK cell-adapted variants contained point mutations in regions of
the HA more distant from the cleavage site. It is proposed that these mutations
are probably responsible, through an unknown mechanism, for enhanced
cleavability of HA in MDCK cells. Such virus variants were apathogenic in
chickens. CEC-adapted variants, on the other hand, contained an insertion of
basic amino acids at the HA cleavage site, in addition to scattered point
mutations. The insertions converted the cleavage sites in the variant virus HAs
so that they came to resemble the cleavage site found in highly pathogenic
avian influenza viruses. CEC variants with such cleavage site modifications
were highly pathogenic for chickens. The lethal outcome of the infection in
chickens demonstrated for the first time that an influenza virus derived from a
mammalian species can be modified during adaptation to a new cell type to such
an extent that the resulting virus variant becomes pathogenic for an avian
species.
Descriptors: chickens microbiology, hemagglutinins viral
metabolism, influenza A virus pathogenicity, pinnipedia microbiology, seals microbiology,
amino acid sequence, base sequence, cell line, chick embryo, dogs,
electrophoresis, gel, two dimensional, hemagglutinins viral genetics,
influenza A virus genetics, molecular sequence data, mutation, peptide
hydrolases metabolism, species specificity, virus replication.
Liem, N.T. (2005). Lack of H5N1 avian influenza
transmission to hospital employees, Hanoi, 2004. Emerging Infectious
Diseases 11(2): 210-5. ISSN:
1080-6040.
NAL
Call Number: RA648.5.E46
Abstract: To establish whether human-to-human
transmission of influenza A H5N1 occurred in the healthcare setting in Vietnam,
we conducted a cross-sectional seroprevalence survey among hospital employees
exposed to 4 confirmed and 1 probable H5N1 case-patients or their clinical
specimens. Eighty-three (95.4%) of 87 eligible employees completed a
questionnaire and provided a serum sample, which was tested for antibodies to
influenza A H5N1. Ninety-five percent reported exposure to >1 H5N1
case-patients; 59 (72.0%) reported symptoms, and 2 (2.4%) fulfilled the
definition for a possible H5N1 secondary case-patient. No study participants
had detectable antibodies to influenza A H5N1. The data suggest that the H5N1
viruses responsible for human cases in Vietnam in January 2004 are not readily
transmitted from person to person. However, influenza viruses are genetically
variable, and transmissibility is difficult to predict. Therefore, persons
providing care for H5N1 patients should continue to take measures to protect
themselves.
Descriptors: patient to professional disease transmission,
health personnel, influenza transmission, avian influenza A virus growth and
development, Western blotting, child, preschool child, adolescent, adult, viral
blood antibodies, cross sectional studies, influenza immunology, influenza
virology, avian influenza A virus immunology, middle-aged, neutralization
tests, questionnaires, seroepidemiologic studies, Vietnam epidemiology.
Lin, Y.P., M. Shaw, V. Gregory, K. Cameron, W. Lim,
A. Klimov, K. Subbarao, Y. Guan, S. Krauss, K. Shortridge, R. Webster, N. Cox,
and A. Hay (2000). Avian-to-human transmission of H9N2 subtype influenza A
viruses: relationship between H9N2 and H5N1 human isolates. Proceedings
of the National Academy of Sciences of the United States of America 97(17):
9654-8. ISSN: 0027-8424.
NAL
Call Number: 500 N21P
Abstract: In 1997, 18 cases of influenza in Hong Kong
(bird flu) caused by a novel H5N1 (chicken) virus resulted in the deaths of six
individuals and once again raised the specter of a potentially devastating
influenza pandemic. Slaughter of the poultry in the live bird markets removed
the source of infection and no further human cases of H5N1 infection have
occurred. In March 1999, however, a new pandemic threat appeared when influenza
A H9N2 viruses infected two children in Hong Kong. These two virus isolates are
similar to an H9N2 virus isolated from a quail in Hong Kong in late 1997.
Although differing in their surface hemagglutinin and neuraminidase components,
a notable feature of these H9N2 viruses is that the six genes encoding the
internal components of the virus are similar to those of the 1997 H5N1 human
and avian isolates. This common feature emphasizes the apparent propensity of
avian viruses with this genetic complement to infect humans and highlights the
potential for the emergence of a novel human pathogen.
Descriptors: bird diseases transmission, influenza
transmission, influenza A virus avian genetics, influenza A virus genetics,
influenza A virus immunology, quail virology, antigens, viral chemistry,
antigens, viral genetics, antigens, viral immunology, binding sites, bird diseases epidemiology, child, preschool,
conserved sequence genetics, genes viral genetics, hemagglutinins viral
chemistry, hemagglutinins viral genetics, hemagglutinins viral immunology, Hong
Kong epidemiology, infant, influenza epidemiology, avian chemistry, avian
classification, avian immunology, influenza A virus chemistry, influenza A virus classification, molecular
sequence data, neuraminidase chemistry, neuraminidase genetics, neuraminidase
immunology, phylogeny, species specificity, variation genetics genetics.
Lin, Y.P., L.L. Shu, S. Wright, W.J. Bean, G.B.
Sharp, K.F. Shortridge, and R.G. Webster (1994). Analysis of the influenza
virus gene pool of avian species from southern China. Virology
198(2): 557-566. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Although Southern China has been considered
the epicenter of human influenza pandemics, little is known about the genetic
composition of influenza viruses in lower mammals or birds in that region. To
provide information on the molecular epidemiology of these viruses, we used dot
blot hybridization and phylogenetic methods to study the internal genes (PB1,
PB2, PA, NP, M, and NS) of 106 avian influenza A viruses isolated from a total
of 11,798 domestic ducks, chickens, and geese raised in Southern China
including Hong Kong. All 636 genes examined were characteristic of avian
influenza viruses; no human or swine influenza genes were detected. Thus,
influenza virus reassortants do not appear to be maintained in the domesticated
birds of Southeast Asia, eliminating opportunities for further gene
reassortment. Phylogenetic analysis showed that the internal genes of these
viruses belong to the Eurasian avian lineage, supporting geographical
separation of the major avian lineages. The PB1 genes were most similar to
A/Singapore/57 (H2N2) and Hong Kong (H3N2) viral genes, supporting an avian
origin for the recent human H2N2 and H3N2 pandemic strains. The majority of
internal genes from avian influenza viruses in Southern China belong to the
Eurasian lineage and are similar to viruses that have recently been transmitted
to humans, swine, and horses. This study provides evidence that the
transmission of avian influenza viruses and their genes to other species is
unidirectional and that the transmission of mammalian influenza virus strains
to domestic poultry is probably not a factor in the generation of new pandemic
strains.
Descriptors: poultry, China, Hong Kong, avian influenza
virus, genes, phylogeny, nucleotide sequence, mankind, epidemiology, Asia, cell
structure, chromosomes, domestic animals, domesticated birds, East Asia,
evolution, genomes, influenza virus, livestock, nucleus, useful animals, viruses, pandemics, sequence
homology, gene flow, comparisons, man.
Lina, B. (2004). A gripe das aves desperta o
terror de uma pandemia. [Avian influenza causes fear about a pandemic.]. Servir
Lisbon, Portugal 52(2): 93-5. ISSN:
0871-2379.
Descriptors: influenza, avian epidemiology, influenza,
avian transmission.
Lindstrom, S.E., N.J. Cox, and A. Klimov (2004). Evolutionary
analysis of human H2N2 and early H3N2 influenza viruses: evidence for genetic
divergence and multiple reassortment among H2N2 and/or H3N2 viruses. International
Congress Series 1263: 184-190.
Abstract: Pandemic influenza H2N2 viruses emerged in
humans in 1957 and caused widespread morbidity and mortality in humans until
1968 when they were displaced by emerging H3N2 viruses. Although it is known
that both the appearance and disappearance of H2N2 viruses involved
reassortment between human and avian influenza viruses, genetic
characterization of these viruses is limited. In this study, detailed genetic
analysis of all eight gene segments of human H2N2 viruses isolated from 1957
until 1968 from geographically diverse regions was undertaken to establish a
better understanding of the evolutionary nature of this virus. In addition, a
number of human H3N2 viruses isolated from 1968 until 1972 were examined to
investigate genetic events associated with the emergence of pandemic H3N2
viruses in humans. Phylogenic analysis of all gene segments of human H2N2
viruses consistently demonstrated divergent evolution. Genes of late H2N2
isolates were located in either of two distinct clades (I and II). Analysis of
H3N2 viruses of 1968 revealed that all gene segments that were retained from
H2N2 viruses were most similar to H2N2 virus genes of clade I. However, genes
of both lineages were found to cocirculate among H3N2 isolates of 1969-1971.
Furthermore, each gene segment demonstrated unique phylogenic topologies,
indicating multiple reassortment events between late H2N2 and/or H3N2 viruses.
The H3N2 viruses of 1972 analyzed here appeared to possess the genome
constellation that represents the ancestral virus of contemporary H3N2 viruses.
This constellation was first observed among isolates of 1970 and was distinct
from that found among the earliest human H3N2 viruses from 1968. This evidence
demonstrates that establishment of H3N2 viruses in humans was associated with
multiple-reassortment events that contributed to genetic diversity among
viruses.
Descriptors: influenza, H2N2, H3N2, evolution,
reassortment, hemagglutinin, neuraminidase, nucleoprotein, influenza virus
genetics.
Lipatov, A.S., A.K. Gitel'man, E.A. Govorkova, and
Y.U.A. Smirnov (1995). Izmeneniya biologicheskikh i fiziko-khimicheskikh
svojstv gemagglyutinina H2 ptich' ego virusa grippa A v protsesse adaptatsii k
novomu khozyainu. [Alteration of the biological and physicochemical
characteristics of hemagglutinin H2 of avian influenza A virus in the course of
adaptation to a new host]. Voprosy Virusologii 40(5): 208-211.
NAL
Call Number: 448.8 P942
Abstract: Avian influenza A virus with H2 hemagglutinin
has been adapted to mice for the first time. Alterations in the hemagglutinin
of adapted variants of the virus as a result of adaptation to a new host are
described. Hemagglutinin of a hightly virulent adapted variant differed from
the parental avirulent strain by antigenic structure, electrophoretic mobility,
and receptor activity during interactions with murine red cells.
Descriptors: laboratory animals, avian influenza virus,
pathotypes, host pathogen relations, adaptation, agglutinins, immunological
factors, biological properties, chemicophysical properties, experimental
infection, in vivo experimentation, mice, biotypes, disease transmission,
experimentation, infection, influenza virus, mammals, orthomyxoviridae,
pathogenesis, pathology, proteins, Rodentia, useful animals, viruses.
Lipatov, A.S., A.K. Gitelman, E.A. Govorkova, and
Y.U.A. Smirnov (1995 ). Changes of morphological, biological and antigenic
properties of avian influenza A virus haemagglutinin H2 in the course of
adaptation to new host. Acta Virologica 39(5-6): 279-81. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: The alterations of avian influenza A virus
haemagglutinin (HA) H2 as a result of adaptation to mice were first
investigated in this study. HA of mouse-adapted (MA) variant was somewhat
different from that of the original strain in electrophoretical mobility,
antigenic structure and in haemagglutination activity with mouse red blood
cells.
Descriptors: hemagglutinins viral immunology, influenza A
virus avian immunology, adaptation, physiological, cell line, chick embryo,
dogs, electrophoresis, polyacrylamide gel, erythrocytes immunology, fowl plague
immunology, fowl plague virology, hemagglutination tests, hemagglutinin
glycoproteins, influenza virus, hemagglutinins viral chemistry, mice.
Lipatov, A.S., A.K. Gitelman, and Y.U.A. Smirnov
(1996). Differences between original strains and their mouse-adapted variants
of human (H1) and avian (H2) influenza A viruses in the reaction with
cross-neutralizing monoclonal antibody recognizing conformational epitope. Acta
Virologica 40(4): 227-30. ISSN:
0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: Human (H1) and avian (H2) influenza A viruses
and their mouse-adapted (MA) variants were studied in radioimmunoprecipitation
assay (RIPA) and infectivity neutralization test using a monoclonal antibody
(MoAb) directed against a conserved antigenic epitope in the stem region of the
haemagglutinin (HA) and reacting both with H1 and H2 subtypes of HA. Whereas
the MA variant of avian influenza A virus differed from the original strain in
RIPA and neutralization tests, no differences were observed between the
original human strain and its MA variant, as well as between the original H1
and H2 strains.
Descriptors: antibodies, viral immunology, antigens, viral
immunology, epitopes, b lymphocyte immunology, hemagglutinin glycoproteins,
influenza virus immunology, influenza A virus avian immunology, human
immunology, adaptation, physiological, antibodies, monoclonal immunology, cell
line, chick embryo, cross reactions, dogs, glycosylation, mice, neutralization
tests, protein conformation, variation genetics.
Lipkind, M. and Y. Weisman (1989). Ecological
studies and diagnosis of animal influenza and animal paramyxoviruses in Israel.
II. Animal influenza: a review on decade studies. Israel Journal of
Veterinary Medicine 45(4): 263-287.
ISSN: 0334-9152.
NAL
Call Number: 41.8 R25
Descriptors: DNA hybridization, influenza,
paramyxoviruses, disease transmission, reviews, turkeys, wild birds, ducks, pigs, horses, review,
Israel, ecological study.
Lipkind, M., Y. Weisman, E. Shihmanter, D. Shoham, C.
Yuval, and A. Aronovici (1980). Evidence for the interspecific transfer of
an avian influenza virus. Israel Journal of Medical Sciences 16(6):
475. ISSN: 0021-2180.
NAL
Call Number: R97.I87
Descriptors: avian influenza virus, transfer,
turkeys, birds, ducks, Israel.
Lisovskaya, K.V., L.M. Garmashova, and T.E. Medvedeva
(1981). Analysis of ts mutations of cold-adapted influenza
A/Leningrad/134/57 virus variants. Acta Virologica 25(6):
415-7. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: By recombination of ts mutants of fowl plague
virus belonging to different complementation groups with two cold-adapted
variants of human influenza virus, the number and gene localization of ts
mutations occurring in these variants was determined. In the course of
passaging of human influenza virus at lowered temperature, the number of genes
with ts mutations increased.
Descriptors: genes viral, influenza A virus avian
genetics, human genetics, cold, genetic complementation test, mutation,
recombination, genetic.
Liu, J.H., K. Okazaki, G.R. Bai, W.M. Shi,
A. Mweene, and H. Kida (2004). Interregional transmission of the internal
protein genes of H2 influenza virus in migratory ducks from North America to
Eurasia. Virus Genes 29(1):
81-6. ISSN: 0920-8569.
NAL
Call Number: QH434.V57
Abstract: H2 influenza virus caused a pandemic in 1957
and has the possibility to cause outbreaks in the future. To assess the
evolutionary characteristics of H2 influenza viruses isolated from migratory
ducks that congregate in Hokkaido, Japan, on their flyway of migration from
Siberia in 2001, we investigated the phylogenetic relationships among these
viruses and avian and human viruses described previously. Phylogenetic analysis
showed that the PB2 gene of Dk/Hokkaido/107/01 (H2N3) and the PA gene of
Dk/Hokkaido/95/01 (H2N2) belonged to the American lineage of avian virus and
that the other genes of the isolates belonged to the Eurasian lineage. These
results indicate that the internal protein genes might be transmitted from American
to Eurasian avian host. Thus, it is further confirmed that interregional
transmission of influenza viruses occurred between the North American and
Eurasian birds. The fact that reassortants could be generated in the migratory
ducks between North American and Eurasian avian virus lineage further stresses
the importance of global surveillance among the migratory ducks.
Descriptors: ducks virology, emigration and immigration,
influenza A virus, avian genetics, influenza, avian virology, viral proteins
genetics, Asia, Europe, avian influenza A virus classification, molecular
sequence data, North America, phylogeny, sequence analysis, DNA.
Liu, M., Y. Guan, M. Peiris, S. He, R.J. Webby, D.
Perez, and R.G. Webster (2003). The quest of influenza A viruses for new
hosts. Avian Diseases 47(Special Issue): 849-856. ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: There is increasing evidence that stable
lineages of influenza viruses are being established in chickens. H9N2 viruses
are established in chickens in Eurasia, and there are increasing reports of
H3N2, H6N1, and H6N2 influenza viruses in chickens both in Asia and North
America. Surveillance in a live poultry market in Nanchang, South Central
China, reveals that influenza viruses were isolated form 1% of fecal samples
taken from healthy poultry over the course of 16 months. The highest isolation
rates were from chickens (1.3%) and ducks (1.2%), followed by quail (0.8%),
then pigeon (0.5%). H3N6, H9N2, H2N9, and H4N6 viruses were isolated from
multiple samples, while single isolates of HlN1, H3N2, and H3N3 viruses were
made. Representatives of each virus subtype were experimentally inoculated into
both quail and chickens. All the viruses replicated in the trachea of quail,
but efficient replication in chickens was confined to 25% of the tested
isolates. In quail, these viruses were shed primarily by the aerosol route,
raising the possibility that quail may be the "route modulator" that
changes the route of transmission of influenza viruses from fecal-oral to
aerosol transmission. Thus, quail may play an important role in the natural
history of influenza viruses. The pros and cons of the use of inactivated and recombinant
fowl pox-influenza vaccines to control the spread of avian influenza are also
evaluated.
Descriptors: epidemiology, infection, live poultry market,
transmission route, aerosol, fecal, oral, viral, natural history.
Lu, X., D. Cho, H. Hall, T. Rowe, H. Sung, W. Kim, C. Kang, I. Mo, N.
Cox, A. Klimov, and J. Katz (2003). Pathogenicity and antigenicity of a new
influenza A (H5N1) virus isolated from duck meat. Journal of Medical
Virology 69(4): 553-559. ISSN:
0146-6615.
Abstract: Avian influenza A viruses are the ancestral
origin of all human influenza viruses. The outbreak of highly pathogenic (HP)
avian H5N1 in Hong Kong in 1997 highlighted the potential of these viruses to
infect and cause severe disease in humans. Since 1999, HP H5N1 viruses were
isolated several times from domestic poultry in Asia. In 2001, a HP H5N1 virus,
A/Duck/Anyang/AVL-1/2001 (Dk/Anyang), was isolated from imported frozen duck
meat in Korea. Because of this novel source of HP H5N1 virus isolation,
concerns were raised about the potential for human exposure and infection; we
therefore compared the Dk/Anyang virus with HP H5N1 viruses isolated from
humans in 1997 in terms of antigenicity and pathogenicity for mammals. At high
doses, Dk/Anyang virus caused up to 50% mortality in BALB/c mice, was isolated
from the brains and lymphoid organs of mice, and caused lymphopenia. Overall
Dk/Anyang virus was substantially less pathogenic for mice than the H5N1 virus
isolated from a fatal human case in 1997. Likewise, Dk/Anyang virus was
apathogenic for ferrets. Dk/Anyang virus was antigenically distinguishable by
hemagglutination-inhibition (HI) assay from human H5N1 viruses isolated in 1997
and avian H5N1 viruses isolated in 2001 in Hong Kong. Nevertheless, prior
infection with Dk/Anyang virus protected mice from death after secondary
infection with HP human H5N1 viruses. These results indicate that compared with
HP human H5N1 viruses, Dk/Anyang virus is substantially less pathogenic for
mammalian species. Nevertheless, the novel source of isolation of this avian
H5N1 virus must be considered when evaluating the potential risk to public
health.
Descriptors: infection, avian influenza, viral disease,
duck meat, meat product.
Lu, X., T.M. Tumpey, T. Morken, S.R. Zaki, N.J. Cox,
and J.M. Katz (1999). A mouse model for the evaluation of pathogenesis and
immunity to influenza A (H5N1) viruses isolated from humans. Journal of
Virology 73(7): 5903-11. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: During 1997 in Hong Kong, 18 human cases of
respiratory illness, including 6 fatalities, were caused by highly pathogenic
avian influenza A (H5N1) viruses. Since H5 viruses had previously been isolated
only from avian species, the outbreak raised questions about the ability of
these viruses to cause severe disease and death in humans. To better understand
the pathogenesis and immunity to these viruses, we have used the BALB/c mouse
model. Four H5N1 viruses replicated equally well in the lungs of mice without
prior adaptation but differed in lethality for mice. H5N1 viruses that were
highly lethal for mice were detected in multiple organs, including the brain.
This is the first demonstration of an influenza A virus that replicates
systemically in a mammalian species and is neurotropic without prior
adaptation. The mouse model was also used to evaluate a strategy of vaccination
against the highly pathogenic avian H5N1 viruses, using an inactivated vaccine
prepared from nonpathogenic A/Duck/Singapore-Q/F119-3/97 (H5N3) virus that was
antigenically related to the human H5N1 viruses. Mice administered vaccine
intramuscularly, with or without alum, were completely protected from lethal
challenge with H5N1 virus. Protection from infection was also observed in 70% of
animals administered vaccine alone and 100% of mice administered vaccine with
alum. The protective effect of vaccination correlated with the level of
virus-specific serum antibody. These results suggests a strategy of vaccine
preparedness for rapid intervention in future influenza pandemics that uses
antigenically related nonpathogenic viruses as vaccine candidates.
Descriptors: influenza prevention and control, influenza
virology, influenza A virus avian immunology, avian pathogenicity, uman
immunology, human pathogenicity, cell line, disease models, animal, disease
outbreaks, dogs, influenza epidemiology, influenza immunology, avian growth and
development, avian isolation and purification, human growth and development,
human isolation and purification, influenza vaccine immunology, mice, inbred
BALB c, vaccines, inactivated immunology.
Lu, X.H., D. Cho, H. Hall, T. Rowe, I.P. Mo, H.W. Sung, W.J. Kim, C.
Kang, N. Cox, A. Klimov, and J.M. Katz (2003). Pathogenesis of and immunity
to a new influenza A (H5N1) virus isolated from duck meat. Avian
Diseases 47(Special Issue): 1135-1140.
ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: The outbreak of avian influenza H5N1 in Hong
Kong in 1997 raised concerns about the potential for the H5 subtype to cause a
human pandemic. In 2001 a new H5N1 virus, A/Duck Meat/Anyang/AVL-1/2001
(A/Dkmt), was isolated from imported duck meat in Korea. The pathogenesis of
this virus was investigated in mice. A/Dkmt virus had low infectivity but was
lethal for mice at high doses, and at lethal doses, the virus replicated in the
brains of infected mice. A/Dkmt virus cross-reacted poorly with ferret antisera
raised against human H5N1 viruses, but prior infection with A/Dkmt virus
protected mice from death after secondary infection with human H5N1 virus.
Descriptors: infection, avian influenza, infectious
disease, respiratory system disease, viral disease, disease pathogenesis duck
meat, contamination, poultry product, influenza pandemic, viral immunity.
Ludwig, S., A. Haustein, E.F. Kaleta, and C.
Scholtissek (1994). Recent influenza A (H1N1) infections of pigs and turkeys
in northern Europe. Virology 202(1): 281-286. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The most recent introduction of an avian
influenza A virus without reassortment into mammals occurred in 1979 when H1N1
strains could be isolated from diseased pigs in northern Europe. This newly
introduced avian virus formed a stable lineage in pigs and, in the meantime,
spread all over Europe In 1991 highly pathogenic H1N1 strains closely related
to a contemporary swine virus were isolated from turkeys of a breeding farm
near Bremen, Germany. Outbreaks in several farms in Germany, France, and the
Netherlands indicate that the "avian-like" swine viruses can easily
be reintroduced into an avian population causing severe economical losses.
Descriptors: swine, Germany, Netherlands, France,
turkeys, swine influenza virus, avian
influenza virus, animal viruses, proteins, genes, nucleotide sequence,
artiodactyla, birds, cell structure, chromosomes, domestic animals, Europe,
Galliformes, genomes, influenza virus, livestock, mammals, Mediterranean
countries, nucleus, suidae, useful animals, viruses, western Europe, spread,
amino acid sequences, comparisons.
Ludwig, S., L. Stitz, O. Planz, H. Van, W.M. Fitch,
and C. Scholtissek (1995). European swine virus as a possible source for the
next influenza pandemic? Virology 212(2): 555-561. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: According to phylogenetic data, about 100
years ago an avian influenza virus passed me species barrier (possibly first)
to pigs and (possibly from there) to humane. In 1979 an avian influenza A virus
(as a whole, without reassortment) again entered the pig population in northern
Europe, forming a stable lineage. Here it is shown that the early North
European swine viruses exhibit higher than normal evolutionary rates and are
highly variable with respect to plaque morphology and neutralizability by
monoclonal antibodies. Our results are consistent with the idea that, in order
to pass the species barrier, an influenza A virus needs a mutator mutation to
provide an additional number of variants, from which the new host might select
the best fitting ones. A mutator mutation could be of advantage under such
stress conditions and might enable a virus to pass the species barrier as a
whole even twice, as it seems to have happened about 100 years ago. This
stressful situation should be over for the recent swine lineage, since the
viruses seem to be adapted already to the new host in that the most recent
isolates--at least in northern Germany--are genetically stable and seem to have
lost the putative mutator mutation again.
Descriptors: Europe, swine influenza virus, avian influenza
virus, influenza virus, mankind, phylogeny, agglutinins, monoclonal antibodies,
viruses, antigen antibody reactions, mutation, antibodies, evolution, genetics,
immune response, immunity, immunological factors, influenza virus,
orthomyxoviridae, proteins, viruses, human influenza virus, mutator mutations,
species barriers, northern Europe, viral hemagglutinins, viral morphology,
virus neutralization, barriers.
Makarova, K.S., Y.I. Wolf, E.P. Tereza, and V.A. Ratner
(1998). Different patterns of molecular evolution of influenza A viruses in
avian and human populations. Genetika 34(7): 890-896. ISSN: 0016-6758.
NAL
Call Number: QH431.A1G4
Abstract: Patterns of molecular evolution of the
influenza virus proteins and genes are discussed. The subsets of all viral
genes corresponding to statistically significant clusters on dendrogram were
shown to fall into two distinct groups. The first group was characterized by
the presence of an exact linear relationship between the year of the strain
isolation and the evolutionary distance. The subsets of human influenza virus
genes belong to this group. A method for eliminating the "frozen"
strains from the subsets and for calculating the evolutionary rates without
construction of phylogenetic trees has been elaborated. The substitution rates
calculated according to this technique agreed with the data obtained
previously. A linear relationship was not observed in the second group. This
group was predominantly composed of avian influenza virus genes. The lack of
linear correlation pointed to the cocirculation of a large amount of different
influenza virus genomic segments in the avian population. An approach for an
examination of the role of intragenic recombination in the development of the
antigenic subtypes of hemagglutinin is suggested. Our results suggest that
recombination did not play a considerable role in this process, and that all
modern subtypes of this protein were probably formed before the introduction of
the influenza viruses into the human population. These findings are consistent
with the hypothesis that influenza viruses penetrated into human population
from their pools in avian populations.
Descriptors: evolution and adaptation, genetics, influenza
virus, human, avian.
Makarova, K.S., Y.U.I. Wulf, E.P. Tereza, and V.A.
Ratner (1998). Razlichie rezhimov molekuliarnoi evoliutsii virusov grippa A
v populiatsiiakh ptits i cheloveka. [Different patterns of molecular evolution
of influenza A viruses in avian and human population]. Genetika 34(7): 890-6.
ISSN: 0016-6758.
NAL
Call Number: QH431.A1G4
Abstract: Patterns of molecular evolution of the
influenza virus proteins and genes are discussed. The subsets of all viral
genes corresponding to statistically significant clusters on dendrogram were
shown to fall into two distinct groups. The first group was characterized by
the presence of an exact linear relationship between the year of the strain
isolation and the evolutionary distance. The subsets of human influenza virus
genes belong to this group. A method for eliminating the "frozen"
strains from the subsets and for calculating the evolutionary rates without
construction of phylogenetic trees has been elaborated. The substitution rates
calculated according to this technique agreed with the data obtained
previously. A linear relationship was not observed in the second group. This
group was predominantly composed of avian influenza virus genes. The lack of
linear correlation pointed to the cocirculation of a large amount of different
influenza virus genomic segments in the avian population. An approach for an
examination of the role of intragenic recombination in the development of the
antigenic subtypes of hemagglutinin is suggested. Our results suggest that recombination
did not play a considerable role in this process, and that all modern subtypes
of this protein were probably formed before the introduction of the influenza
viruses into the human population. These findings are consistent with the
hypothesis that influenza viruses penetrated into human population from their
pools in avian populations.
Descriptors: birds genetics, evolution, molecular, genes
viral, influenza A virus avian genetics, human genetics, viral proteins
genetics.
Makarova, N.V., H. Ozaki, H. Kida, R.G. Webster, and
D.R. Perez (2003). Replication and transmission of influenza viruses in
Japanese quail. Virology 310(1): 8-15. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Quail have emerged as a potential
intermediate host in the spread of avian influenza A viruses in poultry in Hong
Kong. To better understand this possible role, we tested the replication and
transmission in quail of influenza A viruses of all 15 HA subtypes. Quail
supported the replication of at least 14 subtypes. Influenza A viruses
replicated predominantly in the respiratory tract. Transmission experiments
suggested that perpetuation of avian influenza viruses in quail requires
adaptation. Swine influenza viruses were isolated from the respiratory tract of
quail at low levels. There was no evidence of human influenza A or B virus
replication. Interestingly, a human-avian recombinant containing the surface
glycoprotein genes of a quail virus and the internal genes of a human virus
replicated and transmitted readily in quail; therefore, quail could function as
amplifiers of influenza virus reassortants that have the potential to infect
humans and/or other mammalian species.
Descriptors: infection, molecular genetics, respiratory
system, adaptation.
Marois, P., A. Boudreault, E. DiFranco, and V.
Pavilanis (1971). Response of ferrets and monkeys to intranasal infection
with human, equine and avian influenza viruses. Canadian Journal of
Comparative Medicine Revue Canadienne De Medecine Comparee 35(1):
71-6. ISSN: 0008-4050.
NAL
Call Number: 41.8 C162
Descriptors: Carnivora, influenza veterinary, monkey
diseases microbiology, nose microbiology, orthomyxoviridae pathogenicity,
respiratory tract infections microbiology, antigen antibody reactions, birds,
cross reactions, haplorhini, hemagglutination inhibition tests, horses, immune
sera, influenza immunology, orthomyxoviridae isolation and purification,
respiratory tract infections immunology, turkeys, virus replication.
Mase, M., T. Imada, Y. Sanada, M. Etoh, N. Sanada, K.
Tsukamoto, Y. Kawaoka, and S. Yamaguchi (2001). Imported parakeets harbor
H9N2 influenza A viruses that are genetically closely related to those
transmitted to humans in Hong Kong. Journal of Virology 75(7):
3490-4. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: In 1997 and 1998, H9N2 influenza A viruses
were isolated from the respiratory organs of Indian ring-necked parakeets (Psittacula
Krameri manillensis) that had been imported from Pakistan to Japan. The two
isolates were closely related to each other (>99% as determined by
nucleotide analysis of eight RNA segments), indicating that H9N2 viruses of the
same lineage were maintained in these birds for at least 1 year. The
hemagglutinins and neuraminidases of both isolates showed >97% nucleotide
identity with those of H9N2 viruses isolated from humans in Hong Kong in 1999,
while the six genes encoding internal proteins were >99% identical to the
corresponding genes of H5N1 viruses recovered during the 1997 outbreak in Hong
Kong. These results suggest that the H9N2 parakeet viruses originating in
Pakistan share an immediate ancestor with the H9N2 human viruses. Thus,
influenza A viruses with the potential to be transmitted directly to humans may
be circulating in captive birds worldwide.
Descriptors: influenza transmission, influenza A virus
avian classification, nucleoproteins, parakeets virology, amino acid sequence,
Hong Kong, avian genetics, mice, inbred BALB c, molecular sequence data,
phylogeny, RNA viral analysis, viral core proteins genetics.
Massin, P., S. van der Werf, and N. Naffakh (2001). Residue
627 of PB2 is a determinant of cold sensitivity in RNA replication of avian
influenza viruses. Journal of Virology 75(11): 5398-404. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Human influenza A viruses replicate in the
upper respiratory tract at a temperature of about 33 degrees C, whereas avian
viruses replicate in the intestinal tract at a temperature close to 41 degrees
C. In the present study, we analyzed the influence of low temperature (33
degrees C) on RNA replication of avian and human viruses in cultured cells. The
kinetics of replication of the NP segment were similar at 33 and 37 degrees C
for the human A/Puerto-Rico/8/34 and A/Sydney/5/97 viruses, whereas replication
was delayed at 33 degrees C compared to 37 degrees C for the avian
A/FPV/Rostock/34 and A/Mallard/NY/6750/78 viruses. Making use of a genetic
system for the in vivo reconstitution of functional ribonucleoproteins, we
observed that the polymerase complexes derived from avian viruses but not human
viruses exhibited cold sensitivity in mammalian cells, which was determined
mostly by residue 627 of PB2. Our results suggest that a reduced ability of the
polymerase complex of avian viruses to ensure replication of the viral genome
at 33 degrees C could contribute to their inability to grow efficiently in
humans.
Descriptors: influenza A virus avian metabolism, human
metabolism, RNA viral metabolism, viral proteins metabolism, cell line, mutation,
viral genetics, temperature, time factors, transcription, genetic, viral
proteins genetics, virus replication.
Matrosovich, M., A. Tuzikov, N. Bovin, A. Gambaryan,
A. Klimov, M.R. Castrucci, I. Donatelli, and Y. Kawaoka (2000). Early
alterations of the receptor-binding properties of H1, H2, and H3 avian
influenza virus hemagglutinins after their introduction into mammals. Journal
of Virology 74(18): 8502-12. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: Interspecies transmission of influenza A
viruses circulating in wild aquatic birds occasionally results in influenza
outbreaks in mammals, including humans. To identify early changes in the
receptor binding properties of the avian virus hemagglutinin (HA) after
interspecies transmission and to determine the amino acid substitutions
responsible for these alterations, we studied the HAs of the initial isolates
from the human pandemics of 1957 (H2N2) and 1968 (H3N2), the European swine
epizootic of 1979 (H1N1), and the seal epizootic of 1992 (H3N3), all of which
were caused by the introduction of avian virus HAs into these species. The
viruses were assayed for their ability to bind the synthetic
sialylglycopolymers 3'SL-PAA and 6'SLN-PAA, which contained, respectively,
3'-sialyllactose (the receptor determinant preferentially recognized by avian
influenza viruses) and 6'-sialyl(N-acetyllactosamine) (the receptor determinant
for human viruses). Avian and seal viruses bound 6'SLN-PAA very weakly, whereas
the earliest available human and swine epidemic viruses bound this polymer with
a higher affinity. For the H2 and H3 strains, a single mutation, 226Q-->L,
increased binding to 6'SLN-PAA, while among H1 swine viruses, the 190E-->D
and 225G-->E mutations in the HA appeared important for the increased
affinity of the viruses for 6'SLN-PAA. Amino acid substitutions at positions
190 and 225 with respect to the avian virus consensus sequence are also present
in H1 human viruses, including those that circulated in 1918, suggesting that
substitutions at these positions are important for the generation of H1 human
pandemic strains. These results show that the receptor-binding specificity of
the HA is altered early after the transmission of an avian virus to humans and
pigs and, therefore, may be a prerequisite for the highly effective replication
and spread which characterize epidemic strains.
Descriptors: hemagglutinin glycoproteins, influenza virus
metabolism, influenza A virus avian metabolism, receptors, virus
metabolism, amino acid sequence, amino
acid substitution, disease outbreaks, ducks virology, hemagglutinin
glycoproteins, influenza virus chemistry, avian isolation and purification,
models, molecular, molecular sequence data, mutation, missense, phylogeny,
protein binding, seals virology, sequence alignment, sialic acids metabolism,
species specificity, swine virology.
Matrosovich, M., N. Zhou, Y. Kawaoka, and R. Webster
(1999). The surface glycoproteins of H5 influenza viruses isolated from
humans, chickens, and wild aquatic birds have distinguishable properties. Journal
of Virology 73(2): 1146-55. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: In 1997, 18 confirmed cases of human
influenza arising from multiple independent transmissions of H5N1 viruses from
infected chickens were reported from Hong Kong. To identify possible phenotypic
changes in the hemagglutinin (HA) and neuraminidase (NA) of the H5 viruses
during interspecies transfer, we compared the receptor-binding properties and
NA activities of the human and chicken H5N1 isolates from Hong Kong and of H5N3
and H5N1 viruses from wild aquatic birds. All H5N1 viruses, including the human
isolate bound to Sia2-3Gal-containing receptors but not to Sia2-6Gal-containing
receptors. This finding formally demonstrates for the first time that receptor
specificity of avian influenza viruses may not restrict initial avian-to-human
transmission. The H5N1 chicken viruses differed from H5 viruses of wild aquatic
birds by a 19-amino-acid deletion in the stalk of the NA and the presence of a
carbohydrate at the globular head of the HA. We found that a deletion in the NA
decreased its ability to release the virus from cells, whereas carbohydrate at
the HA head decreased the affinity of the virus for cell receptors. Comparison
of amino acid sequences from GenBank of the HAs and NAs from different avian
species revealed that additional glycosylation of the HA and a shortened NA
stalk are characteristic features of the H5 and H7 chicken viruses. This
finding indicates that changes in both HA and NA may be required for the
adaptation of influenza viruses from wild aquatic birds to domestic chickens
and raises the possibility that chickens may be a possible intermediate host in
zoonotic transmission.
Descriptors: hemagglutinin glycoproteins, influenza virus
metabolism, influenza A virus avian metabolism, human metabolism, alpha
globulins metabolism, amino acid sequence, carbohydrates metabolism, chickens,
fowl plague virology, Hong Kong, horseradish peroxidase metabolism, influenza
veterinary, influenza virology, avian classification, avian isolation and
purification, human classification, human isolation and purification, molecular
sequence data, neuraminidase metabolism, ovomucin metabolism, phenotype,
receptors, virus metabolism, sequence homology, amino acid.
Matrosovich, M.N., A.S. Gambaryan, S. Teneberg, V.E.
Piskarev, S.S. Yamnikova, D.K. Lvov, J.S. Robertson, and K.A. Karlsson (1997). Avian
influenza A viruses differ from human viruses by recognition of
sialyloligosaccharides and gangliosides and by a higher conservation of the HA
receptor-binding site. Virology 233(1): 224-234. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Avian influenza virus strains representing
most hemagglutinin (HA) subtypes were compared with human influenza A (H1N1,
H3N2) and B virus isolates, including those with no history of passaging in
embryonated hen's eggs, for their ability to bind free N-acetylneuraminic acid
(Neu5Ac) and sialyloligosaccharides in a competitive binding assay and to
attach to gangliosides in a solid-phase adsorption assay. The avian viruses,
irrespective of their HA subtype, showed a higher affinity for sialyl-3-lactose
and the other Neu5Ac2-3Gal-terminated oligosaccharides and a lower affinity for
sialyl-6-lactose than for free Neu5Ac, indicative of specific interactions
between the HA and the 3-linked Gal and poor accommodation of 6-linked Gal in
the avian receptor-binding site (RBS). Human H1 and H3 strains, by contrast,
were unable to bind to 3-linked Gal, interacting instead with the asialic
portion of sialyl-6-(N-acetyllactosamine). Different parts of this moiety were
recognized by H3 and H1 subtype viruses (Gal and GlcNAc, respectively).
Comparison of the HA amino acid sequences revealed that residues in positions
138, 190, 194, 225, 226, and 228 are conserved in the avian RBS, while the
human HAs harbor substitutions at these positions, A characteristic feature of
avian viruses was their binding to Neu5Ac2-3Gal-containing gangliosides. This
property of avian precursor viruses was preserved in early human H3 isolates,
but was gradually lost with further circulation of the H3 HA in humans.
Consequently, later human H3 isolates, as well as H1 and type B human strains,
were unable to bind to short Neu5Ac2-3Gal-terminated gangliosides, an incompatibility
that correlated with higher glycosylation of the HA globular head of human
viruses. Our results suggest that the RBS is highly conserved among HA subtypes
of avian influenza virus, while that of human viruses displays distinctive
genotypic and phenotypic variability.
Descriptors: biochemistry and molecular biophysics,
evolution and adaptation, genetics, infection, microbiology, avian influenza A
virus, biochemistry and biophysics, conservation, gangliosides, genotypic
variability, hemagglutinin receptor binding site, hemagglutinin subtypes, human
influenza A virus, human influenza B virus, H1N1 subtype, H3N2 subtype,
infection phenotypic variability, sialyloligosaccharides.
Matrosovich, M.N., S. Krauss, and R.G. Webster (
2001). H9N2 influenza A viruses from poultry in Asia have human virus-like
receptor specificity. Virology 281(2): 156-62. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: influenza A virus avian metabolism, poultry
virology, receptors, virus metabolism, amino acid substitution, Asia, binding
sites, fowl plague transmission, fowl plague virology, hemagglutinin
glycoproteins, influenza virus genetics, hemagglutinin glycoproteins, influenza
virus metabolism, avian classification, avian genetics, human classification,
human genetics, human metabolism, mutation, neuraminidase genetics,
neuraminidase metabolism, phylogeny, viral envelope proteins genetics, viral
envelope proteins metabolism.
Matrosovich, M.N., T.Y. Matrosovich, T. Gray, N.A.
Roberts, and H.D. Klenk (2004). Human and avian influenza viruses target
different cell types in cultures of human airway epithelium. Proceedings
of the National Academy of Sciences of the United States of America
101(13): 4620-4. ISSN: 0027-8424.
NAL
Call Number: 500 N21P
Abstract: The recent human infections caused by H5N1,
H9N2, and H7N7 avian influenza viruses highlighted the continuous threat of new
pathogenic influenza viruses emerging from a natural reservoir in birds. It is
generally believed that replication of avian influenza viruses in humans is
restricted by a poor fit of these viruses to cellular receptors and
extracellular inhibitors in the human respiratory tract. However, detailed
mechanisms of this restriction remain obscure. Here, using cultures of
differentiated human airway epithelial cells, we demonstrated that influenza
viruses enter the airway epithelium through specific target cells and that
there were striking differences in this respect between human and avian
viruses. During the course of a single-cycle infection, human viruses
preferentially infected nonciliated cells, whereas avian viruses as well as the
egg-adapted human virus variant with an avian virus-like receptor specificity
mainly infected ciliated cells. This pattern correlated with the predominant
localization of receptors for human viruses (2-6-linked sialic acids) on
nonciliated cells and of receptors for avian viruses (2-3-linked sialic acids)
on ciliated cells. These findings suggest that although avian influenza viruses
can infect human airway epithelium, their replication may be limited by a
nonoptimal cellular tropism. Our data throw light on the mechanisms of
generation of pandemic viruses from their avian progenitors and open avenues
for cell level-oriented studies on the replication and pathogenicity of
influenza virus in humans.
Descriptors: influenza A virus, avian pathogenicity, human
pathogenicity, respiratory mucosa microbiology, bronchi, cell line, dogs, avian
isolation and purification, avian physiology, human isolation and purification,
human physiology, kidney, lectins, microscopy, confocal, nasal mucosa
microbiology, sialic acids analysis, trachea.
Matrosovich, M.N., T.Y. Matrosovich, T. Gray, N.A.
Roberts, and H.D. Klenk (2004). Neuraminidase is important for the
initiation of influenza virus infection in human airway epithelium. Journal
of Virology 78(22): 12665-7. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: Influenza virus neuraminidase (NA) plays an
essential role in release and spread of progeny virions, following the
intracellular viral replication cycle. To test whether NA could also facilitate
virus entry into cell, we infected cultures of human airway epithelium with
human and avian influenza viruses in the presence of the NA inhibitor
oseltamivir carboxylate. Twenty- to 500-fold less cells became infected in
drug-treated versus nontreated cultures (P < 0.0001) 7 h after virus
application, indicating that the drug suppressed the initiation of infection.
These data demonstrate that viral NA plays a role early in infection, and they
provide further rationale for the prophylactic use of NA inhibitors.
Descriptors: bronchi virology, nasal mucosa virology,
neuraminidase physiology, orthomyxoviridae physiology, trachea virology,
acetamides pharmacology, orthomyxoviridae enzymology.
Matsuoka, Y., H. Chen, N. Cox, K. Subbarao, J. Beck,
and D. Swayne (2003). Safety evaluation in chickens of candidate human vaccines
against potential pandemic strains of influenza. Avian Diseases
47(Special Issue): 926-930. ISSN:
0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: Two candidate formalin-inactivated vaccines,
made from high-growth reassortant viruses with the HA and NA genes from avian
viruses in a background of genes derived from A/Puerto Rico/8/34 (PR8), were
prepared against H5N1 and H9N2 subtypes (designated as H5N1/PR8 and H9N2/PR8, respectively).
These viruses bear the genotypes, antigenicity, and attenuation in mouse models
that are desirable in candidate vaccines. The pathogenicity of the newly
generated avian-human reassortant vaccine viruses was also evaluated in
chickens. Neither H5N1/PR8 nor H9N2/PR8 were highly pathogenic for chickens. No
clinical signs, gross legions, or histological lesions were observed in
chickens that were administered H5N1/PR8 either intranasally (i.n.) or
intravenously (i.v.), and virus was not detected in oropharyngeal or cloacal
swabs. When H9N2/PR8 was administered i.n., no clinical signs, gross lesions,
or histological lesions were observed and no virus was detected in cloacal
swabs. However, virus was isolated at low titer from oropharyngeal swabs of all
eight chickens. Although no clinical signs were observed when H9N2/PR8 was
administered i.v., mild tracheitis was seen in one of two chickens. Moderate
amounts of antigen were observed in tracheal respiratory epithelium, and low
titers of virus were recovered from oropharyngeal and cloacal swabs of some
chickens. In summary, both reassortant vaccine viruses replicated poorly in
chickens. These studies suggest that these candidate vaccine viruses carry a
low risk of transmission to chickens.
Descriptors: epidemiology, infection, avian influenza,
infectious disease, prevention and control, respiratory system disease, viral
disease.
Matsuura, Y., R. Yanagawa, and H. Noda (1979). Experimental
infection of mink with influenza A viruses. Brief report. Archives of
Virology 62(1): 71-6. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Mink were found to be susceptible to the
intranasal inoculation of human, swine, equine and avian influenza A viruses.
The viruses were recovered until the 7th post inoculation (p.i.) day from the
respiratory tract. The inoculated mink showed antibody response against these
viruses. Contact infection in mink with A/Kumamoto/22/77 (H3N2) was possible.
Descriptors: influenza A virus pathogenicity,
orthomyxoviridae infections microbiology, antibodies, viral biosynthesis,
disease models, animal, hemagglutination inhibition tests, influenza A virus
immunology, influenza A virus isolation and purification, orthomyxoviridae
infections immunology, orthomyxoviridae infections transmission, respiratory
system microbiology.
McManus, K. (2004). Asian avian influenza--a call
to action. Australian Veterinary Journal 82(3): 135. ISSN: 0005-0423.
NAL
Call Number: 41.8 Au72
Descriptors: chickens, disease outbreaks veterinary, avian
influenza, prevention and control, southeastern Asia, epidemiology, disease
outbreaks prevention and control, influenza A virus.
Melville, D.S. and K.F. Shortridge (2004). Influenza:
time to come to grips with the avian dimension. Lancet Infectious
Diseases 4(5): 261-2. ISSN:
1473-3099.
Descriptors: disease outbreaks prevention and control,
avian influenza epidemiology, avian influenza prevention and control, zoonoses
epidemiology, animal husbandry methods, southeastern Asia epidemiology,
chickens, ducks.
Meslin, F.X., K. Stohr, and D. Heymann (2000). Public
health implications of emerging zoonoses. Revue Scientifique Et
Technique Office International Des Epizooties 19(1): 310-7. ISSN: 0253-1933.
NAL
Call Number: SF781.R4
Abstract: Many new, emerging and re-emerging diseases
of humans are caused by pathogens which originate from animals or products of
animal origin. A wide variety of animal species, both domestic and wild, act as
reservoirs for these pathogens, which may be viruses, bacteria or parasites.
Given the extensive distribution of the animal species affected, the effective
surveillance, prevention and control of zoonotic diseases pose a significant
challenge. The authors describe the direct and indirect implications for public
health of emerging zoonoses. Direct implications are defined as the
consequences for human health in terms of morbidity and mortality. Indirect
implications are defined as the effect of the influence of emerging zoonotic
disease on two groups of people, namely: health professionals and the general
public. Professional assessment of the importance of these diseases influences
public health practices and structures, the identification of themes for
research and allocation of resources at both national and international levels.
The perception of the general public regarding the risks involved considerably
influences policy-making in the health field. Extensive outbreaks of zoonotic
disease are not uncommon, especially as the disease is often not recognised as
zoonotic at the outset and may spread undetected for some time. However, in
many instances, the direct impact on health of these new, emerging or
re-emerging zoonoses has been small compared to that of other infectious
diseases affecting humans. To illustrate the tremendous indirect impact of
emerging zoonotic diseases on public health policy and structures and on public
perception of health risks, the authors provide a number of examples, including
that of the Ebola virus, avian influenza, monkeypox and bovine spongiform encephalopathy.
Recent epidemics of these diseases have served as a reminder of the existence
of infectious diseases and of the capacity of these diseases to occur
unexpectedly in new locations and animal species. The need for greater
international co-operation, better local, regional and global networks for
communicable disease surveillance and pandemic planning is also illustrated by
these examples. These diseases have contributed to the definition of new
paradigms, especially relating to food safety policies and more generally to
the protection of public health. Finally, the examples described emphasise the
importance of intersectorial collaboration for disease containment, and of
independence of sectorial interests and transparency when managing certain health
risks.
Descriptors: communicable diseases, emerging epidemiology,
disease outbreaks prevention and control, public health, zoonoses epidemiology,
zoonoses etiology, communicable diseases, emerging prevention and control,
communicable diseases, emerging transmission, international cooperation,
morbidity, risk factors, world health.
Mohammad Yousaf (2004). Avian influenza outbreak
hits the industry again. World Poultry 20(3): 22-25. ISSN: 1388-3119.
NAL
Call Number: SF481.M54
Descriptors: disease control, disease prevention, disease
surveys, disease transmission, epidemiology, clinical aspects, diagnostic
techniques, outbreaks, pathogenicity, poultry industry, public health, World
Health Organization, zoonoses, human diseases, avian influenza virus.
Mohan, R., Y.M. Saif, G.A. Erickson, G.A. Gustafson,
and B.C. Easterday (1981). Serologic and epidemiologic evidence of infection
in turkeys with an agent related to the swine influenza virus. Avian
Diseases 25(1): 11-6. ISSN:
0005-2086.
NAL
Call Number: 41.8 Av5
Descriptors: influenza veterinary, influenza A virus,
porcine immunology, influenza A virus immunology, poultry diseases
epidemiology, turkeys, antibodies, viral
analysis, hemagglutination tests veterinary, immunodiffusion veterinary, influenza
diagnosis, influenza epidemiology, avian immunology, poultry diseases
diagnosis.
Molibog, E.V., T.V. Pysina, and A.S. Gorbunova (
1968). Sootnoshenie mezhdu eliuikuiushchei i neiraminidaznoi aktivost'iu
virusov gruppa tipa A cheloveka, mlekopitaiushchikh i ptits. [Relationship
between eluting and neuraminidase activity of human, mammalian and avian
influenza type A viruses]. Voprosy Virusologii 13(5): 623-7.
ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Descriptors: neuraminidase analysis, orthomyxoviridae
enzymology, orthomyxoviridae physiology.
Monto, A.S. (2005). The threat of an avian
influenza pandemic. New England Journal of Medicine 352(4):
323-5. ISSN: 1533-4406.
NAL
Call Number: 448.8 N442
Descriptors: acetamides therapeutic use, antiviral agents
therapeutic use, disease outbreaks prevention and control, influenza
epidemiology, influenza transmission, influenza A virus, avian influenza
classification, avian influenza genetics, avian influenza pathogenicity, birds,
disease transmission prevention and control, genome, viral, influenza drug
therapy, avian influenza transmission, avian influenza virology, neuraminidase
antagonists and inhibitors, neuraminidase metabolism, virulence, zoonoses
transmission, zoonoses virology.
Moore, J.T., L.M. Spence, T.D. Sanders, and A.K.
Adams (1999). Human influenza: viral mutations and altered tropisms. Clinical
Laboratory Science Journal of the American Society for Medical Technology
12(2): 67-9. ISSN: 0894-959X.
NAL
Call Number: RB37.A1C5
Abstract: Influenza is a virus that is capable of
causing a pandemic of the human race. Influenza has the ability to infect
humans by mutating and altering its pathogenic characteristics. Efforts must be
made worldwide to educate people about the possibilities of a potential
outbreak. Awareness of optimal conditions which could lead to viral mutation
and human to human transmission of a neogenetic strain of influenza appears to
be a key deterrent against future cases.
Descriptors: influenza genetics, influenza transmission,
influenza A virus genetics, mutation, adolescent, adult, birds, child,
preschool, disease outbreaks, Hong Kong epidemiology, infant, influenza
physiopathology, influenza virology, influenza A virus avian genetics, middle
aged, species specificity.
Morse, S.S. (2004). Factors and determinants of
disease emergence. Revue Scientifique Et Technique Office International
Des Epizooties 23(2): 443-51. ISSN:
0253-1933.
NAL
Call Number: SF781.R4
Abstract: Emerging infectious diseases can be defined as
infections that have newly appeared in a population or are rapidly increasing
in incidence or geographic range. Many of these diseases are zoonoses,
including such recent examples as avian influenza, severe acute respiratory
syndrome, haemolytic uraemic syndrome (a food-borne infection caused by certain
strains of Escherichia coli) and probably human immunodeficiency
virus/acquired immune deficiency syndrome. Specific factors precipitating the
emergence of a disease can often be identified. These include ecological,
environmental or demographic factors that place people in increased contact
with the natural host for a previously unfamiliar zoonotic agent or that
promote the spread of the pathogen. These factors are becoming increasingly
prevalent, suggesting that infections will continue to emerge and probably
increase. Strategies for dealing with the problem include focusing special
attention on situations that promote disease emergence, especially those in
which animals and humans come into contact, and implementing effective disease
surveillance and control.
Descriptors: epidemiology, infection, public health,
vector biology, veterinary medicine, SARS, severe acute respiratory syndrome,
haemolytic uraemic syndrome, Escherichia coli, control, demographic
factors, disease emergence, disease surveillance, ecological factors,
environmental factors, geographic range, zoonosis.
Mounts, A.W., H. Kwong, H.S. Izurieta, Y. Ho, T. Au,
M. Lee, C. Buxton Bridges, S.W. Williams, K.H. Mak, J.M. Katz, W.W. Thompson,
N.J. Cox, and K. Fukuda (1999). Case-control study of risk factors for avian
influenza A (H5N1) disease, Hong Kong, 1997. Journal of Infectious
Diseases 180(2): 505-8. ISSN:
0022-1899.
NAL
Call Number: 448.8 J821
Abstract: In May 1997, a 3-year-old boy in Hong Kong
died of a respiratory illness related to influenza A (H5N1) virus infection,
the first known human case of disease from this virus. An additional 17 cases
followed in November and December. A case-control study of 15 of these patients
hospitalized for influenza A (H5N1) disease was conducted using controls
matched by age, sex, and neighborhood to determine risk factors for disease.
Exposure to live poultry (by visiting either a retail poultry stall or a market
selling live poultry) in the week before illness began was significantly
associated with H5N1 disease (64% of cases vs. 29% of controls, odds ratio,
4.5, P=.045). By contrast, travel, eating or preparing poultry products, recent
exposure to persons with respiratory illness, including persons with known
influenza A (H5N1) infection, were not associated with H5N1 disease.
Descriptors: influenza etiology, influenza A virus avian
isolation and purification, adolescent, adult, case control studies, child,
preschool, Hong Kong, infant, influenza virology, matched pair analysis, middle
aged, poultry, risk factors.
Murakami, Y., K. Nerome, Y. Yoshioka, S. Mizuno, and
A. Oya (1988). Difference in growth behavior of human, swine, equine, and
avian influenza viruses at a high temperature. Archives of Virology
100(3-4): 231-44. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Growth characteristics of a wide range of
influenza A viruses from different mammals and bird species were examined in an
established line of canine kidney (MDCK) cells at an ordinary (37 degrees C)
and a high temperature (42 degrees C). Although all viruses employed in the
present study possessed a capability of replicating at 37 degrees C, virus
growth at 42 degrees C showed considerable variation and reflected differences
in the natural hosts of the isolates. All reference strains and isolates from
bird species grew well in the MDCK cells maintained at 42 degrees C, but human
viruses did not, showing an asymmetrical growth behavior. In contrast to this,
growth of swine and equine viruses showed growth characteristics intermediate
between human and avian viruses. Of the two swine viruses examined, replication
of one strain occurred equally well at both temperatures and another failed to
grow at 42 degrees C. Similarly, two of the three equine viruses tested
belonging to H3N8 antigenic subtypes grew at 42 degrees C. However, the results
obtained from comparison of plaque sizes and growth curves indicated that the
replication of the above swine and equine viruses was restricted under a
stringent temperature when compared to avian viruses. The detailed analysis of
cloned viruses revealed that some of the swine and equine viruses contained two
variants which are readily distinguished by growth behavior at 42 degrees C.
Genome analysis of parental and virus clones by oligonucleotide mapping and
migration profiles of RNA segments did not detect any differences among the
above variants exhibiting the asymmetrical growth characteristics at 42 degrees
C.
Descriptors: influenza A virus avian growth and
development, human growth and development, influenza A virus growth and
development, cell line, genes viral, horses, avian genetics, human genetics,
porcine genetics, porcine growth and development, influenza A virus genetics,
plaque assay, RNA viral genetics, temperature.
Murphy, B.R., A.J. Buckler White, W.T. London, J.
Harper, E.L. Tierney, N.T. Miller, L.J. Reck, R.M. Chanock, and V.S. Hinshaw
(1984). Avian-human reassortant influenza A viruses derived by mating avian
and human influenza A viruses. Journal
of Infectious Diseases 150(6): 841-50.
ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Abstract: Reassortant influenza A viruses were produced
by mating an avian virus (A/Mallard/NY/78, A/Mallard/Alberta/78, or
A/Pintail/Alberta/79) with a wild-type human influenza A virus. From each
mating a reassortant virus was obtained that contained the genes coding for the
hemagglutinin and neuraminidase surface antigens of the human influenza A
wild-type virus and the six other RNA segments ("internal genes") of
the avian influenza A virus parent. The avian-human reassortant influenza
viruses produced resembled their avian virus parent in that they produced
plaques on MDCK monolayers at 42 C, a temperature restrictive for the human
influenza viruses. In the trachea of squirrel monkeys, each avian-human
reassortant influenza virus was as restricted in its replication as was its
avian influenza virus parent. Thus, one or more of the six internal genes of
each avian parent virus was responsible for restriction of the reassortant
virus in monkeys. The A/Washington/80 X A/Mallard/NY/78 reassortant virus
retained its phenotype of restricted replication in monkeys after five serial
passages in vivo. It also failed to transmit to cagemates or induce resistance
to wild-type virus challenge, and it did not initiate a systemic or enteric
infection. These findings form the basis for evaluation of these attenuated
avian-human reassortant influenza A viruses as live attenuated vaccines for
humans.
Descriptors: crosses, genetic, influenza A virus avian
genetics, human genetics, neuraminidase genetics, chickens, child, ducks,
hemagglutinins viral genetics, immunization, avian physiology, human
physiology, saimiri, virus replication.
Murphy, B.R., A.J. Buckler White, W.T. London, and
M.H. Snyder (1989). Characterization of the M protein and nucleoprotein
genes of an avian influenza A virus which are involved in host range
restriction in monkeys. Vaccine 7(6): 557-61. ISSN: 0264-410X.
NAL
Call Number: QR189.V32
Abstract: A reassortant virus possessing RNA segment 7,
which codes for the M1 and M2 proteins, of the avian influenza A/Mallard/New
York/6750/78 (H2N2) virus and the other seven RNA segments of the human
influenza A/Udorn/307/72 (H3N2) virus had been shown previously to be markedly
restricted in replication in the respiratory tract of squirrel monkeys. In
contrast, a reassortant possessing segment 7 of another avian influenza virus,
A/Pintail/Alberta/119/79 (H4N6), and the seven other RNA segments from the
A/Udorn/72 virus was not restricted. The nucleotide and deduced amino acid
sequence of the RNA segment 7 of each virus was determined to identify the
structural basis for the attenuation phenotype specified by RNA segment 7 of
the A/Mallard/78 virus. Analysis of the deduced amino acid sequences revealed
only two amino acid differences in the M1 protein and one difference in the M2
protein, suggesting that the attenuation phenotype of a reassortant virus
possessing segment 7 of the A/Mallard/78 virus may be specified by one to three
amino acids. Reassortant viruses possessing RNA segment 6, which codes for the
nucleoprotein, of either avian influenza virus and the other seven RNA segments
of a human influenza virus were also restricted in replication in squirrel
monkeys. A comparison of the deduced amino acid sequences of the two avian
nucleopeoteins demonstrated only three amino acid differences indicating that
these two avian viruses possess NP genes that are highly related. The high
degree of relatedness of both the NP and M proteins of these two avian viruses
contrasts with their divergent surface antigens.(ABSTRACT TRUNCATED AT 250
WORDS)
Descriptors: genes viral, influenza A virus avian
genetics, nucleoproteins genetics, viral core proteins, viral matrix proteins
genetics, viral proteins genetics, amino acid sequence, base sequence, human
genetics, RNA viral analysis, saimiri, virus replication.
Murphy, B.R., M.L. Clements, E.L. Tierney, R.E.
Black, J. Stienberg, and R.M. Chanock (1985). Dose response of influenza
A/Washington/897/80 (H3N2) avian-human reassortant virus in adult volunteers.
Journal of Infectious Diseases 152(1): 225-9. ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Descriptors: antibodies, viral biosynthesis, influenza A
virus avian immunology, human immunology, influenza vaccine immunology, adult,
dose response relationship, immunologic, influenza microbiology, influenza
transmission, avian genetics, human genetics, recombination, genetic,
vaccination, vaccines, attenuated.
Murphy, B.R., V.S. Hinshaw, D.L. Sly, W.T. London,
N.T. Hosier, F.T. Wood, R.G. Webster, and R.M. Chanock (1982). Virulence of
avian influenza A viruses for squirrel monkeys. Infection and Immunity
37(3): 1119-26. ISSN: 0019-9567.
NAL
Call Number: QR1.I57
Descriptors: cebidae microbiology, influenza A virus avian
pathogenicity, saimiri microbiology, cell line, dogs, ducks microbiology,
ferrets microbiology, hamsters, avian growth and development, human growth and
development, lung microbiology, mesocricetus microbiology, plaque assay,
turbinates microbiology, virus replication.
Murphy, B.R., D.L. Sly, E.L. Tierney, N.T. Hosier,
J.G. Massicot, W.T. London, R.M. Chanock, R.G. Webster, and V.S. Hinshaw
(1982). Reassortant virus derived from avian and human influenza A viruses
is attenuated and immunogenic in monkeys. Science 218(4579):
1330-2. ISSN: 0036-8075.
NAL
Call Number: 470 Sci2
Abstract: An influenza A reassortant virus that
contained the hemagglutinin and neuraminidase genes of a virulent human virus,
A/Udorn/72 (H3N2), and the six other influenza A virus genome segments from an
avirulent avian virus, A/Mallard/New York/6750/78 (H2N2), was evaluated for its
level of replication is squirrel monkeys and hamsters. In monkeys, the reassortant
virus was as attenuated and as restricted in its level of replication in the
upper and lower respiratory tract as its avian influenza virus parent.
Nonetheless, infection with the reassortant induced significant resistant to
challenge with virulent human influenza virus. In hamsters, the reassortant
virus replicated to a level intermediate between that of its parents. These
findings suggest that the nonsurface antigen genes of the avian parental virus
are the primary determinants of restriction of replication of the reassortant
virus in monkeys. Attenuation of the reassortant virus for primates is achieved
by inefficient functioning of the avian influenza genes in primate cells, while
antigenic specificity of the human influenza virus is provided by the
neuraminidase and hemagglutinin genes derived from the human virus. This
approach could lead to the development of a live influenza A virus vaccine that
is attenuated for man if the avian influenza genes are similarly restricted in
human cells.
Descriptors: influenza A virus avian genetics, human
genetics, influenza vaccine immunology, antigens, surface genetics, epitopes
genetics, epitopes immunology, hamsters, hemagglutinins genetics,
hemagglutinins immunology, neuraminidase genetics, neuraminidase immunology,
saimiri, vaccines, attenuated immunology.
Naffakh, N., J.C. Manuguerra, and S. Van der Werf
(2002). Grippe: Zoonose et transmission inter-especes. [Influenza viruses: Zoonosis and interspecies
transmission]. Virologie Montrouge 6(Special): S73-S82. ISSN: 1267-8694.
Abstract: Influenza A viruses have been isolated from a
wide range of species. Aquatic birds, in which all 15 hemagglutinin subtypes
have been found, are believed to be the reservoir of influenza A viruses from
which new virus subtypes can episodically be transmitted to new hosts.
Generally, avian influenza viruses replicate poorly in humans. However,
adaptation of an avian virus to the human host may occur either through genetic
reassortment or following direct transmission, and may result in influenza
pandemics, as has been the case in 1918, 1957 and 1968. Several observations
suggest that pigs, in which both avian and human influenza viruses replicate,
are involved as a link and a mixing vessel in interspecies transmissions of influenza
viruses. In addition, domestic poultry seem to serve as intermediate hosts for
the acquisition of determinants that increase the potential of transmission of
influenza viruses to mammals. The molecular bases for the host-specificity of
human or avian influenza A viruses are not fully understood. The hemagglutinin
and neuraminidase are considered as possible determinants of host-restriction
because of different receptor specificities. In addition, genetic studies have
indicated that gene segments encoding internal proteins, and especially the PB2
segment, harbor host-range determinants. This notion was strengthened by the
fact that the six internal genes of avian H5N1 and H9N2 viruses that were
responsible for respiratory disease in humans in Hong Kong in 1997 and 1999,
respectively, were found to be very similar. However, the multiple genetic
features of internal genes that contribute to host-specificity of influenza A
viruses and to their potential for interspecies transmission, as well as the
molecular mechanisms involved, are still to be understood.
Descriptors: biochemistry and molecular biophysics,
infection, influenza, respiratory system disease, viral disease.
Naffakh, N., P. Massin, N. Escriou, B. Crescenzo
Chaigne, and S. van der Werf (2000). Genetic analysis of the compatibility
between polymerase proteins from human and avian strains of influenza A
viruses. Journal of General Virology 81(Pt. 5): 1283-91. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: In order to determine how efficiently the
polymerase proteins derived from human and avian influenza A viruses can
interact with each other in the context of a mammalian cell, a genetic system
that allows the in vivo reconstitution of active ribonucleoproteins was used.
The ability to achieve replication of a viral-like reporter RNA in COS-1 cells
was examined with heterospecific mixtures of the core proteins (PB1, PB2, PA
and NP) from two strains of human viruses (A/Puerto Rico/8/34 and
A/Victoria/3/75), two strains of avian viruses (A/Mallard/NY/6750/78 and
A/FPV/-Rostock/34), and a strain of avian origin (A/Hong Kong/156/97) that was
isolated from the first human case of H5N1 influenza in Hong Kong in 1997. In
accordance with published observations on reassortant viruses, PB2 amino acid
627 was identified as a major determinant of the replication efficiency of
heterospecific complexes in COS-1 cells. Moreover, the results showed that
replication of the viral-like reporter RNA was more efficient when PB2 and NP
were both derived from the same avian or human virus or when PB1 was derived
from an avian virus, whatever the origin of the other proteins. Furthermore,
the PB1 and PB2 proteins from the A/Hong- Kong/156/97 virus exhibited
intermediate properties with respect to the corresponding proteins from avian
or human influenza viruses, suggesting that some molecular characteristics of
PB1 and PB2 proteins might at least partially account for the ability of the
A/Hong Kong/156/97 virus to replicate in humans.
Descriptors: influenza A virus avian genetics, influenza A
virus human genetics, nucleoproteins, RNA replicase, viral core proteins
genetics, viral core proteins metabolism, cos cells, chloramphenicol o
acetyltransferase, cloning, molecular, DNA, complementary, DNA directed RNA
polymerases genetics, DNA directed RNA polymerases metabolism, influenza A
virus avian metabolism, influenza A virus human metabolism, molecular sequence
data, plasmids genetics, sequence analysis, DNA, transcription, genetic,
transfection, viral proteins genetics, viral proteins metabolism, virus
replication.
Nagai, Y., K. Otsuki, N. Abe, Y. Kawaoka, H. Kida,
T. Kurata, T. Sata, M. Tashiro, N. Yamaguchi, and H. Yoshikura (2004). [Round
table discussion on highly pathogenic H5N1 avian influenza]. Uirusu
Journal of Virology 54(1): 123-41.
ISSN: 0042-6857.
Descriptors: influenza A virus, avian pathogenicity,
virulence, Asia epidemiology, disease outbreaks prevention and control,
influenza epidemiology, influenza prevention and control, influenza
transmission, influenza virology, avian influenza A virus classification, avian
influenza A virus genetics, avian influenza A virus immunology, avian influenza
epidemiology, avian influenza prevention and control, avian influenza
transmission, avian influenza virology, poultry, receptors, virus physiology,
viral vaccines, zoonoses epidemiology, zoonoses transmission, zoonoses
virology.
Nakajima, K., E. Nobusawa, and S. Nakajima (1984). Genetic
relatedness between A/Swine/Iowa/15/30(H1N1) and human influenza viruses. Virology
139(1): 194-8. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The nucleotide sequences of the M and NS1
genes of influenza virus A/Swine/Iowa/15/30 (A/SW/IW/30)(H1N1) were determined
with cloned DNAs and compared with reported sequences of human and avian
influenza viruses. A/SW/IW/30 virus was found to be closely similar to
A/PR/8/34(H1N1) virus in the nucleotide sequences of the M and NS1 genes, the
base differences between the two strains being 64 out of 1027 nucleotides in
the M gene and 52 out of 740 in the NS1 gene. Based on the assumptions that
these two viruses were derived from a common ancestor and that the rate of base
changes per year was the same in man and in swine, it was estimated that the
progenitor virus was in circulation during the period from 1915 to 1920. This
estimation was compatible with the epidemiological findings suggesting that the
progenitor of the swine influenza virus was the agent of the 1918 influenza
pandemic. Furthermore, the M and NS1 gene sequences of A/FPV/Rostock/34(H7N6)
virus were much closer to those of A/SW/IW/30 and A/PR/8/34 viruses than to
A/duck/Alberta/60/76(H12N5) virus, but not as close as the A/SW/IW/30 virus was
to A/PR/8/34 virus.
Descriptors: influenza A virus human genetics, influenza A
virus, porcine genetics, influenza A virus genetics, base sequence, evolution,
genes viral.
Nerome, K., Y. Kanegae, K.F. Shortridge, S. Sugita,
and M. Ishida (1995). Genetic analysis of porcine H3N2 viruses originating
in southern China. Journal of General Virology 76(Pt. 3):
613-24. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: From immunological and phylogenetic analyses
of H3 influenza viruses isolated from pigs and ducks in the People's Republic
of China (China), Hong Kong, Taiwan and Japan, between 1968 and 1982, we
arrived at the following conclusions. The H3 haemagglutinin and N2
neuraminidase genes from swine isolates can be segregated into four mammalian
lineages, including: (i) the earliest human strains; (ii) early swine strains
including Hong Kong isolates from 1976-1977; (iii) an intermediate strain
between the early swine and recent human strains; and (iv) recent human
strains. In this study we found an unusual swine strain (sw/Hong Kong/127/82)
belonging to the third lineage which behaved like those of the early swine-like
lineage in the haemagglutination inhibition test; but neuraminidase inhibition
profiles with monoclonal antibodies indicated that this virus is related to
late human strains. On the basis of pairwise comparisons of complete or partial
nucleotide sequences the genes encoding the three polymerase proteins (PB2,
PB1, PA), the nucleoprotein, the membrane protein and possibly the
nonstructural proteins of sw/Hong Kong/127/82 are of the swine H1N1 lineage,
whereas genes encoding the two surface glycoproteins belong to the human H3N2
lineage. In contrast, all RNA segments of one swine isolate (sw/Hong
Kong/81/78) are similar to those of recent human H3N2 viruses. This study
indicated that frequent interspecies infections between human and swine hosts
appeared to occur during 1976-82. Although the evolutionary rates of human
(0.0122/site/year), swine (0.0127/site/year) and avian (0.0193/site/year) virus
genes are similar when based upon synonymous substitutions, nonsynonymous
substitutions indicated that viral genes derived from human and swine viruses
evolved about three times faster (0.0026-0.0027/site/year) than those of avian
viruses (0.0008/site/year). Furthermore, the evolutionary mechanism by which
human and swine H3 haemagglutinin genes evolve at a similar rate, based on
nonsynonymous substitutions, appeared to be quite different from previous
evidence which showed that human H1 haemagglutinin genes evolved three times
faster than those of swine viruses. However, comparison of the number of
nonsynonymous substitutions in the antigenic sites (A-E) of haemagglutinin
molecules demonstrated that swine viruses evolve at a rate that is about one
fifth to one tenth that of human viruses, reflecting the conservative nature of
the antigenic structure in the former.
Descriptors: evolution, genes viral genetics,
hemagglutinins viral genetics, influenza A virus, porcine genetics, influenza
A virus genetics, amino acid sequence, antibodies, monoclonal, antibodies,
viral, antigenic variation genetics, China, hemagglutinins viral analysis,
hemagglutinins viral immunology, Hong Kong, influenza A virus avian genetics,
influenza A virus avian immunology, influenza A virus human genetics, influenza
A virus human immunology, influenza A virus, porcine immunology, influenza A
virus immunology, molecular sequence data, neuraminidase analysis,
neuraminidase genetics, RNA viral genetics, sequence analysis, DNA, sequence
homology, amino acid, sequence homology, nucleic acid, swine.
Nerome, K., Y. Yoshioka, C.A. Torres, A. Oya, P.
Bachmann, K. Ottis, and R.G. Webster (1984). Persistence of Q strain of H2N2
influenza virus in avian species: antigenic, biological and genetic analysis of
avian and human H2N2 viruses. Archives of Virology 81(3-4):
239-50. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: The characteristics of an avian influenza
virus were compared in detail with those of human Asian (H2N2) influenza
viruses. Antigenic analysis by different antisera against H2N2 viruses and
monoclonal antibodies to both the hemagglutinin and neuraminidase antigens
showed that an avian isolate, A/duck/Munchen/9/79 contained hemagglutinin and
neuraminidase subunits closely related to those of the early human H2N2 viruses
which had been prevalent in 1957. However, this avian virus gave low HI titers
with absorbed and non-absorbed antisera to different human H2N2 viruses
isolated in 1957. Like human Q phase variant, such as A/RI/5-/57 (H2N2),
hemagglutination of the above avian strain was not inhibited by the purified
non-specific gamma-inhibitor from guinea pig serum. Growth behavior at
restrictive temperature (42 degrees C) clearly differentiate the avian H2N2
virus from human influenza viruses, showing that the former virus grew well in
MDCK cells at 42 degrees C but not the latters. Genomic analysis of these
viruses revealed that the oligonucleotide map of H2N2 virus isolated from a
duck was quite different from those of human H2N2 viruses from 1957 to 1967.
The oligonucleotide mapping also indicated that different H2N2 influenza virus
variants had co-circulated in humans in 1957.
Descriptors: influenza A virus avian immunology, influenza
A virus human immunology, hemagglutinins viral immunology, influenza A virus avian
genetics, influenza A virus human genetics, influenza A virus growth and
development, neuraminidase immunology, RNA viral genetics.
Nestorowicz, A., Y. Kawaoka, W.J. Bean, and R.G.
Webster (1987). Molecular analysis of the hemagglutinin genes of Australian
H7N7 influenza viruses: role of passerine birds in maintenance or transmission?
Virology 160(2): 411-8. ISSN:
0042-6822.
NAL
Call Number: 448.8 V81
Abstract: In 1985 a fowl plague-like disease occurred
in chickens in Lockwood, Victoria, Australia and caused high mortality. An H7N7
influenza virus was isolated from the chickens (A/Chicken/Victoria/1/85);
additionally, an antigenically similar virus was isolated from starlings
(A/Starling/Victoria/5156/85) and serological evidence of H7N7 virus infection
was found in sparrows. Antigenic analysis with monoclonal antibodies to H7,
oligonucleotide mapping of total vRNA, and sequence analysis of the HA genes
established that the chicken and starling influenza viruses were closely
related and probably came from the same source. There was high nucleotide
sequence homology (95.3%) between the HA genes of A/Chick/Vic/85 and a fowl
plague-like virus isolated from chickens in Victoria 9 years earlier
[A/Fowl/Vic/76 (H7N7)]. The sequence homologies indicated that the
A/Chick/Vic/85 and A/Fowl/Vic/76 were derived from a common recent ancestor,
while another recent H7N7 virus, Seal/Mass/1/80 originated from a different
evolutionary lineage. Experimental infection of chickens and starlings with
A/Chick/Vic/1/85 (H7N7) was associated with high mortality (100%), transmission
to contact birds of the same species, and virus in all organs. In sparrows
one-third of the birds died after infection and virus was isolated from most
organs; transmission to contact sparrows did not occur. In contrast, the H7N7
virus replicated in ducks and spread to contact ducks but caused no mortality.
These studies establish that the host species plays a role in determining the
virulence of avian influenza viruses, and provide the first evidence for
transmission of virulent influenza viruses between domestic poultry and
passerine birds. They support the hypothesis that potentially virulent H7N7
influenza viruses could be maintained in ducks where they cause no apparent
disease and may sometimes spread to other wild birds and domestic poultry.
Descriptors: birds microbiology, hemagglutinins viral
genetics, influenza A virus avian genetics, amino acid sequence, animals, wild
microbiology, Australia, base sequence, chickens microbiology, disease reservoirs,
genes viral, molecular sequence data, nucleotide mapping, RNA viral genetics,
species specificity, virus replication.
Nettles, V.F., J.M. Wood, and R.G. Webster (1985). Wildlife
surveillance associated with an outbreak of lethal H5N2 avian influenza in
domestic poultry. Avian Diseases 29(3): 733-41. ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: Wildlife surveillance was conducted for
influenza viruses in conjunction with the 1983-84 lethal H5N2 avian influenza
epizootic in domestic poultry in Pennsylvania, New Jersey, Maryland, and
Virginia. Virus-isolation attempts made on cloacal and tracheal swabs from
4,466 birds and small rodents within the quarantined areas and 1,511 waterfowl
in nearby Maryland yielded only a single H5N2 isolate from a pen-raised chukar
in Pennsylvania. Antibodies against hemagglutinin type 5 and/or neuraminidase
type 2 were found in 33% of the aquatic birds tested; however, this finding
could not be used to confirm previous H5N2 avian influenza virus activity because
of the possibility of prior infections with multiple influenza subtypes. The
low prevalence of lethal H5N2 avian influenza virus in wild birds and small
rodents strongly indicated that these animals were not responsible for
dissemination of the disease among poultry farms during the outbreak.
Descriptors: birds microbiology, disease outbreaks
veterinary, fowl plague transmission, disease reservoirs microbiology,
hemagglutinins viral analysis, neuraminidase analysis, orthomyxoviridae
isolation and purification, paramyxoviridae isolation and purification,
Pennsylvania.
Nguyen, D.C., T.M. Uyeki, S. Jadhao, T. Maines, M.
Shaw, Y. Matsuoka, C. Smith, T. Rowe, X. Lu, H. Hall, X. Xu, A. Balish, A.
Klimov, T.M. Tumpey, D.E. Swayne, L.P. Huynh, H.K. Nghiem, H.H. Nguyen, L.T.
Hoang, N.J. Cox, and J.M. Katz (2005). Isolation and characterization of
avian influenza viruses, including highly pathogenic H5N1, from poultry in live
bird markets in Hanoi, Vietnam, in 2001. Journal of Virology 79(7):
4201-12. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Since 1997, outbreaks of highly pathogenic
(HP) H5N1 and circulation of H9N2 viruses among domestic poultry in Asia have
posed a threat to public health. To better understand the extent of
transmission of avian influenza viruses (AIV) to humans in Asia, we conducted a
cross-sectional virologic study in live bird markets (LBM) in Hanoi, Vietnam,
in October 2001. Specimens from 189 birds and 18 environmental samples were
collected at 10 LBM. Four influenza A viruses of the H4N6 (n = 1), H5N2 (n =
1), and H9N3 (n = 2) subtypes were isolated from healthy ducks for an isolation
frequency of over 30% from this species. Two H5N1 viruses were isolated from
healthy geese. The hemagglutinin (HA) genes of these H5N1 viruses possessed
multiple basic amino acid motifs at the cleavage site, were HP for
experimentally infected chickens, and were thus characterized as HP AIV. These
HA genes shared high amino acid identities with genes of other H5N1 viruses
isolated in Asia during this period, but they were genetically distinct from
those of H5N1 viruses isolated from poultry and humans in Vietnam during the
early 2004 outbreaks. These viruses were not highly virulent for experimentally
infected ducks, mice, or ferrets. These results establish that HP H5N1 viruses
with properties similar to viruses isolated in Hong Kong and mainland China
circulated in Vietnam as early as 2001, suggest a common source for H5N1
viruses circulating in these Asian countries, and provide a framework to better
understand the recent widespread emergence of HP H5N1 viruses in Asia.
Descriptors: avian influenza A virus classification, avian
influenza A virus isolation and purification, avian influenza virology, poultry
virology, viral antigens, chickens virology, ducks virology, molecular
epidemiology, ferrets, geese virology, avian influenza A virus genetics, avian
influenza A viruspathogenicity, mice, molecular sequence data, neuraminidase
genetics, phylogeny, sequence analysis, serotyping, Vietnam, virulence.
Nicholson, K.G., A.E. Colegate, A. Podda, I.
Stephenson, J. Wood, E. Ypma, and M.C. Zambon (2001). Safety and
antigenicity of non-adjuvanted and MF59-adjuvanted influenza
A/Duck/Singapore/97 (H5N3) vaccine: A randomised trial of two potential vaccines
against H5N1 influenza. Lancet 357(9272): 1937-1943. ISSN: 0099-5355.
NAL
Call Number: 448.8 L22
Abstract: Background: In 1997, pathogenic avian
influenza A/Hong Kong/97 (H5N1) viruses emerged as a pandemic threat to human
beings. A non-pathogenic variant, influenza A/Duck/Singapore/97 (H5N3), was
identified as a leading vaccine candidate. We did an observer-blind, phase I,
randomised trial in healthy volunteers to assess safety, tolerability, and
antigenicity of MF59-adjuvanted and non-adjuvanted vaccines. Methods: 32
participants were randomly assigned MF59, and 33 non-adjuvanted vaccine. Two
doses were given 3 weeks apart, of 7.5, 15, or 30 mug haemagglutinin surface-antigen
influenza A H5N3 vaccine. Antibody responses were measured by haemagglutination
inhibition, microneutralisation, and single radial haemolysis (SRH). The
primary outcome was geometric mean antibody titre 21 days after vaccination.
Findings: The A/Duck/Singapore vaccines were safe and well tolerated. Antibody
response to non-adjuvanted vaccine was poor, the best response occurring after
two 30 mug doses: one, four, four, and one person of eleven seroconverted by
haemagglutination inhibition, microneutralisation, H5N3 SRH, and H5N1 SRH,
respectively. The geometric mean titres of antibody, and seroconversion rates,
were significantly higher after MF59 adjuvanted vaccine. Two 7.5 mug doses of
MF59 adjuvanted vaccine gave the highest seroconversion rates:
haemagglutination inhibition, six of ten; microneutralisation, eight of ten;
H5N3 SRH, ten of ten; H5N1 SRH, nine of ten. Geometric mean titre of antibody
to the pathogenic virus, A/Hong Kong/489/97 (H5N1), was about half that to
A/Duck/Singapore virus. Interpretation: Non-adjuvanted A/Duck/Singapore/97
(H5N3) vaccines are poorly immunogenic and doses of 7.5-30 mug haemagglutinin
alone are unlikely to give protection from A/Hong Kong/97 (H5N1) virus.
Addition of MF59 to A/Duck/Singapore/97 vaccines boost the antibody response to
protection levels. Our findings have implications for development and
assessment of vaccines for future pandemics.
Descriptors: infection, pharmacology, influenza,
respiratory system disease, viral disease, antigenicity safety.
Nicholson, K.G., J.M. Wood, and M. Zambon (2003). Influenza.
Lancet 362(9397): 1733-1745.
ISSN: 0099-5355.
NAL
Call Number: 448.8 L22
Descriptors: epidemiology, humans, infection, influenza,
vaccination, clinical techniques, pandemic prevention.
Niculescu, I.T., E. Zilisteanu, L. Cretescu, M.
Matepiuc, and V. Roman (1972). Relationship between human and animal
infections with A2 /Hong Kong/68 - like strains of influenza virus. Archives
Roumaines De Pathologie Experimentales Et De Microbiologie 31(4 Suppl):
545-52. ISSN: 0004-0037.
NAL
Call Number: 448.3 Ar22
Descriptors: influenza epidemiology, orthomyxoviridae
immunology, birds, cross reactions, influenza A virus avian immunology,
influenza A virus human immunology, influenza A virus, porcine immunology,
Romania, swine.
Ninomiya, A., A. Takada, K. Okazaki, K.F. Shortridge,
and H. Kida (2002). Seroepidemiological evidence of avian H4, H5, and H9
influenza A virus transmission to pigs in southeastern China. Veterinary
Microbiology 88(2): 107-14. ISSN:
0378-1135.
NAL
Call Number: SF601.V44
Abstract: Pig serum samples collected in southeastern
China were examined for antibodies to influenza A viruses. Since the
hemagglutination inhibition (HI) test does not accurately detect antibodies to
the hemagglutinins (HAs) of "avian" influenza viruses, we utilized
the neutralization (NT) test to detect subtype-specific antibodies to the HA of
avian viruses in pig sera. Neutralizing antibodies to H1, H3, H4, and H5
influenza viruses were detected in the serum samples collected in 1977-1982 and
1998, suggesting that pigs in China have been sporadically infected with avian
H4 and H5 viruses in addition to swine and human H1 and H3 viruses. Antibodies
to H9 virus, on the other hand, were found only in the sera collected in 1998,
not in those collected in 1977-1982, correlating with the recent spread in
poultry and subsequent isolation of H9N2 viruses from pigs and humans in 1998.
The present results indicate that avian influenza viruses have been transmitted
to pig populations in southeastern China.
Descriptors: antibodies, viral blood, influenza
veterinary, influenza A virus immunology, swine diseases epidemiology, China
epidemiology, hemagglutination inhibition tests veterinary, hemagglutinins
viral, influenza epidemiology, influenza transmission, influenza A virus avian
immunology, influenza A virus human immunology, influenza A virus, porcine
immunology, influenza A virus classification, neutralization tests veterinary,
poultry, seroepidemiologic studies, specific pathogen free organisms, swine,
swine diseases blood, swine diseases transmission, swine diseases virology.
Normile, D. (2005). Avian flu. First human case in
Cambodia highlights surveillance shortcomings. Science 307(5712):
1027. ISSN: 1095-9203.
NAL
Call Number: 470 Sci2
Descriptors: influenza epidemiology, influenza virology,
influenza A virus, avian, influenza, avian epidemiology, population
surveillance, adult, southeastern Asia epidemiology, Cambodia epidemiology,
disease outbreaks veterinary, influenza transmission, poultry.
Normile, D. (2004). Infectious diseases. Stopping
Asia's avian flu: a worrisome third outbreak. Science 303(5657):
447. ISSN: 1095-9203.
NAL
Call Number: 470 Sci2
Descriptors: disease outbreaks veterinary, influenza virology,
influenza A virus, avian classification, avian influenza pathogenicity, avian
influenza epidemiology, avian virology, birds, chickens, China epidemiology,
disease reservoirs, influenza epidemiology, influenza prevention and control,
influenza transmission, avian influenza prevention and control, avian influenza
transmission, Japan epidemiology, Korea epidemiology, Vietnam epidemiology.
Normile, D. and M. Enserink (2004). Infectious
diseases. Avian influenza makes a comeback, reviving pandemic worries. Science
305(5682): 321. ISSN: 1095-9203.
NAL
Call Number: 470 Sci2
Descriptors: disease outbreaks veterinary, influenza
epidemiology, influenza virology, influenza A virus, avian pathogenicity, avian
influenza epidemiology, Asia epidemiology, birds, evolution, molecular, avian
genetics, avian influenza virology, poultry, recombination, genetic.
Okazaki, K. (1983). Studies on susceptibility of
mink to influenza viruses--serological evidence of human influenza virus
infection in mink, contact infection of mink with avian influenza viruses, and
application of mink for evaluation of influenza vaccine. Japanese
Journal of Veterinary Research 31(2): 95.
ISSN: 0047-1917.
NAL
Call Number: 41.8 V6446
Descriptors: avian influenza virus, human influenza virus,
mink, susceptibility, studies, serological evidence.
Okazaki, K., A. Takada, T. Ito, M. Imai, H. Takakuwa,
M. Hatta, H. Ozaki, T. Tanizaki, T. Nagano, A. Ninomiya, V.A. Demenev, M.M.
Tyaptirganov, T.D. Karatayeva, S.S. Yamnikova, D.K. Lvov, and H. Kida (2000). Precursor
genes of future pandemic influenza viruses are perpetuated in ducks nesting in
Siberia. Archives of Virology 145(5): 885-93. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Influenza A viruses of different subtypes
were isolated from fecal samples of ducks in their nesting areas in Siberia in
summer from 1996 to 1998. Phylogenetic analysis of the NP genes of the isolates
in Siberia and those in Hokkaido, Japan on their flyway of migration from
Siberia to the south in autumn revealed that they belong to the Eurasian
lineage of avian influenza viruses. It is noted that the genes of the isolates
in Siberia are closely related to those of H5N1 influenza virus strains
isolated from chickens and humans in Hong Kong in 1997 as well as to those of
isolates from domestic birds in southern China. The results indicate that
influenza viruses perpetuated in ducks nesting in Siberia should have
contributed genes in the emergence of the H5N1 virus in Hong Kong. Vaccine
prepared from avirulent A/duck/Hokkaido/4/96 (H5N3) influenza virus was potent
enough to protect mice from challenge with lethal dose of the pathogenic H5N1
virus [19]. Intensive surveillance study of aquatic birds especially in Siberia
is, therefore, stressed to provide information on the future pandemic influenza
virus strains and for vaccine preparation.
Descriptors: ducks virology, genes viral, influenza A
virus avian genetics, base sequence, DNA primers genetics, disease reservoirs, fowl
plague immunology, fowl plague prevention and control, influenza A virus avian
classification, influenza A virus avian pathogenicity, influenza vaccine
pharmacology, Japan, mice, nucleoproteins genetics, phylogeny, poultry, Siberia, viral proteins
genetics.
Okazaki, K., R. Yanagawa, and H. Kida (1983). Contact
infection of mink with 5 subtypes of avian influenza virus. Archives of
Virology 77(2-4): 265-269. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Descriptors: avian influenza virus, transmission,
epidemiology, host range, mink.
Olofsson, S., U. Kumlin, K. Dimock, and N. Arnberg
(2005). Avian influenza and sialic acid receptors: more than meets the eye?
Lancet Infectious Diseases 5(3): 184-8.
ISSN: 1473-3099.
Abstract: Given our recent discoveries that the ocular
human pathogens adenovirus serotype 37 and enterovirus serotype 70 use sialic
acid linked to galactose via alpha2,3 glycosidic bonds as a cellular receptor,
we propose that the presence of this receptor in the eye also explains the ocular
tropism exhibited by zoonotic avian influenza A viruses such as subtype H5N1 in
Hong Kong in 1997, H7N7 in the Netherlands in 2003, H7N2 in the USA in 2003,
and H7N3 in Canada in 2004. We also draw attention to the implications this
hypothesis may have for epizootic and zoonotic influenza, and the initiation of
future pandemics.
Descriptors: Adenoviridae classification, eye diseases
virology, avian influenza pathology, cell surface physiology receptors,
zoonoses virology, Adenoviridae pathology, birds, avian influenza epidemiology,
avian influenza transmission, serotyping, zoonoses transmission, sialic acid.
Olsen, C.W. (2002). The emergence of novel swine
influenza viruses in North America. Virus Research 85(2): 199-210. ISSN: 0168-1702.
NAL
Call Number: QR375.V6
Abstract: Since 1997, novel viruses of three different
subtypes and five different genotypes have emerged as agents of influenza among
pigs in North America. The appearance of these viruses is remarkable because
there were no substantial changes in the overall epidemiology of swine
influenza in the United States and Canada for over 60 years prior to this time.
Viruses of the classical H1N1 lineage were virtually the exclusive cause of
swine influenza from the time of their initial isolation in 1930 through 1998.
Antigenic drift variants of these H1N1 viruses were isolated in 1991-1998, but
a much more dramatic antigenic shift occurred with the emergence of H3N2
viruses in 1997-1998. In particular, H3N2 viruses with genes derived from human,
swine and avian viruses have become a major cause of swine influenza in North
America. In addition, H1N2 viruses that resulted from reassortment between the
triple reassortant H3N2 viruses and classical H1N1 swine viruses have been
isolated subsequently from pigs in at least six states. Finally, avian H4N6
viruses crossed the species barrier to infect pigs in Canada in 1999.
Fortunately, these H4N6 viruses have not been isolated beyond their initial
farm of origin. If these viruses spread more widely, they will represent
another antigenic shift for our swine population, and could pose a threat to
the world's human population. Research on these novel viruses may offer
important clues to the genetic basis for interspecies transmission of influenza
viruses.
Descriptors: influenza virology, influenza A virus,
porcine physiology, Canada epidemiology, fowl plague transmission, influenza A
virus avian, influenza A virus, porcine
classification, influenza A virus, porcine genetics, influenza A virus, porcine immunology, North
America epidemiology, species specificity, swine, United States, variation
genetics.
Olsen, C.W., S. Carey, L. Hinshaw, and A.I. Karasin
(2000). Virologic and serologic surveillance for human, swine and avian
influenza virus infections among pigs in the north-central United States. Archives
of Virology 145(7): 1399-419. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Influenza virus infection in pigs is both an
animal health problem and a public health concern. As such, surveillance and
characterization of influenza viruses in swine is important to the veterinary
community and should be a part of human pandemic preparedness planning. Studies
in 1976/1977 and 1988/1989 demonstrated that pigs in the U.S. were commonly
infected with classical swine H1N1 viruses, whereas human H3 and avian
influenza virus infections were very rare. In contrast, human H3 and avian H1
viruses have been isolated frequently from pigs in Europe and Asia over the
last two decades. From September 1997 through August 1998, we isolated 26
influenza viruses from pigs in the north central United States at the point of
slaughter. All 26 isolates were H1N1 viruses, and phylogenetic analyses of the
hemagglutinin and nucleoprotein genes from 11 representative viruses
demonstrated that these were classical swine H1 viruses. However, monoclonal
antibody analyses revealed antigenic heterogeneity among the HA proteins of the
26 viruses. Serologically, 27.7% of 2,375 pigs tested had
hemagglutination-inhibiting antibodies against classical swine H1 influenza
virus. Of particular significance, however, the rates of seropositivity to
avian H1 (7.6%) and human H3 (8.0%) viruses were substantially higher than in
previous studies.
Descriptors: influenza veterinary, influenza virology,
influenza A virus avian isolation and purification, influenza A virus human
isolation and purification, influenza A virus, porcine isolation and
purification, swine diseases virology, amino acid sequence, influenza
epidemiology, molecular sequence data,
seroepidemiologic studies, swine, swine diseases epidemiology, United
States epidemiology.
Osterhaus, A.D., R.A. Fouchier, and T. Kuiken (2004).
The aetiology of SARS: Koch's postulates fulfilled. Philosophical
Transactions of the Royal Society of London. Series B Biological Sciences
359(1447): 1081-2. ISSN: 0962-8436.
NAL
Call Number: 501 L84Pb
Abstract: Proof that a newly identified coronavirus,
severe acute respiratory syndrome coronavirus (SARS-CoV) is the primary cause
of severe acute respiratory syndrome (SARS) came from a series of studies on
experimentally infected cynomolgus macaques (Macaca fascicularis).
SARS-CoV-infected macaques developed a disease comparable to SARS in humans;
the virus was re-isolated from these animals and they developed
SARS-CoV-specific antibodies. This completed the fulfilment of Koch's
postulates, as modified by Rivers for viral diseases, for SARS-CoV as the
aetiological agent of SARS. Besides the macaque model, a ferret and a cat model
for SARS-CoV were also developed. These animal models allow comparative
pathogenesis studies for SARS-CoV infections and testing of different
intervention strategies. The first of these studies has shown that pegylated
interferon-alpha, a drug approved for human use, limits SARS-CoV replication
and lung damage in experimentally infected macaques. Finally, we argue that,
given the worldwide nature of the socio-economic changes that have predisposed
for the emergence of SARS and avian influenza in Southeast Asia, such changes
herald the beginning of a global trend for which we are ill prepared.
Descriptors: disease models, animal, ferrets, Macaca
fascicularis, SARS virus, severe acute respiratory syndrome etiology,
zoonoses transmission, cats, severe acute respiratory syndrome physiopathology,
severe acute respiratory syndrome transmission.
Otsuki, K., K. Yamazaki, Y. Kawaoka, and M. Tsubokura
(1987). Infectivity for mice of avian influenza A viruses of H7N7, H5N3 and
H2N2 subtypes isolated from migratory waterfowls in San-in District, Western
Japan. Nippon Juigaku Zasshi Japanese Journal of Veterinary Science
49(1): 199-201. ISSN: 0021-5295.
NAL
Call Number: 41.8 J27
Descriptors: birds microbiology, influenza A virus avian
pathogenicity, mice microbiology, influenza A virus avian isolation and
purification, Japan.
Oxford, J.S., R. Lambkin, A. Sefton, R. Daniels, A.
Elliot, R. Brown, and D. Gill (2005). A hypothesis: the conjunction of
soldiers, gas, pigs, ducks, geese and horses in northern France during the
Great War provided the conditions for the emergence of the "Spanish"
influenza pandemic of 1918-1919. Vaccine 23(7): 940-5.
ISSN: 0264-410X.
NAL
Call Number: QR189.V32
Abstract: The Great Influenza Pandemic of 1918-1919 was
a cataclysmic outbreak of infection wherein over 50 million people died
worldwide within 18 months. The question of the origin is important because
most influenza surveillance at present is focussed on S.E. Asia. Two later
pandemic viruses in 1957 and 1968 arose in this region. However we present
evidence that early outbreaks of a new disease with rapid onset and
spreadability, high mortality in young soldiers in the British base camp at
Etaples in Northern France in the winter of 1917 is, at least to date, the most
likely focus of origin of the pandemic. Pathologists working at Etaples and
Aldershot barracks later agreed that these early outbreaks in army camps were
the same disease as the infection wave of influenza in 1918. The Etaples camp
had the necessary mixture of factors for emergence of pandemic influenza
including overcrowding (with 100,000 soldiers daily changing), live pigs, and
nearby live geese, duck and chicken markets, horses and an additional factor 24
gases (some of them mutagenic) used in large 100 ton quantities to contaminate
soldiers and the landscape. The final trigger for the ensuing pandemic was the
return of millions of soldiers to their homelands around the entire world in
the autumn of 1918.
Descriptors: communicable diseases, emerging history,
disease outbreaks, influenza history, military personnel history, world war I,
ducks, France, geese, history, 20th century, horses, influenza A virus, avian
pathogenicity, swine.
Ozaki, H., E.A. Govorkova, C. Li, X. Xiong, R.G.
Webster, and R.J. Webby (2004). Generation of high-yielding influenza A
viruses in African green monkey kidney (Vero) cells by reverse genetics. Journal
of Virology 78(4): 1851-7. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: Influenza A viruses are the cause of annual
epidemics of human disease with occasional outbreaks of pandemic proportions.
The zoonotic nature of the disease and the vast viral reservoirs in the aquatic
birds of the world mean that influenza will not easily be eradicated and that
vaccines will continue to be needed. Recent technological advances in reverse
genetics methods and limitations of the conventional production of vaccines by
using eggs have led to a push to develop cell-based strategies to produce
influenza vaccine. Although cell-based systems are being developed, barriers
remain that need to be overcome if the potential of these systems is to be
fully realized. These barriers include, but are not limited to, potentially
poor reproducibility of viral rescue with reverse genetics systems and poor
growth kinetics and yields. In this study we present a modified A/Puerto
Rico/8/34 (PR8) influenza virus master strain that has improved viral rescue
and growth properties in the African green monkey kidney cell line, Vero. The
improved properties were mediated by the substitution of the PR8 NS gene for
that of a Vero-adapted reassortant virus. The Vero growth kinetics of viruses
with H1N1, H3N2, H6N1, and H9N2 hemagglutinin and neuraminidase combinations
rescued on the new master strain were significantly enhanced in comparison to
those of viruses with the same combinations rescued on the standard PR8 master
strain. These improvements pave the way for the reproducible generation of
high-yielding human and animal influenza vaccines by reverse genetics methods.
Such a means of production has particular relevance to epidemic and pandemic
use.
Descriptors: influenza A virus avian growth and
development, influenza A virus human growth and development, influenza vaccine,
reassortant viruses growth and development, vero cells virology, Cercopithecus
aethiops, influenza A virus avian genetics, influenza A virus human
genetics, reassortant viruses genetics, viral nonstructural proteins genetics,
virus cultivation, virus replication.
Papparella, V., A. Fioretti, L.F. Menna, JM Bruce (ed.),
and S. M. (1987). On the danger of certain avian respiratory diseases to
human health. In: Environmental aspects of respiratory disease in
intensive pig and poultry houses, including the implications for human health.
Report Eur 10820 EN, Aberdeen, UK, Commission of he European Communities:
Luxembourg, p. 127-132.
Descriptors: zoonoses, public health, humans, Newcastle disease virus, avian
influenza virus.
Park, C.H., K. Matsuda, Y. Sunden, A. Ninomiya, A.
Takada, H. Ito, T. Kimura, K. Ochiai, H. Kida, and T. Umemura (2003). Persistence
of viral RNA segments in the central nervous system of mice after recovery from
acute influenza A virus infection. Veterinary Microbiology 97(3-4):
259-68. ISSN: 0378-1135.
NAL
Call Number: SF601.V44
Abstract: One-hundred thirty-seven BALB/c mice were
intranasally inoculated with neurotropic avian influenza A virus (H5N3).
Thirty-nine of these mice died within 16 days post-inoculation (PID) and 98 of
the mice recovered from the infection. To investigate whether viral antigens
and genomes persist in the central nervous system (CNS) of recovered mice,
immunohistochemistry and reverse transcription-polymerase chain reaction
(RT-PCR) methods were performed. Histopathologically, mild interstitial
pneumonia and non-suppurative encephalomyelitis restricted to the basal part of
the frontal lobe of the cerebrum, brain stem and thoracic spinal cord were
observed in BALB/c mice until 40 PID. Small amounts of viral antigens were
detected in the brain and spinal cord and some viral RNA segments (NA, NP, M,
PA, HA, NS, PB1) were intermittently detected in the CNS until 48 PID.
Immunosuppression of these mice by dexamethazone (DEX) treatment did not
increase the frequency of detection of the lesions, viral antigens or genomes.
These findings suggest that viral genomes of neurovirulent influenza virus
persist with restricted transcriptive activity in the CNS of the mice even
after clinical recovery from the infection.
Descriptors: central nervous system virology, fowl plague
virology, influenza A virus avian isolation and purification, RNA viral
analysis, brain pathology, brain virology, central nervous system pathology,
disease models, animal, fowl plague mortality, fowl plague pathology,
immunohistochemistry veterinary, influenza A virus avian genetics, mice, mice
inbred BALB c, random allocation, reverse transcriptase polymerase chain
reaction veterinary, specific pathogen free organisms.
Parry, J. (2004). Death toll mounts in avian flu
outbreak. BMJ Clinical Research 328(7434): 243. ISSN: 1468-5833.
Descriptors: disease outbreaks, fowl plague virology,
influenza mortality, Asia, southeastern epidemiology, birds, influenza A virus
avian, influenza A virus human.
Parry, J. (2004). WHO investigates possible human
to human transmission of avian flu. BMJ Clinical Research 328(7435):
308. ISSN: 1468-5833.
Descriptors: influenza, avian transmission, zoonoses
transmission, influenza, avian epidemiology, poultry, Vietnam epidemiology.
Parry, J. (2004). WHO warns that avian flu could still
be in the environment. BMJ Clinical Research 328(7437): 426. ISSN: 1468-5833.
Descriptors: influenza, avian epidemiology, birds,
Carnivora, cat diseases epidemiology, cats, poultry, world health, World Health
Organization.
Pasick, J., K. Handel, J. Robinson, J. Copps, D.
Ridd, K. Hills, H. Kehler, C. Cottam Birt, J. Neufeld, Y. Berhane, and S. Czub
(2005). Intersegmental recombination between the haemagglutinin and matrix
genes was responsible for the emergence of a highly pathogenic H7N3 avian influenza
virus in British Columbia. Journal of General Virology 86(Pt. 3):
727-31. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: In February 2004 a highly pathogenic avian
influenza (HPAI) outbreak erupted in British Columbia. Investigations indicated
that the responsible HPAI H7N3 virus emerged suddenly from a low pathogenic
precursor. Analysis of the haemagglutinin (HA) genes of the low and high
pathogenic viruses isolated from the index farm revealed the only difference to
be a 21 nt insert at the HA cleavage site of the highly pathogenic avian
influenza virus. It was deduced that this insert most probably arose as a
result of non-homologous recombination between the HA and matrix genes of the
same virus. Over the course of the outbreak, a total of 37 isolates with, and 3
isolates without inserts were characterized. The events described here appear
very similar to those which occurred in Chile in 2002 where the virulence shift
of another H7N3 virus was attributed to non-homologous recombination between
the HA and nucleoprotein genes.
Descriptors: veterinary disease outbreaks, hemagglutinins
viral genetics, avian influenza A virus genetics, avian influenza epidemiology,
genetic recombination, viral matrix proteins genetics, British Columbia.
Peiris, J.S., Y. Guan, D. Markwell, P. Ghose, R.G.
Webster, and K.F. Shortridge (2001). Cocirculation of avian H9N2 and
contemporary "human" H3N2 influenza A viruses in pigs in southeastern
China: potential for genetic reassortment? Journal of Virology
75(20): 9679-86. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Pigs are permissive to both human and avian
influenza viruses and have been proposed to be an intermediate host for the
genesis of pandemic influenza viruses through reassortment or adaptation of
avian viruses. Prospective virological surveillance carried out between March
1998 and June 2000 in Hong Kong, Special Administrative Region, People's
Republic of China, on pigs imported from southeastern China, provides the first
evidence of interspecies transmission of avian H9N2 viruses to pigs and
documents their cocirculation with contemporary human H3N2 (A/Sydney/5/97-like,
Sydney97-like) viruses. All gene segments of the porcine H9N2 viruses were
closely related to viruses similar to chicken/Beijing/1/94 (H9N2), duck/Hong
Kong/Y280/97 (H9N2), and the descendants of the latter virus lineage. Phylogenetic
analysis suggested that repeated interspecies transmission events had occurred
from the avian host to pigs. The Sydney97-like (H3N2) viruses isolated from
pigs were related closely to contemporary human H3N2 viruses in all gene
segments and had not undergone genetic reassortment. Cocirculation of avian
H9N2 and human H3N2 viruses in pigs provides an opportunity for genetic
reassortment leading to the emergence of viruses with pandemic potential.
Descriptors: influenza A virus avian isolation and purification,
influenza A virus human isolation and purification, swine virology, antibodies,
viral blood, carrier state epidemiology, carrier state veterinary, cell line,
China epidemiology, influenza epidemiology, influenza veterinary, influenza A
virus avian classification, influenza A virus avian genetics, influenza A virus
human classification, influenza A virus human genetics, molecular sequence
data, phylogeny, sequence homology, nucleic acid, seroepidemiologic studies.
Perdue, M.L. (2003). Molecular diagnostics in an
insecure world. Avian Diseases 47(Special Issue): 1063-1068. ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: As of October 2001, the potential for use of
infectious agents, such as anthrax, as weapons has been firmly established. It
has been suggested that attacks on a nations' agriculture might be a preferred
form of terrorism or economic disruption that would not have the attendant
stigma of infecting and causing disease in humans. Highly pathogenic avian
influenza virus is on every top ten list available for potential agricultural
bioweapon agents, generally following foot and mouth disease virus and
Newcastle disease virus at or near the top of the list. Rapid detection
techniques for bioweapon agents are a critical need for the first-responder
community, on a par with vaccine and antiviral development in preventing spread
of disease. There are several current approaches for rapid, early responder
detection of biological agents including influenza A viruses. There are also
several proposed novel approaches in development. The most promising existing
approach is real-time fluorescent PCR analysis in a portable format using
exquisitely sensitive and specific primers and probes. The potential for
reliable and rapid early-responder detection approaches are described, as well
as the most promising platforms for using real-time PCR for avian influenza, as
well as other potential bioweapon agents.
Descriptors: immune system, infection, molecular genetics,
molecular diagnostics clinical techniques, diagnostic techniques, real time
fluorescent polymerase chain reaction, real time fluorescent PCR, genetic
techniques, laboratory techniques, agricultural bioweapon agents, bioterrorism,
economic disruption, rapid disease detection.
Perez, D.R., R.J. Webby, E. Hoffmann, and R.G.
Webster (2003). Land-based birds as potential disseminators of
avian/mammalian reassortant influenza A viruses. Avian Diseases
47(Special Issue): 1114-1117. ISSN:
0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: Chickens, quail, and other land-based birds
are extensively farmed around the world. They have been recently implicated in
zoonotic outbreaks of avian influenza in Hong Kong. The possibility that
land-based birds could act as mixing vessels or disseminators of avian/mammalian
reassortant influenza A viruses with pandemic potential has not been evaluated.
In this report, we investigated whether chickens and Japanese quail are
susceptible to a mammalian influenza virus (A/swine/Texas/4199-2/98 (H3N2)).
This virus did not grow in chickens and replicated to low levels in Japanese
quail but did not transmit. Replacing the H3 gene of this virus for one of the
avian H9 viruses resulted in transmission of the avian/swine reassortant virus
among quail but not among chickens. Our findings demonstrated that Japanese
quail could provide an environment in which viruses like the
A/swine/Texas/4199-2/98 (H3N2) virus could further reassort and generate
influenza viruses with pandemic potential.
Descriptors: epidemiology, infection, avian influenza,
infectious disease, respiratory system disease, viral disease, pandemic
potentials, zoonotic influenza outbreaks.
Perkins, L.E.L. and D.E. Swayne (2003). Comparative
susceptibility of selected avian and mammalian species to a Hong Kong-Origin
H5N1 high-pathogenicity avian influenza virus. Avian Diseases
47(Special Issue): 956-967. ISSN:
0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: Seventeen avian species and two mammalian
species were intranasally inoculated with the zoonotic A/chicken/Hong
Kong/220/97 (chicken/HK) (H5N1) avian influenza (AI) virus in order to
ascertain a relative range of susceptible hosts and the pathobiology of the
resultant disease. A direct association was demonstrated between viral
replication and the severity of disease, with four general gradations being
observed among these species. These gradations included the following: 1)
widespread dissemination with rapid and high mortality, 2) neurological disease
relative to viral neurotropism, 3) asymptomatic infection or only mild
transient depression associated with minor viral replication, and 4) absence of
disease relative to minimal to no viral replication. This investigation not
only demonstrates that the chicken/HK virus could infect multiple avian
species, but also that the virulence of the chicken/HK virus varied
significantly among avian species, including those species that are members of
the same order.
Descriptors: epidemiology, infection, avian influenza,
infectious disease, respiratory system disease, viral disease, inoculation,
clinical techniques, therapeutic and prophylactic techniques, disease severity,
disease susceptibility, host susceptibility, pathobiology, viral neurotropism,
viral replication.
Perkins, L.E.L. and D.E. Swayne (2002). Pathogenicity
of a Hong Kong-origin H5N1 highly pathogenic avian influenza virus for emus,
geese, ducks, and pigeons. Avian Diseases 46(1): 53-63. ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: The H5N1 type A influenza viruses that
emerged in Hong Kong in 1997 are a unique lineage of type A influenza viruses
with the capacity to transmit directly from chickens to humans and produce
significant disease and mortality in-both of these hosts. The objective of this
study was to ascertain the susceptibility of emus (Dramaius novaehollandiae),
domestic geese (Anser anser domesticus), domestic ducks (Anas
platyrhynchos), and pigeons (Columba livia) to intranasal (i.n.)
inoculation with the A/chicken/Hong Kong/220/97 (H5N1) highly pathogenic avian
influenza virus. No mortality occurred within 10 days postinoculation (DPI) in
the four species investigated, and clinical disease, evident as neurologic
dysfunction, was observed exclusively in emus and geese. Grossly, pancreatic
mottling and splenomegaly were identified in these two species. In addition,
the geese had cerebral malacia and thymic and bursal atrophy. Histologically,
both the emus and geese developed pancreatitis, meningoencephalitis, and mild
myocarditis. Influenza viral antigen was demonstrated in areas with histologic
lesions up to 10 DPI in the geese. Virus was reisolated from oropharyngeal and
cloacal swabs and from the lung, brain, and kidney of the emus and geese.
Moderate splenomegaly was observed grossly in the ducks. Viral infection of the
ducks was pneumotropic, as evidenced by mild inflammatory lesions in the
respiratory tract and virus reisolation from oropharyngeal swabs and from a
lung. Pigeons were resistant to HK/220 infection, lacking gross and histologic
lesions, viral antigen, and reisolation of virus. These results imply that emus
and geese are susceptible to i.n. inoculation with the HK/220 virus, whereas
ducks and pigeons are more resistant. These latter two species probably played
a minimal epidemiologic role in the perpetuation of the H5N1 Hong Kong-origin
influenza viruses.
Descriptors: infection, veterinary medicine, H5N1 avian
influenza virus infection, etiology, mortality, viral disease, bursal atrophy,
joint disease, cerebral malacia, nervous system disease, meningoencephalitis,
nervous system disease, myocarditis, heart disease, neurologic dysfunction,
nervous system disease, pancreatic mottling, digestive system disease,
endocrine disease, pancreas, pancreatitis, digestive system disease,
respiratory tract inflammation, respiratory system disease, splenomegaly, blood
and lymphatic disease, thymic atrophy, endocrine disease, thymus.
Permin, A. (2004). Avian influenza is spreading.
Now avian influenza is also in pigs [Aviaer influenza breder sig nu ogsa aviaer
influenza hos svin]. Dansk Veterinaertidsskrift 87(19): 10-11. ISSN: 0106-6854.
NAL
Call Number: 41.9 D23
Descriptors: avian influenza virus, pigs, poultry.
Permin, A. (2003). A veterinarian dies from avian
influenza virus infection. Dansk Veterinaertidsskrift 86(13): 13-15. ISSN: 0106-6854.
NAL
Call Number: 41.9 D23
Descriptors: avian influenza virus, zoonoses, human death,
Denmark, Holland.
Pilet, C. (1980). Proceedings of an International
Symposium, held on September 13 and 14, 1979 at the Ecole Nationale Veterinaire
d'Alfort, France. Comparative Immunology, Microbiology and Infectious
Diseases. Special Issue on Animal and Human Influenzas 3(1/2): xvi +
246. ISSN: 0147-9571.
NAL
Call Number: QR180.C62
Descriptors: influenza virus, humans, zoonoses, equine,
porcine, avian, symposium.
Pilet, C., G. Dauphin, and S. Zientara (2004). Actualites
en pathologie comparee: sur quelques maladies animales menacantes pour l'homme.
[Advances in comparative pathology: some zoonoses threatening man]. Bulletin
De L'Academie Nationale De Medecine 188(5): 823-36. ISSN: 0001-4079.
Abstract: The last major human epidemics of infectious
diseases have arisen from animals. Some of them are especially threatening. The
authors call attention to the danger of spread of avian influenza, either
directly or indirectly through genetic rearrangements. They underline the role
of animals in the epidemiology of SARS, West Nile virus, hepatitis E, NIPA and
Hendra virus, ehrlichiosis and Lyme disease. The authors recommend health
surveillance not only in humans but also in animals; the teaching of zoonoses,
and research on animal diseases transmissible to humans.
Descriptors: virus diseases transmission, zoonoses.
Podcherniaeva, R.I.A., V.K. Blinova, M.V. Ronina,
E.I. Sklianskaia, and N.V. Kaverin (1980). Antigennye rekombinanty virusov
grippa cheloveka s virusami, vydelennymi ot dikikh ptits. [Antigenic
recombinants of human influenza viruses with viruses isolated from wild birds].
Voprosy Virusologii (4): 419-24.
ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Antigenic recombinants obtained by crossing
of different human and animal influenza viruses were studied for some genetic
markers and specific proteins in the resulting recombinants were analyses. In a
number of cases the origin of inner virion proteins (NP and M) from one or the
other parent and nonstructural NS proteins was established.
Descriptors: antigens, viral genetics, birds microbiology,
influenza A virus avian genetics, influenza A virus human genetics,
recombination, genetic, antigens, viral analysis, genetic markers, species
specificity, viral proteins genetics.
Podchernyaeva, R.J., R.G. Webster, V.V. Skovorodka,
A.I. Klimov, and V.M. Zhdanov (1989). Molecular and biological properties of
a variant of avian influenza A/Seal/Massachusetts/1/80 (H7N7) virus that is
pathogenic for mice. Acta Virologica 33(1): 38-42. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: A/Seal/Mass/80 influenza virus has been shown
to be closely related antigenically and genetically to avian influenza H7N7 viruses,
however, the virus does not replicate efficiently in avian species but does
replicate in most mammals, except mice (Hinshaw et al., Infect. Immun., 34,
351-361, 1981). In order to develop a model defining the molecular changes that
occur during acquisition of virulence, the A/Seal/Mass/80 virus was adapted to
growth in mouse lungs. The adaptation was accompanied by changes in a number of
properties of the haemagglutinin as well as by changes in other genes of the
virus as determined by RNA: RNA hybridization.
Descriptors: influenza A virus pathogenicity, genes viral,
hemagglutinins viral, influenza A virus genetics, lethal dose 50, lung
microbiology, mice, neutralization tests, nucleic acid hybridization, RNA viral
analysis, serial passage, variation genetics, virulence.
Poli, G. and L. Bonizzi (2004). Avian influenza:
not a danger [Influenza aviare: nessun pericolo]. Informatore Agrario
60(11): 33-34. ISSN: 0020-0689.
NAL
Call Number: 281.8 In32
Descriptors: avian influenza virus, disease prevention,
disease transmission, hygiene, occupational transmission, poultry, poultry
farming.
Pollack, C.V.J., C.W. Kam, and Y.K. Mak (1998). Update:
isolation of avian influenza A(H5N1) viruses from human beings--Hong Kong,
1997-1998. Annals of Emergency Medicine 31(5): 647-9. ISSN: 0196-0644.
Descriptors: disease outbreaks, influenza transmission,
influenza virology, influenza A virus human,
poultry diseases transmission, poultry diseases virology, adolescent,
adult, case control studies, chickens, child, child, preschool, ducks, Hong
Kong epidemiology, infant, influenza epidemiology, influenza veterinary, middle
aged, neutralization tests, population surveillance, poultry diseases
epidemiology.
Pospisil, Z., P. Lany, J. Buchta, D. Zendulkova, P.
Cihal, and B. Tumova (2001). Swine influenza surveillance and the impact of
human influenza epidemics on pig herds in the Czech Republic. Acta
Veterinaria (Czech Republic) 70(3): 327-332. ISSN: 0001-7213.
NAL
Call Number: SF604.B7
Abstract: Epizootiological and virological surveys
carried out between 1995 and mid-2000 corroborated the findings from the end of
the 1970s that swine influenza did not cause any serious problems in pig herds
in the Czech Republic. In the present study, no antibodies against either swine
influenza virus, types A (H1N1) and A (H3N2), or avian influenza virus, A
(H1N1), were demonstrated and no influenza virus was isolated. In contrast,
antibodies against the human influenza virus isolated during the 1995 epidemic
were found. The dynamics of antibody formation indicated that the human virus
gradually disappeared from the pig population. It is possible that the human
virus was introduced to the pig herds by infected animal attendants, in whom
antibodies against this virus were also found. During the second human
influenza epidemic in 1998/99, however, pigs remained free from antibody
response to influenza virus.
Descriptors: swine, swine influenza virus, serotypes,
antibodies, zoonoses, disease transmission, disease surveillance, Czech
Republic, biological differences, domestic animals, Eastern Europe,
epidemiology, Europe, immunological factors, influenza virus, livestock,
orthomyxoviridae, pathogenesis, Suidae, useful animals, viruses.
Potter, P. (2004). "One medicine" for
animal and human health. Emerging Infectious Diseases 10(12):
2269-2270. ISSN: 1080-6040.
NAL
Call Number: RA648.5.E46
Descriptors: AIDS, acquired immunodeficiency syndrome,
Ebola virus disease, SARS, severe acute respiratory syndrome, West Nile fever,
avian influenza, bovine spongiform encephalopathy, prion disease, Edward Hicks
artist, zoonosis, biography, history, epidemiology.
Profeta, M.L. and G. Palladino (1986). Serological
evidence of human infections with avian influenza viruses. Brief report. Archives
of Virology 90(3-4): 355-60. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Two hundred ninety-four subjects from Milan
were tested for serum hemagglutination-inhibiting (HI) and
neuraminidase-inhibiting (NI) antibodies to five avian influenza viruses. No HI
antibodies were found in all the serum samples. On the contrary, NI antibodies
to each strain were detected depending on the year of birth of the subjects.
Descriptors: influenza immunology, influenza A virus avian
immunology, hemagglutination inhibition tests, hemagglutinins viral immunology,
influenza microbiology, influenza A virus avian pathogenicity, neuraminidase
antagonists and inhibitors, neuraminidase immunology.
Prokudina, E.N., N.P. Semenova, V.M. Chumakov, E.I.
Burtseva, and A.N. Slepushkin (2003). Differences in oligomerization of the
nucleocapsid protein of epidemic human influenza A(H1N1), A(H3N2) and B
viruses. Voprosy Virusologii 48(3): 27-31. ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: A comparative analysis of involving the
nucleocapsid protein (NP) into shaping-up of SDS-resistant oligomers was
carried out presently in circulating epidemic strains of human influenza,
viruses A and B. The study results of viral isolates obtained from clinical samples
and recent standard strains revealed that the involvement of NP in the
SDS-resistant oligomers, which are different in various subtypes of influenza A
viruses. According to this sign, the human viruses A(9H3N2) are close to the
avian ones, in which, as proved by us previously, virtually the entire NP
transforms itself into the oligomers resistant to SDS. About 10-20% of NP are
involved in shaping-up the virus influenza A(H1N1) of SDS-resistant oligomers.
No SDS-resistant NP-oligomers were detected in influenza of type B. It is
suggested that the prevalence of human viruses A(H3N2) in NP-oligomers are the
peculiarities of NP structure and of the presence of the PB1 protein from avian
influenza virus.
Descriptors: computer applications, infection, molecular
genetics, SDS page, SDS polyacrylamide gel electrophoresis, electrophoretic
techniques, laboratory techniques, comparative analysis laboratory techniques.
Prokudina, E.N., N.P. Semenova, I.A. Rudneva, V.M.
Chumakov, and S.S. Yamnikova (2001). Avian and human influenza a virus
strains possess different intracellular nucleoprotein oligomerization
efficiency. Acta Virologica 45(4): 201-7. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: We have previously shown
(Prokudina-Kantorovich EN and Semenova NP, Virology 223, 51-56, 1996) that the
nucleoprotein (NP) of influenza A virus forms in infected cells oligomers which
in the presence of SDS and 2-mercaptoethanol (ME) as reducing agent are stable
at room temperature (RT) and dissociate at 100 degrees C. Here we report that
the efficiency of intracellular NP oligomerization depends on the host origin
of influenza A virus strain. Thus, in the cells infected with avian influenza A
virus strains the viral NP was almost completely oligomerized and only traces
of monomeric NP were detected by polyacrylamide gel electrophoresis (PAGE) in
unboiled samples. However, in the cells infected with human influenza A virus
strains, besides oligomeric NP also a significant amount of non-oligomerized
monomeric NP was detected in unboiled samples. In purified virions of avian and
human strains the same difference in NP monomers/oligomers ratio was detected
as in the infected cells. A reassortant having all internal protein genes from
a human strain and the glycoprotein genes from an avian strain revealed the
same intracellular pattern of NP monomers/oligomers ratio as its parental human
virus. These findings suggest that the type of NP oligomerization is controlled
by the NP gene. The possible connection between the accumulation of
protease-sensitive monomeric NP in cells infected with a human influenza strain
and the parallel accumulation of cleaved NP in these cells is discussed.
Descriptors: influenza A virus metabolism, nucleoproteins
metabolism, viral core proteins metabolism, biopolymers analysis, cell line,
dogs, influenza A virus avian metabolism, influenza A virus human metabolism,
influenza A virus genetics, nucleoproteins analysis, nucleoproteins genetics,
reassortant viruses metabolism, species specificity, viral core proteins
analysis, viral core proteins genetics.
Pysina, T.V. and A.S. Gorbunova (1970). Sootnosheniia
mezhdu patogennost'iu virusov grippa ptits dlia laboratornykh zhivotnykh i
infitsirovaniem avifauny. [Relation between the pathogenicity of avian
influenza viruses for laboratory animals and infection of avifauna]. Voprosy
Virusologii 15(3): 298-301. ISSN:
0507-4088.
NAL
Call Number: 448.8 P942
Descriptors: bird diseases microbiology, orthomyxoviridae
pathogenicity, bird diseases epidemiology, chickens, Czechoslovakia, ducks,
England, influenza epidemiology,
influenza microbiology, mice, Scotland, Siberia, South Africa, tissue culture,
virus cultivation.
Quirk, M. (2004). USA to manufacture two million
doses of pandemic flu vaccine. Lancet Infectious Diseases 4(11): 654. ISSN: 1473-3099.
Descriptors: influenza prevention and control, influenza A
virus, avian immunology, influenza vaccines supply and distribution, drug
industry, United States, vaccination.
Quirk, M. (2004). Zoo tigers succumb to avian
influenza. Lancet Infectious Diseases 4(12): 716. ISSN: 1473-3099.
Descriptors: disease outbreaks veterinary, food
contamination, influenza, avian epidemiology, tigers, animal feed standards,
animal feed virology, newborn animals, zoo animals, chickens, disease susceptibility
veterinary, avian influenza mortality, avian influenza transmission, Thailand
epidemiology.
Raleigh, P.J. (2004). Avian influenza. Irish
Veterinary Journal 57(3): 154-156.
ISSN: 0368-0762.
NAL
Call Number: 41.8 Ir4
Descriptors: avian influenza virus, diagnosis, disease
control, disease prevention, disease transmission, fowl diseases, lesions,
poultry, viral replication, zoonoses, fowl, reviews.
Rassool, G.H. (2004). Unprecedented spread of
avian influenza requires broad collaboration. Journal of Advanced
Nursing 46(5): 567. ISSN: 0309-2402.
Descriptors: disease outbreaks prevention and control,
influenza A virus, avian influenza, avian influenza prevention and control,
avian influenza transmission, international cooperation, zoonoses transmission.
Ready, T. (2004). Race for pandemic flu vaccine
rife with hurdles. Nature Medicine 10(3): 214. ISSN: 1078-8956.
Descriptors: influenza prevention and control, influenza A
virus, avian immunology, influenza vaccines, chickens, clinical trials,
influenza virology.
Reid, A.H., J.K. Taubenberger, and T.G. Fanning
(2004). Evidence of an absence: the genetic origins of the 1918 pandemic
influenza virus. Nature Reviews Microbiology 2(11): 909-14. ISSN: 1740-1526.
Abstract: Annual outbreaks of influenza A infection are
an ongoing public health threat and novel influenza strains can periodically
emerge to which humans have little immunity, resulting in devastating
pandemics. The 1918 pandemic killed at least 40 million people worldwide and
pandemics in 1957 and 1968 caused hundreds of thousands of deaths. The
influenza A virus is capable of enormous genetic variation, both by continuous,
gradual mutation and by reassortment of genome segments between viruses. Both
the 1957 and 1968 pandemic strains are thought to have originated as
reassortants in which one or both human-adapted viral surface proteins were
replaced by proteins from avian influenza strains. Analyses of the genes of the
1918 pandemic virus, however, indicate that this strain might have had a
different origin. The haemagglutinin and nucleoprotein genome segments in
particular are unlikely to have come directly from an avian source that is
similar to those that are currently being sequenced. Determining whether a
pandemic influenza virus can emerge by different mechanisms will affect the
scope and focus of surveillance and prevention efforts.
Descriptors: influenza history, influenza virology,
influenza A virus, human genetics, variation genetics, viral proteins genetics,
disease outbreaks, hemagglutinin glycoproteins, influenza virus genetics,
history, 20th century, influenza epidemiology, mutation, neuraminidase
genetics, nucleoproteins genetics, reassortant viruses genetics, viral matrix
proteins genetics, viral nonstructural proteins genetics.
Reina, J. (2002). Factores de virulencia y
patogenicidad en las cepas gripales (virus influenza tipo A) aviares y humanas.
[Factors affecting the virulence and pathogenicity of avian and human viral
strains (influenza virus type A)]. Enfermedades Infecciosas y
Microbiologia Clinica 20(7): 346-53.
ISSN: 0213-005X.
Abstract: Most studies performed in avian viral strains
seem to indicate that virulence is a polygenic phenomenon. However,
hemagglutinin and neuraminidase and the genes codifying these substances (genes
4 and 6) play an essential role in viral pathogenesis. Avian strains can be
classified as avirulent or virulent according to the ability of hemagglutinin
to be activated by endoproteases of the respiratory tract only or by proteases
from other tissues. This ability is based on the progressive development of
mutations that lead to the substitution of the normal amino acids at the point
of hemagglutinin hydrolysis by the other basic amino acids that determine the
amplification of the spectrum of hydrolysis and activation. Neuraminidase
participates in the acquisition of virulence through its capacity to bind to
plasminogen and by increasing the concentration of activating proteases.
Adaptation to the host, through recognition of the cell receptor, is another
factor determining the virulence and interspecies transmission of avian
strains. From an epidemiological point of view, viral strains should be
subtyped and the activating capacity of hemagglutinin should be determined to
identify their degree of virulence.
Descriptors: influenza A virus avian pathogenicity,
influenza A virus human pathogenicity, hemagglutinins, neuraminidase, peptide
hydrolases, virulence.
Reina, J. (2004). Gripe aviar. Una amenaza
constante para el ser humano. [Avian influenza. A continual threat to human
beings]. Medicina Clinica 122(9): 339-41. ISSN: 0025-7753.
NAL
Call Number: R21.M43
Descriptors: avian influenza, humans, continual threat,
birds, pigs.
Reinhardt, U. and C. Scholtissek (1988). Comparison
of the nucleoprotein genes of a chicken and a mink influenza A H 10 virus. Archives
of Virology 103(1-2): 139-45. ISSN:
0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: The base sequences of the coding region of
the nucleoprotein (NP) genes of two H 10 influenza A viruses, one avian (virus
N) and one mink virus, have been determined by primer extension. When the NP
genes and the NP sequences derived from the only open reading frame of the two
H 10 viruses were compared with those of other human and avian influenza A
viruses, it turned out that the mink virus NP was highly related to that of
other avian strains, but differed from that of the human strains. Comparison of
the NP genes of the mink and avian strains of European origin suggests a direct
lineage between them. Since the NP plays a major role in species specificity,
it is assumed that an avian influenza virus has directly invaded the mink
population.
Descriptors: base sequence, influenza A virus avian
genetics, influenza A virus genetics, nucleoproteins genetics, RNA, viral,
sequence homology, nucleic acid, viral proteins genetics, amino acid sequence,
chickens microbiology, mink microbiology, molecular sequence data.
Renegar, K.B. (1992). Influenza virus infections
and immunity: a review of human and animal models. Laboratory Animal
Science 42(3): 222-32. ISSN:
0023-6764.
NAL
Call Number: 410.9 P94
Abstract: Studies of the pathogenesis of influenza
infection have involved the extensive use of animal models. The development of
the current concepts of immunity to influenza and of the contribution the
secretory immune system makes toward the protection of mucosal surfaces against
influenza infection would have been impossible without this use of animals. The
pathology and clinical signs of influenza infection in both natural and
experimental hosts, the advantages and disadvantages of the most common
experimental influenza infection models, and the contribution of animal models
to the understanding of local and systemic immunity to influenza infection are
discussed.
Descriptors: influenza immunology, influenza veterinary,
antibody formation, disease models, animal, ferrets, fowl plague immunology,
hamsters, haplorhini, horse diseases immunology, horses, influenza A virus avian,
influenza A virus human, influenza A virus, porcine, influenza A virus,
influenza vaccine administration and dosage, mice.
Rezza, G. (2004). Avian influenza: a human
pandemic threat? Journal of
Epidemiology and Community Health 58(10): 807-8. ISSN: 0143-005X.
Descriptors: disease outbreaks, influenza epidemiology,
influenza, avian transmission, zoonoses epidemiology, communicable diseases,
emerging epidemiology, communicable diseases, emerging prevention and control,
influenza prevention and control.
Riberdy, J.M., K.J. Flynn, J. Stech, R.G. Webster,
J.D. Altman, and P.C. Doherty (1999). Protection against a lethal avian
influenza A virus in a mammalian system. Journal of Virology 73(2):
1453-9. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: The question of how best to protect the human
population against a potential influenza pandemic has been raised by the recent
outbreak caused by an avian H5N1 virus in Hong Kong. The likely strategy would
be to vaccinate with a less virulent, laboratory-adapted H5N1 strain isolated
previously from birds. Little attention has been given, however, to dissecting
the consequences of sequential exposure to serologically related influenza A
viruses using contemporary immunology techniques. Such experiments with the
H5N1 viruses are limited by the potential risk to humans. An extremely virulent
H3N8 avian influenza A virus has been used to infect both
immunoglobulin-expressing (Ig+/+) and Ig-/- mice primed previously with a
laboratory-adapted H3N2 virus. The cross-reactive antibody response was very
protective, while the recall of CD8(+) T-cell memory in the Ig-/- mice provided
some small measure of resistance to a low-dose H3N8 challenge. The H3N8 virus
also replicated in the respiratory tracts of the H3N2-primed Ig+/+ mice,
generating secondary CD8(+) and CD4(+) T-cell responses that may contribute to
recovery. The results indicate that the various components of immune memory
operate together to provide optimal protection, and they support the idea that related
viruses of nonhuman origin can be used as vaccines.
Descriptors: influenza prevention and control, influenza A
virus avian immunology, influenza vaccine immunology, base sequence, birds, CD4
positive T lymphocytes immunology, CD8 positive T lymphocytes immunology, DNA,
viral, disease models, animal, immunoglobulins immunology, influenza
immunology, mice, mice inbred BALB c, mice, inbred c57bl, molecular sequence
data.
Rimmelzwaan, G.F., E.C.J. Claas, G. van Amerongen,
J.C. de Jong, and A.D.M.E. Osterhaus (1999). ISCOM vaccine induced
protection against a lethal challenge with a human H5N1 influenza virus. Vaccine
17(11-12): 1355-1358. ISSN: 0264-410X.
NAL
Call Number: QR189.V32
Abstract: Recently avian influenza A viruses of the
H5N1 subtype were shown to infect humans in the Hong Kong area, resulting in
the death of six people. Although these viruses did not efficiently spread
amongst humans, these events illustrated that influenza viruses of subtypes not
previously detected in humans could be at the basis of a new pandemic. In the
light of this pandemic threat we evaluated and compared the efficacy of a
classical non-adjuvanted subunit vaccine and a vaccine based on immune
stimulating complexes (ISCOM) prepared with the membrane glycoproteins of the
human influenza virus A/Hong Kong/156/97 (H5N1) to protect roosters against a
lethal challenge with this virus. The ISCOM vaccine induced protective immunity
against the challenge infection whereas the non-adjuvanted subunit vaccine
proved to be poorly immunogenic and failed to induce protection in this model.
Descriptors: immune system, infection, pharmacology,
lethal viral challenge pandemic protective immunity, induction.
Rimmelzwaan, G.F., J.C. de Jong, T.M. Bestebroer,
A.M. van Loon, E.C. Claas, R.A. Fouchier, and A.D. Osterhaus (2001 ). Antigenic
and genetic characterization of swine influenza A (H1N1) viruses isolated from
pneumonia patients in The Netherlands. Virology 282(2): 301-6. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: influenza A virus, porcine genetics,
influenza A virus, porcine immunology, pneumonia, viral transmission,
pneumonia, viral virology, swine virology, adult, cell line, child, preschool,
ferrets, hemagglutination inhibition tests, immune sera immunology, influenza A
virus, porcine isolation and purification, influenza A virus, porcine
metabolism, likelihood functions, molecular sequence data, Netherlands,
phylogeny, sequence homology, nucleic acid.
Robertson, J.S., M.E.S.C. Robertson, and I.J. Roditi
(1984). Nucleotide sequence of RNA segment 3 of the avian influenza
A/FPV/Rostock/34 and its comparison with the corresponding segment of human
strains A/PR/8/34 and A/NT/60/68. Virus Research 1(1): 73-79. ISSN: 0168-1702.
NAL
Call Number: QR375.V6
Descriptors: avian influenza virus, RNA, nucleotide
sequence, human strains.
Rogers, G.N. and B.L. D'Souza (1989). Receptor
binding properties of human and animal H1 influenza virus isolates. Virology
173(1): 317-22. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: It has been previously reported that several
human H1 influenza viruses isolated prior to 1956, in contrast to human H3
isolates which are quite specific for SA alpha 2,6Gal sequences, apparently
recognize both SA alpha 2,3Gal and SA alpha 2,6Gal sequences (Rogers, G.N., and
Paulson, J.C., Virology 127, 361-373, 1983). In this report human H1 isolates
representative of two epidemic periods, from 1934 to 1957 and from 1977 to
1986, and H1 influenza isolated from pigs, ducks, and turkeys were compared for
their ability to utilize sialyloligosaccharide structures containing terminal
SA alpha 2,3Gal or SA alpha 2,6Gal sequences as receptor determinants. Five of
the eight human isolates from the first epidemic period recognize both SA alpha
2,3Gal and SA alpha 2,6Gal linkages, in agreement with our previous results. Of
the remaining three strains, all isolated towards the end of the first
epidemic, two appear to prefer SA alpha 2,6Gal sequences while the third
preferentially binds SA alpha 2,3Gal sequences. In contrast to the early
isolates, 11 of 13 human strains isolated during the second epidemic period
preferentially bind SA alpha 2,6Gal containing oligosaccharides. On the basis
of changes in receptor binding associated with continued passage in the
laboratory for some of these later strains, it seems likely that human H1
isolates preferentially bind SA alpha 2,6Gal sequences in nature, and that
acquisition of SA alpha 2,3Gal-binding is associated with laboratory passage.
Influenza H1 viruses isolated from pigs were predominantly SA alpha
2,6Gal-specific while those isolated from ducks were primarily SA alpha
2,3Gal-specific. Thus, as has been previously reported for H3 influenza
isolates, receptor specificity for influenza H1 viruses appears to be
influenced by the species from which they were isolated, human isolates binding
preferentially to SA alpha 2,6Gal-containing oligosaccharides while those
isolated from ducks prefer SA alpha 2,3Gal-containing oligosaccharides.
However, unlike the SA alpha 2,6Gal-specific H3 isolates, binding to cell
surface receptors by the H1 influenza viruses is not sensitive to inhibition by
horse serum glycoproteins, regardless of their receptor specificity. These
results suggest that, while the H1 and H3 hemagglutinins appear to be subject
to similar host-derived selective pressures, there appear to be certain
fundamental differences in the detailed molecular interaction of the two
hemagglutinins with their sialyloligosaccharide receptor determinants.
Descriptors: influenza A virus avian metabolism, influenza
A virus human metabolism, influenza A virus, porcine metabolism, influenza A
virus metabolism, orthomyxoviridae metabolism, receptors, virus metabolism,
ducks, hemagglutination inhibition tests, hemagglutination tests, species
specificity, swine, turkeys.
Rogers, G.N. and J.C. Paulson (1983). Receptor
determinants of human and animal influenza virus isolates: differences in
receptor specificity of the H3 hemagglutinin based on species of origin. Virology
127(2): 361-73. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The binding of influenza virus to
erythrocytes and host cells is mediated by the interaction of the viral
hemagglutinin (H) with cell surface receptors containing sialic acid (SA). The
specificity of this interaction for 19 human and animal influenza isolates was
examined using human erythrocytes enzymatically modified to contain cell
surface sialyloligosaccharides with the sequence SA alpha 2,6Gal beta
1,4GlcNAc; SA alpha 2,3Gal beta 1,4(3)GlcNAc; SA alpha 2,3Gal beta 1,3GalNAc;
or SA alpha 2,6GalNAc. Although none of the viruses agglutinated cells
containing the SA alpha 2,6GalNAc linkage, differential agglutination of cells
containing the other three sequences revealed at least three distinct receptor
binding types. Several virus isolates exhibited marked receptor specificity,
binding only to cells containing the SA alpha 2,6Gal or the SA alpha 2,3Gal
linkage, while others bound equally well to cells containing either linkage.
Moreover, some viruses could distinguish between two oligosaccharide receptor
determinants containing the terminal SA alpha 2,3Gal linkage when present in
the SA alpha 2,3Gal beta 1,4(3)GlcNAc sequence or the SA alpha 2,3Gal beta
1,3GalNAc sequence binding cells containing only the former. The observed
receptor specificities were not significantly influenced by the viral
neuraminidases as shown by the use of the potent neuraminidase inhibitor
2-deoxy-2,3-dehydro-N-acetylneuraminic acid. Receptor specificity appeared, to
some extent, to be dependent on the species from which the virus was isolated.
In particular, human isolates of the H3 serotype all agglutinated cells
containing the SA alpha 2,6Gal linkage, but not cells bearing the SA alpha
2,3Gal beta 1,3GalNAc sequence. In contrast, antigenically similar (H3)
isolates from avian and equine species preferentially bound erythrocytes
containing the SA alpha 2,3Gal linkage. This is of particular interest in view
of the identification of the avian virus H3 hemagglutinin as the progenitor of
the H3 hemagglutinin present on the current human Hong Kong viruses.
Descriptors: hemagglutinins viral, influenza A virus
immunology, oligosaccharides metabolism, receptors, virus metabolism,
hemagglutination, viral, hemagglutinin glycoproteins, influenza virus,
influenza A virus avian immunology, influenza A virus human immunology,
influenza A virus, porcine immunology, neuraminidase metabolism, species
specificity.
Rogers, G.N., T.J. Pritchett, J.L. Lane, and J.C.
Paulson (1983). Differential sensitivity of human, avian, and equine
influenza A viruses to a glycoprotein inhibitor of infection: selection of
receptor specific variants. Virology 131(2): 394-408. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Human and animal (avian and equine) influenza
A virus isolates of the H3 serotype exhibit marked differences in their ability
to bind specific sialyloligosaccharide sequences that serve as cell surface
receptor determinants (G. Rogers and J. Paulson, 1983, Virology 127, 361-373).
Whereas human isolates of this subtype strongly agglutinate enzymatically
modified human erythrocytes containing the terminal SA alpha 2,6Gal sequence,
avian and equine isolates preferentially agglutinate erythrocytes bearing the
SA alpha 2, 3Gal sequence. As shown in this report, a glycoprotein found in
horse serum, alpha 2-macroglobulin, is a potent inhibitor of viral adsorption
to the cell surface for human H3 isolates. In contrast, avian and equine
isolates are poorly inhibited suggesting a correlation between receptor
specificity and inhibitor sensitivity. Growth of a human H3 isolate
(A/Memphis/102/72) on MDCK cells in the presence of horse serum resulted in an
overall shift in the virus receptor specificity from preferential binding of
the SA alpha 2,6Gal linkage to preferential binding of the SA alpha 2,3Gal
linkage characteristic of avian and equine isolates. Clonally isolated variants
of A/Memphis/102/72 grown in the presence or absence of horse serum exhibited
binding properties that account for those observed in the field isolates.
Clones which preferentially bound the SA alpha 2,6Gal linkage, like the parent
human virus, were very sensitive to inhibition of hemagglutination by horse
serum and equine alpha 2-macroglobulin. In contrast, receptor variants which
preferentially bound the SA alpha 2,3Gal linkage, like the avian and equine
isolate, were insensitive to such inhibitors. None of the variants was very
sensitive to inhibition of hemagglutination by human alpha 2-macroglobulin.
These results suggest that the presence, in vivo, of a glycoprotein inhibitor
such as equine alpha 2-macroglobulin could suppress infection of influenza
viruses bearing an H3 hemagglutinin with a SA alpha 2,6Gal specific, inhibitor
sensitive phenotype, allowing growth to predominance of a virus which is SA
alpha 2,3Gal specific and inhibitor insensitive as found in avian and equine
isolates.
Descriptors: glycoproteins antagonists and inhibitors,
influenza A virus avian drug effects, influenza A virus human drug effects,
influenza A virus drug effects, receptors, virus drug effects, viral proteins
antagonists and inhibitors, adsorption, chick embryo, ducks, erythrocytes
immunology, erythrocytes microbiology, hemagglutination inhibition tests, hemagglutination
tests, hemagglutinins viral analysis, horses, alpha macroglobulins
pharmacology.
Rohm, C., T. Horimoto, Y. Kawaoka, J. Suss, and R.G.
Webster (1995). Do hemagglutinin genes of highly pathogenic avian influenza
viruses constitute unique phylogenetic lineages? Virology 209(2):
664-670. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Avian influenza A viruses of the H5 and H7
subtypes periodically cause severe outbreaks of disease in poultry. The
question we wished to address in this study is whether these highly pathogenic
strains constitute unique lineages or whether they and related nonpathogenic
viruses are derived from common ancestors in the wild bird reservoir. We
therefore compared the nucleotide and amino acid sequences of the hemagglutinin
(HA) genes of 15 H5 and 26 H7 influenza A viruses isolated over 91 years from a
variety of host species in Eurasia, Africa, Australia, and North America.
Phylogenetic analysis indicated that the HA genes of H5 and H7 viruses that
cause severe disease in domestic birds do not form unique lineages but share
common ancestors with nonpathogenic H5 and H7 viruses. These findings predict
that highly pathogenic avian H5 and H7 influenza A viruses will continue to
emerge from wild bird reservoirs. Another important question is whether H7
influenza viruses found in mammalian species are derived from avian strains. We
included eight equine influenza viruses and one seal isolate in the
phylogenetic analysis of H7 HA genes. We could show that the HA genes of both,
the equine and the seal viruses, shared ancestors with avian H7 HA genes. This
indicates that currently circulating H7 viruses with an avian HA gene may have
the potential to adapt to mammalian species and to cause an influenza outbreak
in the new host.
Descriptors: avian influenza virus, agglutinins, genes,
pathogenicity, phylogeny, nucleotide sequence, chemical composition, biological
properties, cell structure, chromosomes, evolution, genomes, influenza virus,
microbial properties, nucleus, orthomyxoviridae, proteins, viruses, viral
hemagglutinins, structural genes, amino acid sequences.
Romvary, J. and J. Tanyi (1975). Occurrence of
Hong Kong influenza A (H3N2) virus infection in the Budapest zoo. Acta
Veterinaria Academiae Scientiarum Hungaricae 25(2-3): 251-254.
Descriptors: Hong Kong influenza A, epidemiology, Streptopelia
decaocto, zoo animals, birds, dogs, goats, human, fowl, Budapest.
Roslaya, I.G., L.Y.A.S. Zakstel' skaya, and G.E.
Roslyakov (1975). Eksperimental'noe infitsirovanie rechnykh krachek virusom
grippa ptits. [Experimental infection of terns (Sterna hirunda) with a
strain of avian influenza virus isolated from mallard]. Sbornik Trudov
Institut Virusologii Imeni D.I. Ivanoskogo, "Ekologiya Virusov" 3
: 142-146.
Descriptors: avian influenza virus, orthomyxoviridae,
Charadriiformes, terns, Sterna hirunda, mallard.
Rota, P.A., E.P. Rocha, M.W. Harmon, and et al
(1989). Laboratory characterization of a swine influenza virus isolated from
a fatal case of human influenza. Journal of Clinical Microbiology
27(6): 1413-1416. ISSN: 0095-1137.
NAL
Call Number: QR46.J6
Descriptors: zoonoses, influenza virus A and B,
relationships, RNA, Sus scrofa, pigs, swine influenza virus, Wisconsin,
United States.
Rott, R. (1997). Influenza, eine besondere Form
einer Zoonose. [Influenza, a special form of zoonosis]. Berliner Und
Munchener Tierarztliche Wochenschrift 110(7-8): 241-6. ISSN: 0005-9366.
NAL
Call Number: 41.8 B45
Abstract: Findings based on molecular genetics and
phylogeny indicate that avian species represent an important reservoir for
influenza viruses and that virus strains of man and different mammals
originated from avian influenza virus ancestors. In contrast to infectious
agents causing classical zoonoses, influenza viruses have to alter their
genetic make up in order to change their host range. The special, segmented
structure of the viral RNA allows an exchange of gene(s) between two different
influenza viruses (reassortment) resulting in viruses with different
combinations of genome segments and thereby creating new biological properties.
Under the selective pressure of the new host the most adapted virus variants
will succeed which arose from a genetically heterogeneous virus population with
additional mutations. In particular mutations of the genes encoding the
polymerase complex (mutator mutations) would be advantageous for rapid
adaptation in a hostile environment. The generation of influenza viruses
capable of overcoming the species barrier is a rare event since only virus
variants will succeed which are genetically stable and transmissible and which
replicate efficiently in the new host. It is considered likely that pigs act as
intermediate hosts for adaptation of avian viruses to man.
Descriptors: influenza transmission, influenza veterinary,
orthomyxoviridae genetics, zoonoses, birds, mammals, mutation, orthomyxoviridae
pathogenicity, species specificity, swine, variation genetics.
Rott, R., H. Becht, and Orlich (1975). Antigenic
relationship between the surface antigens of avian and equine influenze
viruses. Medical Microbiology and Immunology 161(4): 253-61. ISSN: 0300-8584.
Abstract: Influenza virus Equine 1 (A/equine/Prague/56)
has a hemagglutinin which is antigenically related to the hemagglutinin of fowl
plague virus strain Rostock (FPV) and a neuraminidase which cross-reacts with
the enzyme of virus N (A/chick/Germany/49). After a single injection of
chickens with Equine 1 virus no hemagglutination inhibiting (HI) and
neutralizing antibodies against FPV can be demonstrated, although the birds are
fully protected against a lethal dose of FPV. HI and neutralizing antibodies
against FPV appear after a second injection of Equine 1 virus several weeks
after the first one. Liberation of newly sunthesized FPV from the host cell is
ingibited by antibodies cross-reacting with any antigen of virus surface.
Descriptors: antigens, viral administration and
dosage, arteritis virus, equine
immunology, influenza A virus avian immunology, RNA viruses immunology, binding
sites, antibody, epitopes, fluorescent antibody technique, hemadsorption,
hemagglutination inhibition tests, hemagglutination tests, hemagglutinins viral
isolation and purification, injections, intravenous, neuraminidase analysis,
neutralization tests, plaque assay.
Rovnova, Z.I., E.I. Isaeva, A.L. Platonova, and P.N.
Kosiakov (1989). Antigenno-geneticheskie sviazi virusov grippa cheloveka i
zhivotnykh. [Antigenic-genetic connections between human and animal influenza
viruses]. Voprosy Virusologii 34(5): 553-7. ISSN: 0507-4088.
NAL
Call Number: 448.8 P942
Abstract: A comparative immunological analysis of the
composition of antigenic determinants (AGD) in hemagglutinins of human
influenza A virus (HIAV) of the serosubtypes H1, H2, H3, and in hemagglutinins
of animal influenza viruses (AIV) of the serosubtypes H1, H3-H6, H8-H11 with 25
polyclonal highly active sera was demonstrated. Using original monospecific mon
AGD in HIAV and AIV hemagglutinins was demonstrated. Using original
monospecific antibodies to individual AGD, those AGD contributing to similarity
and differences between HIAV and AIV were determined. It was found that
influenza A. virus strains isolated from man in the USSR in 1986 were identical
in the antigenic structure of hemagglutinin with that isolated from a tern in
1973 (A/tern/Turkmenistan/18/73).
Descriptors: epitopes, genes viral, influenza A virus
avian immunology, human immunology, antigens, viral immunology, cross
reactions, hemagglutination tests, hemagglutinins viral genetics,
hemagglutinins viral immunology, avian genetics, human genetics, neuraminidase
genetics, neuraminidase immunology, species specificity.
Rowe, T., R.A. Abernathy, J. Hu Primmer, W.W.
Thompson, X. Lu, W. Lim, K. Fukuda, N.J. Cox, and J.M. Katz (1999). Detection
of antibody to avian influenza A (H5N1) virus in human serum by using a
combination of serologic assays. Journal of Clinical Microbiology
37(4): 937-43. ISSN: 0095-1137.
NAL
Call Number: QR46.J6
Abstract: From May to December 1997, 18 cases of mild
to severe respiratory illness caused by avian influenza A (H5N1) viruses were
identified in Hong Kong. The emergence of an avian virus in the human
population prompted an epidemiological investigation to determine the extent of
human-to-human transmission of the virus and risk factors associated with
infection. The hemagglutination inhibition (HI) assay, the standard method for
serologic detection of influenza virus infection in humans, has been shown to
be less sensitive for the detection of antibodies induced by avian influenza
viruses. Therefore, we developed a more sensitive microneutralization assay to
detect antibodies to avian influenza in humans. Direct comparison of an HI
assay and the microneutralization assay demonstrated that the latter was
substantially more sensitive in detecting human antibodies to H5N1 virus in
infected individuals. An H5-specific indirect enzyme-linked immunosorbent assay
(ELISA) was also established to test children's sera. The sensitivity and
specificity of the microneutralization assay were compared with those of an
H5-specific indirect ELISA. When combined with a confirmatory H5-specific
Western blot test, the specificities of both assays were improved. Maximum
sensitivity (80%) and specificity (96%) for the detection of anti-H5 antibody
in adults aged 18 to 59 years were achieved by using the microneutralization
assay combined with Western blotting. Maximum sensitivity (100%) and
specificity (100%) in detecting anti-H5 antibody in sera obtained from children
less than 15 years of age were achieved by using ELISA combined with Western
blotting. This new test algorithm is being used for the seroepidemiologic
investigations of the avian H5N1 influenza outbreak.
Descriptors: antibodies, viral blood, influenza A virus
avian immunology, serologic tests methods, adolescent, adult, blotting, western
methods, blotting, western statistics and numerical data, child, preschool,
cross reactions, enzyme linked immunosorbent assay methods, enzyme linked
immunosorbent assay statistics and numerical data, hemagglutination inhibition
tests methods, hemagglutination inhibition tests statistics and numerical data,
Hong Kong epidemiology, influenza epidemiology, influenza immunology, influenza
transmission, avian classification, avian pathogenicity, middle aged,
neutralization tests methods, neutralization tests statistics and numerical
data, sensitivity and specificity, seroepidemiologic studies, serologic tests
statistics and numerical data.
Rowe, T., D.S. Cho, R.A. Bright, L.A. Zitzow, and
J.M. Katz (2003). Neurological manifestations of avian influenza viruses in
mammals. Avian Diseases 47(Special Issue): 1122-1126. ISSN: 0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: The H5N1 viruses isolated from humans in Hong
Kong directly infected both mice and ferrets without prior adaptation to either
host. Two representative viruses, A/Hong Kong/483/97 (HK/483) and A/Hong
Kong/486/97 (HK/486) were equally virulent in outbred ferrets but differed in
their virulence in inbred mice. Both HK/483 and HK/486 replicated systemically
in ferrets and showed neurologic manifestations. In contrast, intranasal infection
of mice with HK/483, but not HK/486, resulted in viral spread to the brain,
neurologic signs, and death. However, HK/486 was able to replicate in the brain
and induce lethal disease following direct intracerebral inoculation.
Descriptors: infection, nervous system, avian influenza,
infectious disease, respiratory system disease, viral disease, neurological
infection manifestations.
Rudneva, I.A., E.I. Sklyanskaya, O.S. Barulina, S.S.
Yamnikova, V.P. Kovaleva, I.V. Tsvetkova, and N.V. Kaverin (1996). Phenotypic
expression of HA-NA combinations in human-avian influenza A virus reassortants.
Archives of Virology 141(6): 1091-9.
ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: Human-avian and human-mammalian influenza A
virus reassortant clones with the neuraminidase (NA) gene of the A/USSR/90/77
(H1N1) strain and hemagglutinin (HA) genes of H3, H4 and H13 subtypes had been
shown in an earlier publication to produce low HA yields in the embryonated
chicken eggs. The low HA titers had been shown to be due, at least in part, to
the formation of virion clusters at 4 degrees C; the clustering was removed by
the treatment with bacterial neuraminidase [Rudneva et al., Arch. Virol (1993)
133: 437-450]. By serial passages of the reassortants in chick embryos
non-aggregating variants were selected: the variants produced HA titers of the
same order as A/USSR/90/77 parent virus. The assessment of the virus yields by
the analysis of the partially purified virus preparations from fixed volumes of
the allantoic fluid revealed that actual virion yields of the initial
reassortants were lower than the yields of their passaged variants or of the
parent viruses. The passaged variant of a reassortant possessing the HA gene of
A/Duck/Ukraine/1/63 (H3N2) virus differed from the original (non-passaged)
reassortant and from the parent A/Duck/Ukraine/1/63 virus in the reaction with
a panel of monoclonal antibodies against H3 hemagglutinin. The data suggest
that some HA-NA combinations may lead to an incomplete functional match between
HA and NA and to the formation of low-yield reassortants, thus representing a
possible limiting factor in the emergence of new HA-NA combinations in natural
conditions.
Descriptors: hemagglutinins viral biosynthesis, influenza
A virus avian metabolism, human metabolism, neuraminidase biosynthesis,
reassortant viruses metabolism, antibodies, monoclonal immunology, antibodies,
viral immunology, antigens, viral immunology, cell line, chick embryo, dogs,
epitopes, hemagglutinin glycoproteins, influenza virus, hemagglutinins viral
genetics, avian genetics, human genetics, neuraminidase genetics, phenotype,
reassortant viruses genetics, serial passage, variation genetics.
Russi Cahill, J.C., M.C. Mogdasy, R.E. Somma Moreira,
and M.H. de Peluffo (1975). Counterimmunoelectrophoresis with influenza
antigens. I. Use of avian plague virus to detect type-specific antibodies to
influenza A in human sera. Journal of Infectious Diseases 131(1):
64-6. ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Abstract:
Avian plague virus was used as antigen
in a counterimmunoelectrophoresis technique. This virus was selected because it
detects only type-specific influenza A antibodies in human sera, avoiding the
possible interference of other antigens with anodic migration. The results with
reference sera, as well as the correlation of positive sera found by
counterimmunoelectrophoresis and complement fixation with the proposed antigen,
in the absence of other types of antibodies to fowl plague virus antigen,
support the conclusion that the counterimmunoelectrophoresis technique reveals
type-specific antibodies. The test is more sensitive than immunodiffusion but
less sensitive than complement fixation. Its sensitivity, simplicity, and
rapidity make it suitable for serologic surveys of human influenza A.
Descriptors: antibodies, viral analysis, antigens, viral,
immunoelectrophoresis, influenza immunology, influenza A virus avian
immunology, antibody specificity, chick embryo, complement fixation tests,
guinea pigs immunology, immune sera,
immunodiffusion.
Saito, T., W. Lim, T. Suzuki, Y. Suzuki, H. Kida,
S.I. Nishimura, and M. Tashiro (2001). Characterization of a human H9N2
influenza virus isolated in Hong Kong. Vaccine 20(1-2): 125-33. ISSN: 0264-410X.
NAL
Call Number: QR189.V32
Abstract: Two H9N2 viruses were isolated, for the first
time, from humans in Hong Kong in 1999. Isolation of influenza viruses with a
novel subtype of the hemagglutinin (HA) drew attention of health care
authorities worldwide from the view of pandemic preparedness. Sequence analysis
of the HA genes reveals that HA of A/Hong Kong/1073/99 (H9N2) is most closely
related to that of A/quail/HK/G1/97 (H9N2) that contains the internal genes
similar to those of Hong Kong/97 (H5N1) viruses. Phylogenetic and antigenic
analyses demonstrated the diversity among H9 HA. A/Hong Kong/1073/99 was shown
to cause a respiratory infection in Syrian hamsters, suggesting that the virus
can replicate efficiently in mammalian hosts. We developed a whole virion test
vaccine with a formalin-inactivated egg-grown HK1073. Intraperitoneal
administration of the vaccine twice to hamsters conferred a complete protection
against challenge infection by the MDCK cell-grown homologous virus. Receptor
specificity of HK1073 appeared different from that of other avian influenza
viruses of H9 subtype which recognize preferentially alpha-2,3 linked sialic
acid. Hemagglutination of HK1073 with guinea pig erythrocytes was inhibited by
both alpha-2,3 and alpha-2,6 linked sialic acid containing polymers. These data
suggested that HK1073 had acquired a broader host range, including humans.
Together with data so far available, the present study suggested that isolation
of the H9 influenza viruses from humans requires precaution against the emergence
of a novel human influenza.
Descriptors: influenza virology, influenza A virus human
isolation and purification, antigens, viral immunology, Asia, cattle, cultured
cells, chick embryo, child, dogs, Europe, glycoconjugates pharmacology, guinea
pigs, hamsters, hemagglutination tests, hemagglutination, viral, hemagglutinin
glycoproteins, influenza virus genetics, hemagglutinin glycoproteins, influenza
virus physiology, Hong Kong, horses, influenza prevention and control,
influenza veterinary, avian classification, avian physiology, human
classification, human genetics, human immunology, human physiology, porcine
classification, porcine physiology, influenza vaccine immunology, lung
virology, mesocricetus, N-acetylneuraminic acid metabolism, North America,
phylogeny, poultry virology, poultry diseases virology, receptors, virus
metabolism, sheep, species specificity, swine, swine diseases virology,
vaccination, vaccines, inactivated, virion immunology, virus cultivation.
Samaan, G. (2005). Rumor surveillance and avian
influenza H5N1. Emerging Infectious Diseases 11(3): 463-6. ISSN: 1080-6040.
NAL
Call Number: RA648.5.E46
Abstract: We describe the enhanced rumor surveillance
during the avian influenza H5N1 outbreak in 2004. The World Health Organization's
Western Pacific Regional Office identified 40 rumors; 9 were verified to be
true. Rumor surveillance informed immediate public health action and prevented
unnecessary and costly responses.
Descriptors: influenza prevention and control, avian influenza
A virus, population surveillance methods, communication, disease outbreaks,
influenza epidemiology, avian influenza epidemiology, World Health
Organization.
Sambhara, S., A. Kurichh, R. Miranda, T. Tumpey, T.
Rowe, M. Renshaw, R. Arpino, A. Tamane, A. Kandil, O. James, B. Underdown, M.
Klein, J. Katz, and D. Burt (2001). Heterosubtypic immunity against human
influenza A viruses, including recently emerged avian H5 and H9 viruses,
induced by FLU-ISCOM vaccine in mice requires both cytotoxic T-lymphocyte and
macrophage function. Cellular Immunology 211(2): 143-53. ISSN: 0008-8749.
NAL
Call Number: QR180.C4
Descriptors: iscoms immunology, influenza prevention and
control, influenza A virus avian immunology, human immunology, influenza
vaccine immunology, macrophages immunology, T lymphocytes, cytotoxic
immunology, antibodies, viral immunology, cross reactions, fowl plague
prevention and control, influenza immunology, mice inbred BALB c, mice, inbred
c57bl, mice, inbred DBA, mice, knockout, time factors.
Schafer, J., M.L. Khristova, T.L. Busse, R.
Sinnecker, I.G. Kharitonenkov, C. Schrader, J. Suss, and D. Bucher (1992). Analysis
of internal proteins of influenza A (H2N2) viruses isolated from birds in East
Germany in 1983. Acta Virologica 36(2): 113-20. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: Proteins and RNAs of influenza A (H2N2)
viruses isolated from birds in 1983 in East Germany were compared antigenically
with those of H2N2 human strains. The electrophoretic mobility of the viral
proteins and of the S1-treated double-stranded RNAs from two human and six
avian strains, as well as the results of EIA-tests using monoclonal antibodies
to their matrix protein and nucleoproteins indicate an antigenic relationship
between the avian isolates and human strains of H2N2 subtype. One of the avian
strains had a reduced amount of matrix protein.
Descriptors: antigens, viral analysis, epitopes analysis,
influenza A virus avian chemistry, human chemistry, RNA viral analysis, viral
matrix proteins analysis, antibodies, monoclonal, ducks, enzyme linked
immunosorbent assay, East Germany.
Schafer, J.R., Y. Kawaoka, W.J. Bean, J. Suss, D.
Senne, and R.G. Webster (1993). Origin of the pandemic 1957 H2 influenza A
virus and the persistence of its possible progenitors in the avian reservoir.
Virology 194(2): 781-8. ISSN:
0042-6822.
NAL
Call Number: 448.8 V81
Abstract: H2N2 influenza A viruses caused the Asian
pandemic of 1957 and then disappeared from the human population 10 years later.
To assess the potential for similar outbreaks in the future, we determined the
antigenicity of H2 hemagglutinins (HAs) from representative human and avian H2
viruses and then analyzed the nucleotide and amino acid sequences to determine
their evolutionary characteristics in different hosts. The results of
longitudinal virus surveillance studies were also examined to estimate the
prevalence of avian H2 isolates among samples collected from wild ducks and
domestic poultry. Reactivity patterns obtained with a large panel of monoclonal
antibodies indicated antigenic drift in the HA of human H2 influenza viruses,
beginning in 1962. Amino acid changes were clustered in two regions of HA1 that
correspond to antigenic sites A and D of the H3 HA. By contrast, the antigenic
profiles of the majority of avian H2 HAs were remarkably conserved through
1991, resembling the prototype Japan 57 (H2N2) strain. Amino acid changes were
distributed throughout HA1, indicating that antibodies do not play a major role
in the selection of avian H2 viruses. Phylogenetic analysis revealed two
geographic site-specific lineages of avian H2 HAs: North American and Eurasian.
Evidence is presented to support interregion transmission of gull H2 viruses.
The human H2 HAs that circulated in 1957-1968 form a separate phylogenetic
lineage, most closely related to the Eurasian avian H2 HAs. There was an
increased prevalence of H2 influenza viruses among wild ducks in 1988 in North
America, preceding the appearance of H2N2 viruses in domestic fowl. As the prevalence
of avian H2N2 influenza viruses increased on turkey farms and in live bird
markets in New York City and elsewhere, greater numbers of these viruses have
come into direct contact with susceptible humans. We conclude that
antigenically conserved counterparts of the human Asian pandemic strain of 1957
continue to circulate in the avian reservoir and are coming into closer
proximity to susceptible human populations.
Descriptors: disease outbreaks, disease reservoirs,
hemagglutinins viral genetics, influenza epidemiology, influenza A virus
genetics, orthomyxoviridae infections epidemiology, Americas epidemiology,
antibodies, monoclonal, antibodies, viral immunology, Asia epidemiology, birds
microbiology, Europe epidemiology, evolution, fowl plague epidemiology, fowl
plague genetics, genes viral genetics, hemagglutinin glycoproteins, influenza
virus, influenza genetics, influenza A virus avian genetics, avian immunology,
human genetics, human immunology, influenza A virus immunology, molecular
sequence data, orthomyxoviridae
infections genetics, phylogeny, population surveillance, time factors.
Schneeberger, P.M., R.A.M. Fouchier, J.M. Broekman,
S.A.G. Kemink, F.W. Rozendaal, M.P.G.
Koopmans, and A.D.M. Osterhaus (2003). A fatal case of infection with avian
influenza A virus (H7N7) of a veterinarian during a highly pathogenic avian
influenza outbreak in the Netherlands. Abstracts of the Interscience
Conference on Antimicrobial Agents and Chemotherapy, Chicago, IL, USA,
September 14-17, 2003 43: 492.
Descriptors: infection, occupational health, avian
influenza A virus, viral pneumonia, veterinarian, human death, Netherlands.
Scholtissek, C. (1994). Source for influenza
pandemics. European Journal of Epidemiology 10(4): 455-8. ISSN: 0393-2990.
NAL
Call Number: RA648.5.E97
Abstract: There are three ways how influenza A viruses
can escape the immune response in the human population: (1) By antigenic drift.
This means by mutation and selection of variants under the selection pressure
of the immune system. These variants have amino acid replacements mainly in the
epitopes of the hemagglutinin. (2) By antigenic shift. This means replacement
of at least the hemagglutinin gene of the prevailing human strain by the
allelic gene of an avian influenza virus by reassortment. (3) As a rare event,
direct or indirect introduction of an avian influenza virus in toto into the
human population. A prior introduction of an avian virus into pigs and an
adaptation to the new host might be a presupposition for its final passage to
humans. In this sense the nowadays situation is reminiscent to that of about
100 years ago, when an avian virus was presumably first introduced into pigs,
and from there into humans. Immediately or some time thereafter the disastrous
Spanish Flu in 1918/19 had killed at least 20,000,000 people in one winter.
Pandemic strains can be created by all three means, however the most common way
is by reassortment. In order to recognize a pandemic strain as soon as possible
a worldwide surveillance system and collaborating laboratories equipped with
corresponding modern technologies are required.
Descriptors: disease outbreaks, influenza epidemiology,
influenza virology, orthomyxoviridae genetics, antigenic variation genetics,
antigens, viral genetics, birds, genes viral genetics, influenza A virus avian
genetics, avian immunology, porcine genetics, porcine immunology,
orthomyxoviridae immunology, swine.
Scholtissek, C., H. Burger, P.A. Bachmann, and C.
Hannoun (1983). Genetic relatedness of hemagglutinins of the H1 subtype of
influenza A viruses isolated from swine and birds. Virology 129(2):
521-3. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The hemagglutinin (HA) gene of the influenza
virus subtype H1N1 isolated from pigs and birds has been analyzed by the
hybridization technique. According to the RNase protection data the HA genes of
recent isolates from pigs in Northern Europe are genetically more closely
related to those of isolates from birds in Europe and North America than to
those of isolates from pigs in the United States, Taiwan, and Italy. Thus, two
different H1N1 subtypes are circulating in the pig population. The results are
consistent with the view that H1N1 viruses can be transmitted from birds to
pigs and/or vice versa.
Descriptors: hemagglutinins viral genetics, influenza A
virus avian genetics, porcine genetics, genetics, birds microbiology, genes
viral, avian immunology, avian isolation and purification, porcine
classification, porcine immunology, porcine isolation and purification, nucleic
acid hybridization, swine microbiology.
Scholtissek, C., J. Stech, S. Krauss, and R.G.
Webster (2002). Cooperation between the hemagglutinin of avian viruses and
the matrix protein of human influenza A viruses. Journal of Virology
76(4): 1781-6. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: To analyze the compatibility of avian
influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M)
proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with
amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and
amantadine-sensitive avian strains. By using antisera against the human virus
HAs and amantadine, we selected reassortants containing the human virus M gene
and the avian virus HA gene. In our system, high virus yields and large,
well-defined plaques indicated that the avian HAs and the human M gene products
could cooperate effectively; low virus yields and small, turbid plaques
indicated that cooperation was poor. The M gene products are among the primary
components that determine the species specificities of influenza A viruses.
Therefore, our system also indicated whether the avian HA genes effectively
reassorted into the genome and replaced the HA gene of the prevailing human influenza
A viruses. Most of the avian HAs that we tested efficiently cooperated with the
M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian
HAs did not effectively cooperate with the most recently isolated human virus
that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and
the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These
results suggest that the currently prevailing human influenza A viruses might
have lost their ability to undergo antigenic shift and therefore are unable to
form new pandemic viruses that contain an avian HA, a finding that is of great
interest for pandemic planning.
Descriptors: hemagglutinin glycoproteins, influenza virus
metabolism, influenza A virus avian genetics, human genetics, reassortant
viruses, viral matrix proteins metabolism, amantadine pharmacology, antiviral
agents pharmacology, cell line, dogs, drug resistance, viral, fowl plague
virology, hemagglutinin glycoproteins, influenza virus genetics, influenza
virology, avian drug effects, avian growth and development, avian metabolism,
human drug effects, human growth and development, human metabolism, kidney
cytology, kidney virology, plaque assay, poultry, viral matrix proteins
genetics.
Scholtissek, C. (1995). Molecular evolution of
influenza viruses. Virus Genes 11(2-3): 209-215. ISSN: 0920-8569.
NAL
Call Number: QH434.V57
Abstract: There are two different mechanisms by which
influenza viruses might evolve: (1) Because the RNA genome of influenza viruses
is segmented, new strains can suddenly be produced by reassortment, as happens,
for example, during antigenic shift, creating new pandemic strains. (2) New
viruses evolve relatively slowly by stepwise mutation and selection, for
example, during antigenic or genetic drift. Influenza A viruses were found in
various vertebrate species, where they form reservoirs that do not easily mix.
While human influenza A viruses do not spread in birds and vice versa, the
species barrier to pigs is relatively low, so that pigs might function as
"mixing vessels" for the creation of new pandemic reassortants in
Southeast Asia, where the probability is greatest for double infection of pigs
by human and avian influenza viruses. Phylogenetic studies revealed that about
100 years ago, an avian influenza A virus had crossed the species barrier,
presumably first to pigs, and from there to humans, forming the new stable
human and classical swine lineages. In 1979, again, an avian virus showed up in
the North European swine population, forming another stable swine lineage. The
North European swine isolates from 1979 until about 1985 were genetically
extremely unstable. A hypothesis is put forward stating that a mutator mutation
is necessary to enable influenza virus to cross the species barrier by
providing the new host with sufficient variants from which it can select the
best fitting ones. As long as the mutator mutation is still present, such a
virus should be able to cross the species barrier a second time, as happened
about 100 years ago. Although the most recent swine isolates from northern
Germany are again genetically stable, we nevertheless should be on the lookout
to see if a North European swine virus shows up in the human population in the
near future.
Descriptors: evolution and adaptation, immune system,
infection, microbiology, veterinary medicine, antigenic drift evolution host
infection molecular evolution pandemic reassortants phylogeny species barrier
virology.
Schultz, U., W.M. Fitch, S. Ludwig, J. Mandler, and
C. Scholtissek (1991). Evolution of pig influenza viruses. Virology
183(1): 61-73. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: There is evidence that the nucleoprotein (NP)
gene of the classical swine virus (A/Swine/1976/31) clusters with the early
human strains at the nucleotide sequence level, while at the level of the amino
acid sequence, as defined by consensus amino acids and in functional tests, its
NP is clearly "avian like." Therefore it was suggested that the Sw/31
NP had been recently under strong selection pressure, possibly caused by
reassortment with other avian influenza genes, whose gene products have to
cooperate intimately with NP (Gammelin et al., 1989. Virology 170, 71-80). This
suggestion has been investigated by sequencing the genes of internal and
nonstructural proteins of Sw/31. The data on these sequences and on the
phylogenetic trees are not in accordance with that suggestion: all these genes
cluster with the early human strains at the nucleotide level while, at the
level of the amino acid sequence, most of them are more closely related to the
avian strains, thus resembling NP in this respect. This indicates that these
genes rather evolved concomitantly with the NP gene. Our data are in agreement
with the suggestion that, at about the time of the Spanish Flu (1918/19), a
human influenza A (H1N1) virus entered the pig population. Furthermore, it is
known that the NP of the human influenza A viruses--in contrast to that of the
avian and swine strains--has been under strong selection pressure to change
(Gammelin et al., 1990. Mol. Biol. Evol. 7, 194-200. Gorman et al., 1990a. J.
Virol. 64, 1487-1497). Thus, after transfer of a human strain into pigs, the
selection pressure might be released, enabling the NP and the other genes of
the swine virus to evolve back to the optimal avian sequences, especially at
the functionally important consensus positions. The swine influenza viruses
circulating since 1979 in Northern Europe--represented by A/Swine/Germany/2/81
(H1N1)--have all genes, so far examined, derived from an avian influenza virus
pool and are different from the classical swine viruses.
Descriptors: influenza A virus, porcine genetics,
phylogeny, RNA replicase, viral proteins genetics, chick embryo, consensus sequence, genes
viral, nucleoproteins genetics, swine, viral core proteins genetics.
Sears, S.D., M.L. Clements, R.F. Betts, H.F. Maassab,
B.R. Murphy, and M.H. Snyder (1988). Comparison of live, attenuated H1N1 and
H3N2 cold-adapted and avian-human influenza A reassortant viruses and
inactivated virus vaccine in adults. Journal of Infectious Diseases
158(6): 1209-19. ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Abstract: The infectivity, immunogenicity, and efficacy
of live, attenuated influenza A/Texas/1/85 (H1N1) and A/Bethesda/1/85 (H3N2)
avian-human (ah) and cold-adapted (ca) reassortant vaccines were compared in
252 seronegative adult volunteers. The immunogenicity and efficacy of the H1N1
reassortant vaccine were also compared with those of the trivalent inactivated
virus vaccine. Each reassortant vaccine was satisfactorily attenuated. The 50%
human infectious dose was 10(4.9) for ca H1N1, 10(5.4) for ah H1N1, 10(6.4) for
ca H3N2, and 10(6.5) TCID50 for ah H3N2 reassortant virus. Within a subtype,
the immunogenicities of ah and ca vaccines were comparable. Five to seven weeks
after vaccination, volunteers were challenged with homologous wild-type
influenza A virus. The magnitude of shedding of virus after challenge was
greater than 100-fold less in H1N1 vaccinees and greater than 10-fold less in
H3N2 vaccinees compared with unimmunized controls. The vaccines were equally
efficacious, as indicated by an 86%-100% reduction in illness. Thus, the ah
A/Mallard/New York/6750/78 and the ca A/Ann Arbor/6/60 reassortant viruses are
comparable.
Descriptors: influenza prevention and control, influenza A
virus avian immunology, human immunology, influenza vaccine, adult, antibodies,
viral biosynthesis, cold, double blind method, enzyme linked immunosorbent
assay, hemagglutination inhibition tests, avian pathogenicity, avian
physiology, human pathogenicity, human physiology, random allocation, vaccines,
attenuated, vaccines, synthetic, virus replication.
Shaw, M., L. Cooper, X. Xu, W. Thompson, S. Krauss,
Y. Guan, N. Zhou, A. Klimov, N. Cox, R. Webster, W. Lim, K. Shortridge, and K.
Subbarao (2002). Molecular changes associated with the transmission of avian
influenza a H5N1 and H9N2 viruses to humans. Journal of Medical Virology
66(1): 107-14. ISSN: 0146-6615.
Abstract: In order to identify molecular changes
associated with the transmission of avian influenza A H5N1 and H9N2 viruses to
humans, the internal genes from these viruses were compared to sequences from
other avian and human influenza A isolates. Phylogenetically, each of the
internal genes of all sixteen of the human H5N1 and both of the H9N2 isolates
were closely related to one another and fell into a distinct clade separate
from clades formed by the same genes of other avian and human viruses. All six
internal genes were most closely related to those of avian isolates circulating
in Asia, indicating that reassortment with human strains had not occurred for
any of these 18 isolates. Amino acids previously identified as host-specific
residues were predominantly avian in the human isolates although most of the
proteins also contained residues observed previously only in sequences of human
influenza viruses. For the majority of the nonglycoprotein genes, three
distinct subgroups could be distinguished on bootstrap analyses of the
nucleotide sequences, suggesting multiple introductions of avian virus strains
capable of infecting humans. The shared nonglycoprotein gene constellations of
the human H5N1 and H9N2 isolates and their detection in avian isolates only
since 1997 when the first human infections were detected suggest that this
particular gene combination may confer the ability to infect humans and cause
disease. J. Med. Virol. 66:107-114, 2002. Published 2002 Wiley-Liss, Inc.
Descriptors: fowl plague transmission, influenza virology,
influenza A virus avian genetics, human genetics, fowl plague virology,
influenza transmission, avian classification, human classification, human
isolation and purification, molecular sequence data, nasopharynx virology,
phylogeny, viral proteins genetics.
Shinshaw, V.S., R.G. Webster, and W.J. Bean. (1981). Application
of recently developed techniques to determine the origin of influenza A viruses
appearing in avian and mammalian species and to develop potent avian influenza
vaccines. In: Proceedings of the First International Symposium on Avian
Influenza, Beltsville, Maryland, USA, p. 134-147.
NAL
Call Number:
aSF995.6.I6I5 1981a
Descriptors: avian influenza virus, techniques,
vaccines, mammalian species, avian species.
Shinya, K., F.D. Silvano, T. Morita, A. Shimada, M.
Nakajima, T. Ito, K. Otsuki, and T. Umemura (1998). Encephalitis in mice
inoculated intranasally with an influenza virus strain originated from a water
bird. Journal of Veterinary Medical Science the Japanese Society of
Veterinary Science 60(5): 627-9.
ISSN: 0916-7250.
NAL
Call Number: SF604.J342
Abstract: Five-week-old ddY mice were inoculated
intranasally with a low virulent (4e) or highly virulent (24a5b) avian
influenza virus strain originated from a water bird. None of mice in the 4e
group showed clinical signs and brain lesions. Of the 24a5b group, two mice
died and one mouse was killed at a moribund state at day 7 post-inoculation
(PI). Four mice of the 24a5b group necropsied at day 5 or 7 PI had mild to
severe encephalitis in the brain stem and the cerebellar white matter.
Influenza virus antigen was detected in neurons, glial cells and vascular
endothelium in the lesions. The distribution of the lesions seems to indicate
the transneuronal invasion of the virus via cranial nerve fibers into the
brain.
Descriptors: birds virology, brain pathology,
encephalitis, viral pathology, influenza pathology, influenza A virus avian
pathogenicity, antigens, viral analysis, brain virology, brain stem pathology,
cerebellum pathology, encephalitis, viral virology, immunohistochemistry, avian
isolation and purification, mice, necrosis, virulence.
Shortridge, K.F. (1982). Avian influenza A viruses
of southern China and Hong Kong: ecological aspects and implications for man.
Bulletin of the World Health Organization 60(1): 129-35. ISSN: 0042-9686.
NAL
Call Number: 449.9 W892B
Descriptors: influenza A virus avian isolation and
purification, chickens, China, ducks, geese, hemagglutination inhibition tests,
Hong Kong, neuraminidase analysis, poultry.
Shortridge, K.F. (1992). Pandemic influenza: a
zoonosis? Seminars in Respiratory Infections 7(1): 11-25. ISSN: 0882-0546.
Abstract: In the last two decades, influenza A viruses
have been found to occur throughout the animal kingdom, mainly in birds,
notably aquatic ones, in which infection is largely intestinal, waterborne, and
asymptomatic. The domestic duck of southern China, raised in countless numbers
all year round mainly as an adjunct to rice farming, is the principal host of
influenza A viruses. Studies based on Hong Kong H3N2 viruses from southern
China suggest that pandemic strains originate from the domestic duck there and
are transmitted to humans via the domestic pig, which acts as a "mixing
vessel" for two-way transmission of viruses. This provides further support
for the hypothesis that the region is a hypothetical influenza epicenter. Rural
dwellers in the epicenter show serological evidence of contact with non-human
influenza A viruses. Two hypotheses are advanced for the range of hemagglutinin
(HA) subtypes of viruses that can cause pandemics (1) circle or cycle limited
to H1, H2, and H3 subtypes, thereby implying that a virus of the H2 subtype
will cause the next pandemic; and (2) spiral, by which any one of the 14 HA
subtypes recorded to date may be involved. Consideration is given to the
temporal and geographical factors and range of hosts, namely the duck, pig, and
human, that need to be submitted to virus surveillance in China and beyond to
attempt to anticipate a future pandemic. Evidence is presented that points
strongly to pandemic influenza being a zoonosis.
Descriptors: ducks microbiology, influenza transmission,
influenza A virus avian pathogenicity, human pathogenicity, porcine
pathogenicity, swine microbiology, zoonoses transmission, China epidemiology,
chronology, disease outbreaks prevention and control, feces microbiology, fresh
water, influenza epidemiology, influenza microbiology, avian isolation and
purification, human isolation and purification, porcine isolation and
purification, reassortant viruses genetics.
Shortridge, K.F., P. Gao, Y. Guan, T. Ito, Y.
Kawaoka, D. Markwell, A. Takada, and R.G. Webster (2000). Interspecies
transmission of influenza viruses: H5N1 virus and a Hong Kong SAR perspective.
Veterinary Microbiology 74(1-2): 141-7.
ISSN: 0378-1135.
NAL
Call Number: SF601.V44
Abstract: This account takes stock of events and
involvements, particularly on the avian side of the influenza H5N1 'bird flu'
incident in Hong Kong SAR in 1997. It highlights the role of the chicken in the
many live poultry markets as the source of the virus for humans. The slaughter
of chicken and other poultry across the SAR seemingly averted an influenza
pandemic. This perspective from Hong Kong SAR marks the coming-of-age of
acceptance of the role of avian hosts as a source of pandemic human influenza
viruses and offers the prospect of providing a good baseline for influenza
pandemic preparedness in the future. Improved surveillance is the key. This is
illustrated through the H9N2 virus which appears to have provided the
'replicating' genes for the H5N1 virus and which has since been isolated in the
SAR from poultry, pigs and humans highlighting its propensity for interspecies
transmission.
Descriptors: influenza transmission, influenza A virus
avian pathogenicity, zoonoses transmission, chickens, disease outbreaks
prevention and control, fowl plague transmission, Hong Kong epidemiology,
influenza mortality, influenza virology, avian genetics.
Shortridge, K.F., A.P. King, and R.G. Webster (1987).
Monoclonal antibodies for characterizing H3N2 influenza viruses that persist
in pigs in China. Journal of Infectious Diseases 155(3):
577-81. ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Descriptors: antigens, viral immunology, influenza A
virus, porcine immunology, influenza A virus immunology, swine microbiology,
viral core proteins, antibodies, monoclonal immunology, antibodies, viral
immunology, antigens, viral analysis, China, cross reactions, epitopes,
hemagglutinins viral immunology, Hong Kong, avian immunology, human immunology,
neuraminidase immunology, nucleoproteins immunology, Taiwan, viral proteins
immunology.
Shortridge, K.F., J.S.M. Peiris, and Y. Guan (2003). The
next influenza pandemic: Lessons from Hong Kong. Society for Applied
Microbiology Symposium Series (32): 70S-79S. ISSN: 1467-4734.
NAL
Call Number: QR1.S64
Abstract: Pandemic influenza is a zoonosis. Studies on
influenza ecology conducted in Hong Kong since the 1970s in which Hong Kong
essentially functioned as an influenza sentinel post indicated that it might be
possible, for the first time, to have influenza preparedness at the baseline
avian level. This appreciation of influenza ecology facilitated recognition of
the H5N1 'bird flu' incident in Hong Kong in 1997 in what was considered to be
an incipient pandemic situation, the chicken being the source of virus for
humans and, if so, was the first instance where a pandemic may have been
averted. The 2001 and 2002 H5N1 incidents demonstrated that it was possible to
have an even higher order of baseline preparedness with the recognition in
chicken of a range of genotypes of H5N1-like viruses before they had the
opportunity to infect humans. Investigations of these incidents revealed a
complex ecology involving variously precursor avian H5N1 virus in geese and
ducks, and H9N2 and H6N1 viruses in quail, the quail possibly functioning as an
avian 'mixing vessel' for key genetic reassortment events for onward
transmission of H5N1 viruses highly pathogenic for chicken and humans. These
findings highlight the importance of systematic virus surveillance of domestic
poultry in recognizing changes in virus occurrence, host range and
pathogenicity as signals at the avian level that could presage a pandemic. For
example, there is now an increasing prevalence of avian influenza viruses in
terrestrial (in contrast to aquatic) poultry. Prior to 1997, no particular
virus subtype other than H4N6 would have been considered a candidate for
pandemicity and this was based, in the absence of any other data, on its high
frequency of occurrence in ducks in southern China. Now, with the isolation of
H5N1 and H9N2 viruses from humans supported by genetic, molecular and
biological studies on these and other avian isolates, there is credible
evidence for the candidacy, in order, of H5N1, H9N2 and H6N1 viruses. These
viruses have been made available for the production of diagnostic reagents and
exploratory vaccines. The 1997 incident upheld the hypothesis that southern
China is an epicentre for the emergence of pandemic influenza viruses. However,
the intensification of the poultry (chicken) industry worldwide coupled with
the spread of viruses such as the Eurasian lineage of H9N2 suggest that the
genesis of a pandemic could take place elsewhere in the world. This
re-emphasizes the importance of systematic virus surveillance of poultry globally
for international public health and for economic and food concerns. Faced with
an incipient pandemic in 1997, Hong Kong brought in international experts to
join the investigative effort. Good teamwork at all levels is essential in
dealing with the many facets. The threat of a pandemic should not be minimized,
nor should governments be lulled into a sense of false security. The media is a
powerful channel and has the responsibility and the avenues to convey and
influence public perception of events. Close liaison between the media and
those on the operational side ensures effective, accurate and timely
dissemination of information. This will enhance public confidence in the
investigative process and in steps taken for its safety and health.
Descriptors: epidemiology, infection, public health,
respiratory system, influenza, respiratory system disease, viral disease,
epidemics, pandemics, viral occurrence.
Shu, L.L., W.J. Bean, and R.G. Webster (1993). Analysis
of the evolution and variation of the human influenza A virus nucleoprotein
gene from 1933 to 1990. Journal of Virology 67(5): 2723-9. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: This study examined the evolution and
variation of the human influenza virus nucleoprotein gene from the earliest
isolates to the present. Phylogenetic reconstruction of the most parsimonious
evolutionary path connecting 49 nucleoprotein sequences yielded a single
lineage. The average calculated rate of mutation was 3.6 nucleotide
substitutions per year (2.3 x 10(-3) substitutions per site per year).
Thirty-two percent of these mutations resulted in amino acid substitutions, and
the remainder were silent mutations. Analysis of virus isolates from China and
elsewhere showed no significant differences in their rate of evolution, genetic
diversity, or mean survival time. The nearly constant rate of change was
maintained through the two antigenic shifts, and there were no obvious changes
in the number or types of mutations associated with the changes in the surface
proteins. A detailed comparison of the changes that have occurred on the main
evolutionary path with those that have occurred on the side branches of the
phylogenetic tree was made. This showed that while 35% of the mutations on the
side branches resulted in amino acid changes, only 21% of those on the main
path affected the protein sequence. These results suggest that although the
rate of change of the human influenza virus nucleoprotein is much higher than
that previously described for avian influenza viruses, there are measurable
constraints on the evolution of the surviving virus lineage. Comparison of the
nucleoproteins of virus isolates adapted to chicken embryos with the
nucleoproteins of those grown only in MDCK cells revealed no consistent differences
between the virus pairs. Thus, although the nucleoprotein is known to be
critical for host specificity, its adaptation to growth in eggs apparently
involves no immediate selective pressures, such as are found with
hemagglutinin.
Descriptors: evolution, genes viral genetics, influenza A
virus human genetics, nucleoproteins, viral core proteins genetics, amino acid
sequence, cultured cells, chick embryo, cloning, molecular, molecular sequence
data, mutagenesis, polymerase chain reaction, sequence analysis, DNA, sequence
homology, amino acid, time factors, variation genetics.
Shu, L.L., Y.P. Lin, S.M. Wright, K.F. Shortridge,
and R.G. Webster (1994). Evidence for interspecies transmission and
reassortment of influenza A viruses in pigs in Southern China. Virology
202(2): 825-833. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The Asian/57, Hong Kong/68, and Russian/77
pandemics of this century appeared or reappeared in China. Interspecies
transmission and genetic reassortment of influenza viruses have been implicated
in the origin of these human pandemic influenzas viruses. Pigs have been
suspected to be the "mixing vessel" where reassortment occurs. To
investigate this possibility, 104 porcine influenza viruses collected at random
from Southern China from 1976 to 1982, including 32 H3N2 isolates and 72 H1N1
isolates, were studied using dot blot hybridization, partial sequencing, and
phylogenetic analysis. There were 29 of 32 H3N2 isolates characteristic of
viruses originally derived from humans; the other 3 isolates were reassortants
containing genes from porcine and human influenza viruses. Phylogenetic
analyses of the polymerase B1 (PB1) genes showed that interspecies transmission
from humans to pigs has happened multiple times in pigs in Southern China. All
72 H1N1 isolates were of porcine origin characteristic of classical porcine
H1N1 influenza virus. Analysis of 624 genes of porcine influenza viruses from
Southern China failed to detect any evidence for avian influenza virus genes.
This contrasts to what is currently found in Europe, where the majority of
porcine influenza virus isolates are of avian origin.
Descriptors: swine, Guangdong, Hong Kong, Taiwan,
mankind, influenza virus, swine
influenza virus, disease transmission, hosts, provenance, phylogeny, genes,
artiodactyla, Asia, biological competition, cell structure, China,
chromosomes, domestic animals, East Asia, evolution, influenza virus,
livestock, mammals, nucleus, parasitism,
pathogenesis, suidae, useful animals, viruses, pandemics, genetic
reassortment, virus mixing vessels, man.
Shu, L.P., G.B. Sharp, Y.P. Lin, E.C.J. Class, S.L.
Krauss, K.F. Shortridge, and R.G. Webster (1996). Genetic reassortment in
pandemic and interpandemic influenza viruses: A study of 122 viruses infecting
humans. European Journal of Epidemiology 12(1): 63-70. ISSN: 0393-2990.
NAL
Call Number: RA648.5.E97
Abstract: The human influenza pandemics of 1957 and
1968 were caused by reassortant viruses that possessed internal gene segments
from avian and human strains. Whether genetic reassortment of human and avian
influenza viruses occurs during interpandemic periods and how often humans are
infected with such reassortants is not known. To provide this information, we
used dot-blot hybridization, partial nucleotide sequencing and subsequent
phylogenetic analysis to examine the 6 internal genes of 122 viruses isolated
in humans between 1933 and 1992 primarily from Asia, Europe, and the Americas.
The internal genes of A/New Jersey/11/76 isolated from a human fatality at Fort
Dix, New Jersey in 1976 were found to be of porcine origin. Although none of
the geographically and temporally diverse collection of 122 viruses was an
avian-human or other reassortant, cognizance was made of the fact that there were
two isolates from children from amongst 546 influenza A isolates obtained from
The Netherlands from 1989-1994 which were influenza A reassortants containing
genes of avian origin, viruses which have infected European pigs since
1983-1985. Thus, genetic reassortment between avian and human influenza strains
does occur in the emergence of pandemic and interpandemic influenza A viruses.
However, in the interpandemic periods the reassortants have no survival
advantage, and the circulating interpandemic influenza viruses in humans do not
appear to accumulate avian influenza virus genes.
Descriptors: epidemiology, genetics, infection,
microbiology, public health, genetic reassortment genetics infection internal
genes interpandemic influenza virus interspecies transmission pandemic
influenza virus pathogen virology zoonotic infections.
Silim, A. (2003). Avian Influenza (H5N1): a menace
for humans? State of things [L'influenza aviaire (H5N1): une menace pour les
humains? Etat de la question]. Medecin Veterinaire Du Quebec 33(3): 122 123.
NAL
Call Number: SF602.M8
Descriptors: avian influenza virus, human, zoonoses,
diagnosis, disease distribution, disease prevalence, disease transmission,
epidemiology, poultry, zoonoses.
Simpson, V.R. (2002). Wild animals as reservoirs
of infectious diseases in the UK. Veterinary Journal 163(2):
128-146. ISSN: 1090-0233.
NAL
Call Number: SF601.V484
Abstract: This review aims to illustrate the extent to
which wildlife act as reservoirs of infectious agents that cause disease in
domestic stock, pet and captive animals and humans. More than 40 agents are
described. In the case of some of these, e.g. Cryptosporidium spp., Escherichia
coli O157 and malignant catarrhal fever, the current evidence is that
wildlife either does not act as a reservoir or is of limited importance.
However, in the case of many important diseases, including bovine tuberculosis,
Weil's disease, Lyme disease, avian influenza, duck virus enteritis and louping
ill, wild animals are considered to be the principal source of infection.
Wildlife may be involved in the epidemiology of other major diseases, such as
neosporosis, Johne's disease, mucosal disease and foot and mouth disease, but
further studies are needed. The UK would benefit from a more positive approach
to the study of wildlife and the infections they harbour.
Descriptors: epidemiology, infection, vector biology,
veterinary medicine, Cryptosporidium infection, parasitic disease,
transmission, Escherichia coli infection, bacterial disease,
transmission, Johne's disease, infectious disease, Lyme disease, bacterial
disease, Weil's disease, bacterial disease, avian influenza, viral disease,
bovine tuberculosis, bacterial disease, duck virus enteritis, digestive system
disease, viral disease, foot and mouth disease, viral disease, malignant
catarrhal fever, bacterial disease, neoplastic disease, mucosal disease,
infectious disease, neosporosis, infectious disease.
Sims, L. (2000). Did Hong Kong H5N1 really
threaten human health? World Poultry (Special): 13-14. ISSN: 1388-3119.
NAL
Call Number: SF481.M54
Descriptors: avian influenza virus, poultry, zoonoses,
disease transmission, human, Hong Kong.
Slingenbergh, J.I., M. Gilbert, K.I. de Balogh, and
W. Wint (2004). Ecological sources of zoonotic diseases. Revue Scientifique Et Technique Office
International Des Epizooties 23(2): 467-84.
ISSN: 0253-1933.
NAL
Call Number: SF781.R4
Abstract: Although of zoonotic origin, pathogens or
infections posing a global threat to human health such as human
immunodeficiency virus, severe acute respiratory syndrome or emerging influenza
type A viruses may actually have little in common with known, established
zoonotic agents, as these new agents merely underwent a transient zoonotic
stage before adapting to humans. Evolution towards person-to-person
transmission depends on the biological features of the pathogen, but may well
be triggered or facilitated by external factors such as changes in human
exposure. Disease emergence may thus be depicted as an evolutionary response to
changes in the environment, including anthropogenic factors such as new
agricultural practices, urbanisation, or globalisation, as well as climate
change. Here the authors argue that in the case of zoonotic diseases emerging in
livestock, change in agricultural practices has become the dominant factor
determining the conditions in which zoonotic pathogens evolve, spread, and
eventually enter the human population. Livestock pathogens are subjected to
pressures resulting from the production, processing and retail environment
which together alter host contact rate, population size and/or microbial
traffic flows in the food chain. This process is illustrated by two study
cases: a) livestock development in the 'Eurasian ruminant street' (the area
extending from central Asia to the eastern Mediterranean basin) and the
adjacent Arabian peninsula b) poultry production in Southeast Asia. In both
scenarios, environmental factors relating to demography, land pressure and
imbalances in production intensification have led to an unstable
epidemiological situation, as evidenced by the highly pathogenic avian
influenza upsurge early in 2004, when the main outbreaks were located in areas
which had both large scale, peri-urban commercial holdings and a high density
of smallholder poultry units.
Descriptors: physiological adaptation, agriculture
methods, animal diseases epidemiology, animal diseases transmission, animal
husbandry methods, animals, environment, molecular evolution, humans,
population density, population dynamics, world health, zoonoses.
Smirnov, Y.A., A.S. Lipatov, A.K. Gitelman, E.C.
Claas, and A.D. Osterhaus (2000). Prevention and treatment of
bronchopneumonia in mice caused by mouse-adapted variant of avian H5N2
influenza A virus using monoclonal antibody against conserved epitope in the HA
stem region. Archives of Virology 145(8): 1733-41. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: The effects of monoclonal antibody (MAb) C179
recognizing a conformational epitope in the middle of the hemagglutinine (HA)
stem region were examined in a mouse model in the experiments of prevention and
treatment of lethal bronchopneumonia caused by influenza A virus of H5 subtype.
To model the lethal infection, avian nonpathogenic strain A/mallard
duck/Pennsylvania/10218/84 (H5N2) was adapted to mice. This resulted in highly
pathogenic pneumovirulent mouse-adapted (MA) variant, which was characterized.
Three amino acid changes were found in the HA1 subunit of HA of MA virus. One
of these was located inside the region of the conformational epitope recognized
by MAb C179. However, this substitution was not significant for the recognition
of HA and virus neutralization by MAb C179 in vitro and in vivo.
Intraperitoneal administration of two different concentrations of MAb C179 one
day before or two days after the virus challenge significantly decreased
mortality rate. These results suggest that MAb C179 is efficient not only in
the prevention and treatment of H1 and H2 influenza virus bronchopneumonia, as
was reported previously, but also of H5-induced bronchopneumonia as well, and
demonstrate in vivo the existence of a common neutralizing epitope in the HAs
of these three subtypes.
Descriptors: antibodies, monoclonal therapeutic use,
antibodies, viral therapeutic use, bronchopneumonia therapy, hemagglutinin
glycoproteins, influenza virus immunology, influenza A virus avian genetics,
pneumonia, viral therapy, antibodies, monoclonal pharmacology, antibodies,
viral pharmacology, bronchopneumonia prevention and control, bronchopneumonia
virology, cell line, disease models, animal, dose response relationship, drug,
epitopes genetics, epitopes immunology, hemagglutinin glycoproteins, influenza
virus genetics, avian drug effects, avian immunology, mice, molecular sequence
data, neutralization tests, pneumonia, viral prevention and control, pneumonia,
viral virology, sensitivity and specificity.
Smirnov, Y.A., A.S. Lipatov, R. Van Beek, A.K.
Gitelman, A.D. Osterhaus, and E.C. Claas (2000). Characterization of
adaptation of an avian influenza A (H5N2) virus to a mammalian host. Acta
Virologica 44(1): 1-8. ISSN: 0001-723X.
NAL
Call Number: 448.3 AC85
Abstract: We have used the mouse model to monitor the
acquisition of virulence of a non-pathogenic influenza A virus upon adaptation
to a new mammalian host. An avian strain, A/Mallard duck/Pennsylvania/10218/84
(H5N2) (Mld/PA/84) was adapted to mice by 23 serial lung-to-lung passages until
a highly virulent mouse-adapted (MA) variant (Mld/PA/84-MA) emerged. This MA
variant was characterized and compared to the parental strain as well as some
of its intermediate passage variants. MA variant caused bronchopneumonia in
mice with a high mortality rate (the virulence of Mld/PA/84-MA measured as log
(EID50/LD50) was 1.75), while the parental, avirulent strain Mld/PA/84 did not
cause illness and mortality in mice (log (EID50/LD50) was 7.25).
Hemagglutination-inhibition (HAI) test with a set of hemagglutinin- (HA) specific
monoclonal antibodies (MAbs) revealed antigenic differences between the
parental strain and MA variant. Mld/PA/84-MA reacted with HA-specific MAbs in
higher titers than the parental strain. The HA genes of the parental strain
Mld/PA/84, the 1st, 3rd, 8th, and 15th intermediate passage variants, and
Mld/PA/84-MA were sequenced. Three amino acid changes at positions 203, 273 and
320 were determined in the HA of MA variant. The first of them, Leu-->Pro
(320), appeared in the HA stem region at the 8th passage. Two other in the HA1
globular region (Ser-->Phe (203) and Glu-->Gly (273)) appeared at the
15th passage. All of these substitutions were associated with the increase of
viral infectivity for mouse lungs and changes in the HA antigenicity. The potential
role of these changes in HA with respect to the process of viral interspecies
transmission and acquisition of virulence for new host is discussed.
Descriptors: adaptation, physiological genetics,
bronchopneumonia virology, influenza A virus avian pathogenicity, amino acid
substitution, antigenic variation, chick embryo, genes viral, hemagglutination
tests, hemagglutinins viral genetics, hemagglutinins viral immunology,
hydrogen-ion concentration, avian genetics, avian immunology, lung immunology,
lung microbiology, mice, molecular sequence data, virulence.
Snyder, M.H., A.J. Buckler White, W.T. London, E.L.
Tierney, and B.R. Murphy (1987). The avian influenza virus nucleoprotein
gene and a specific constellation of avian and human virus polymerase genes
each specify attenuation of avian-human influenza A/Pintail/79 reassortant
viruses for monkeys. Journal of Virology 61(9): 2857-63.
ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Reassortant viruses which possessed the
hemagglutinin and neuraminidase genes of wild-type human influenza A viruses
and the remaining six RNA segments (internal genes) of the avian
A/Pintail/Alberta/119/79 (H4N6) virus were previously found to be attenuated in
humans. To study the genetic basis of this attenuation, we isolated influenza
A/Pintail/79 X A/Washington/897/80 reassortant viruses which contained human
influenza virus H3N2 surface glycoprotein genes and various combinations of
avian or human influenza virus internal genes. Twenty-four reassortant viruses
were isolated and first evaluated for infectivity in avian (primary chick
kidney [PCK]) and mammalian (Madin-Darby canine kidney [MDCK]) tissue culture
lines. Reassortant viruses with two specific constellations of viral polymerase
genes exhibited a significant host range restriction of replication in
mammalian (MDCK) tissue culture compared with that in avian (PCK) tissue
culture. The viral polymerase genotype PB2-avian (A) virus, PB1-A virus, and
PA-human (H) virus was associated with a 900-fold restriction, while the viral
polymerase genotype PB2-H, PB1-A, and PA-H was associated with an 80,000-fold
restriction of replication in MDCK compared with that in PCK. Fifteen
reassortant viruses were subsequently evaluated for their level of replication
in the respiratory tract of squirrel monkeys, and two genetic determinants of
attenuation were identified. First, reassortant viruses which possessed the
avian influenza virus nucleoprotein gene were as restricted in replication as a
virus which possessed all six internal genes of the avian influenza A virus
parent, indicating that the nucleoprotein gene is the major determinant of
attenuation of avian-human A/Pintail/79 reassortant viruses for monkeys.
Second, reassortant viruses which possessed the viral polymerase gene
constellation of PB2-H, PB1-A, and PA-H, which was associated with the greater
degree of host range restriction in vitro, were highly restricted in
replication in monkeys. Since the avian-human influenza reassortant viruses
which expressed either mode of attenuation in monkeys replicated to high titer
in eggs and in PCK tissue culture, their failure to replicate efficiently in
the respiratory epithelium of primates must be due to the failure of viral
factors to interact with primate host cell factors. The implications of these
findings for the development of live-virus vaccines and for the evolution of
influenza A viruses in nature are discussed.
Descriptors: genes viral, influenza A virus genetics,
nucleoproteins genetics, RNA directed DNA polymerase genetics, viral core
proteins, viral proteins genetics, genotype, influenza A virus pathogenicity,
phenotype, saimiri, temperature, virulence, virus replication.
Snyder, M.H., M.L. Clements, R.F. Betts, R. Dolin,
A.J. Buckler White, E.L. Tierney, and B.R. Murphy (1986). Evaluation of live
avian-human reassortant influenza A H3N2 and H1N1 virus vaccines in
seronegative adult volunteers. Journal of Clinical Microbiology
23(5): 852-7. ISSN: 0095-1137.
NAL
Call Number: QR46.J6
Abstract: An avian-human reassortant influenza A virus
deriving its genes coding for the hemagglutinin and neuraminidase from the
human influenza A/Washington/897/80 (H3N2) virus and its six
"internal" genes from the avian influenza A/Mallard/NY/6750/78 (H2N2)
virus (i.e., a six-gene reassortant) was previously shown to be safe,
infectious, nontransmissible, and immunogenic as a live virus vaccine in adult
humans. Two additional six-gene avian-human reassortant influenza viruses
derived from the mating of wild-type human influenza A/California/10/78 (H1N1)
and A/Korea/1/82 (H3N2) viruses with the avian influenza A/Mallard/NY/78 virus
were evaluated in seronegative (hemagglutination inhibition titer, less than or
equal to 1:8) adult volunteers for safety, infectivity, and immunogenicity to
determine whether human influenza A viruses can be reproducibly attenuated by
the transfer of the six internal genes of the avian influenza A/Mallard/NY/78
virus. The 50% human infectious dose was 10(4.9) 50% tissue culture infectious
doses for the H1N1 reassortant virus and 10(5.4) 50% tissue culture infectious
doses for the H3N2 reassortant virus. Both reassortants were satisfactorily
attenuated with only 5% (H1N1) and 2% (H3N2) of infected vaccines receiving
less than 400 50% human infectious doses developing illness. Consistent with
this level of attenuation, the magnitude of viral shedding after inoculation
was reduced 100-fold (H1N1) to 10,000-fold (H3N2) compared with that produced
by wild-type virus. The duration of virus shedding by vaccines was one-third
that of controls receiving wild-type virus. At 40 to 100 50% human infectious
doses, virus-specific immune responses were seen in 77 to 93% of volunteers.
When vaccinees who has received 10(7.5) 50% tissue culture infectious doses of
the H3N2 vaccine were experimentally challenged with a homologous wild-type
human virus only 2 of 19 (11%) vaccinees became ill compared with 7 of 14 (50%)
unvaccinated seronegative controls ( P < 0.025; protective efficacy, 79%).
Thus, three different virulent human influenza A viruses have been
satisfactorily attenuated by the acquisition of the six internal genes of the
avian influenza A/Mallard/NY/78 virus. The observation that this donor virus
can reproducibly attenuate human influenza A viruses indicates that avian-human
influenza A reassortants should be further studied as potential live influenza
A virus vaccines.
Descriptors: hemagglutinins viral immunology, influenza A
virus avian immunology, human immunology, neuraminidase immunology, viral
vaccines immunology, adult, antibodies, viral biosynthesis, avian growth and
development, human growth and development, virus replication.
Snyder, M.H., M.L. Clements, D. Herrington, W.T.
London, E.L. Tierney, and B.R. Murphy (1986). Comparison by studies in
squirrel monkeys, chimpanzees, and adult humans of avian-human influenza A
virus reassortants derived from different avian influenza virus donors. Journal
of Clinical Microbiology 24(3): 467-9.
ISSN: 0095-1137.
NAL
Call Number: QR46.J6
Abstract: We evaluated the abilities of three different
avian influenza A viruses to attenuate the wild-type human influenza
A/Korea/1/82 (H3N2) virus in squirrel monkeys, chimpanzees, and adult
seronegative human volunteers. Two of these, avian influenza A/Mallard/NY/78
and A/Mallard/Alberta/76 viruses, appeared to be satisfactory donors of
attenuating genes for the production of live influenza A reassortant virus
vaccines for human use because the reassortants exhibited an acceptable balance
between attenuation and immunogenicity.
Descriptors: influenza A virus avian immunology, human
immunology, influenza vaccine immunology, antibodies, viral biosynthesis, avian
genetics, avian physiology, human genetics, human physiology, Pan
troglodytes, recombination, genetic, saimiri, vaccines, attenuated, virus
replication.
Snyder, M.H., E.H. Stephenson, H. Young, C.G. York,
E.L. Tierney, W.T. London, R.M. Chanock, and B.R. Murphy (1986). Infectivity
and antigenicity of live avian-human influenza A reassortant virus: comparison
of intranasal and aerosol routes in squirrel monkeys. Journal of
Infectious Diseases 154(4): 709-11.
ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Descriptors: antibodies, viral biosynthesis, influenza A
virus avian immunology, human immunology, influenza vaccine immunology,
administration, intranasal, aerosols, immunization, avian pathogenicity, human
pathogenicity, saimiri, vaccines, attenuated, virulence.
Sokolova, N.L. (1974). Dynamics of the formation
of antihaemagglutinins to various types of avian influenza virus in the serum
of sheep. Sbornik Nauchnykh Trudov Moskovskaya Veterinarnaya Akademiya
73(Pt. 1): 148-149.
Descriptors: avian influenza virus, antibodies, immune
serum, immunization, sheep serum, antihemagglutinins.
Stech, J., X. Xiong, C. Sholtissek, and R.G. Webster
(1999). Independence of evolutionary and mutational rates after transmission
of avian influenza viruses to swine. Journal of Virology 73(3):
1878-1884. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: In 1979, an H1N1 avian influenza virus
crossed the species barrier, establishing a new lineage in European swine.
Because there is no direct or serologic evidence of previous H1N1 strains in
these pigs, these isolates provide a model for studying early evolution of
influenza viruses. The evolutionary rates of both the coding and noncoding
changes of the H1N1 swine strains are higher than those of human and classic
swine influenza A viruses. In addition, early H1N1 swine isolates show a marked plaque heterogeneity that consistently
appears after a few passages. The presence of a mutator mutation was postulated
(C. Scholtissek, S. Ludwig, and W. M. Fitch, Arch. Virol. 131:237-250, 1993) to
account for these observations and the successful establishment of an avian H1N1
strain in swine. To address this question, we calculated the mutation rates of
A/Mallard/New York/6750/78 (H2N2) and A/Swine/Germany/2/81 (H1N1) by using the
frequency of amantadine-resistant mutants. To account for the inherent variability of estimated mutation
rates, we used a probabilistic model for the statistical analysis. The
resulting estimated mutation rates of the two strains were not significantly
different. Therefore, an increased mutation rate due to the presence of a
mutator mutation is unlikely to have led to the successful introduction of
avian H1N1 viruses in European swine.
Descriptors: evolution and adaptation, infection,
molecular genetics, evolutionary rates, independence mutational rates,
independence viral transmission.
Steinhoff, M.C., N.A. Halsey, L.F. Fries, M.H.
Wilson, J. King, B.A. Burns, R.K. Samorodin, V. Perkis, B.R. Murphy, and M.L.
Clements (1991). The A/Mallard/6750/78 avian-human, but not the A/Ann
Arbor/6/60 cold-adapted, influenza A/Kawasaki/86 (H1N1) reassortant virus
vaccine retains partial virulence for infants and children. Journal of
Infectious Diseases 163(5): 1023-8.
ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Abstract: Characteristics of avian-human (ah) and
cold-adapted (ca) influenza A/Kawasaki/9/86 (H1N1) reassortant vaccine viruses
were compared in 37 seronegative adults and 122 seronegative infants and
children. The 50% human infectious dose (HID50) in infants and children was
10(2.9) and 10(2.6) TCID50 for the ah and ca vaccine, respectively. The ah influenza
A/Kawasaki/9/86 reassortant was reactogenic: 24% of infants and children
infected with greater than or equal to 100 HID50 had fever greater than or
equal to 39.4 degrees C. Since H3N2 ah vaccines were previously shown to be
adequately attenuated, it is reasonable to suggest that the genes that code for
hemagglutinin and neuraminidase of the H1N1 virus apparently influence the
reactogenicity of reassortant viruses derived from the avian influenza
A/Mallard/New York/6750/78 donor virus. Because this avian virus does not
reproducibly confer a satisfactory level of attenuation to each subtype of
influenza A virus, it is not a suitable donor virus for attenuation of
wild-type influenza viruses. In contrast, the ca A/Ann Arbor/6/60 donor virus
reliably confers attenuation characteristics to a variety of H1N1 and H3N2
influenza A viruses.
Descriptors: influenza prevention and control, influenza A
virus avian immunology, human immunology, influenza vaccine adverse effects,
adult, child, preschool, infant, influenza etiology, avian pathogenicity, human
pathogenicity, vaccines, attenuated adverse effects, vaccines, synthetic
adverse effects, virulence.
Steinhoff, M.C., N.A. Halsey, M.H. Wilson, B.A.
Burns, R.K. Samorodin, L.F. Fries, B.R. Murphy, and M.L. Clements (1990). Comparison
of live attenuated cold-adapted and avian-human influenza A/Bethesda/85 (H3N2)
reassortant virus vaccines in infants and children. Journal of
Infectious Diseases 162(2): 394-401.
ISSN: 0022-1899.
NAL
Call Number: 448.8 J821
Abstract: Randomized, placebo-controlled studies with
10(3)-10(7) 50% tissue-culture infectious dose (TCID50) of avian-human (ah) and
cold-adapted (ca) influenza A/Bethesda/85 (H3N2) reassortant viruses were
completed in 106 seronegative young children 6-48 months of age. Although the
reassortants differed in six of eight RNA segments, they exhibited similar
properties in level of attenuation, infectivity, immunogenicity, and efficacy.
The 50% human infectious dose was 10(4.6) TCID50 for ah and 10(4.4) for ca
vaccines. Both reassortants were satisfactorily attenuated with restricted
replication and were no more reactogenic than placebo. The mean peak titer of
virus shed was 10(1.5) (ah) to 10(2.0) (ca) TCID50/ml, and each of 37 isolates
tested retained their characteristic vaccine phenotypes. Infection with ah or
ca virus conferred immunity to experimental challenge with homologous virus.
These findings indicate that both ah and ca influenza A/Bethesda/85 (H3N2)
reassortants should be suitable vaccine candidates for use in healthy infants
and young children.
Descriptors: influenza prevention and control, influenza A
virus avian immunology, human immunology, influenza vaccine immunology,
antibodies, viral biosynthesis, child, preschool, cold, dose response relationship,
immunologic, double blind method, enzyme linked immunosorbent assay,
immunoglobulin G biosynthesis, infant, avian isolation and purification, human
isolation and purification, randomized controlled trials, vaccines, attenuated
immunology, vaccines, synthetic immunology.
Stephenson, I., K.G. Nicholson, J.M. Wood, M.C.
Zambon, and J.M. Katz (2004). Confronting the avian influenza threat:
vaccine development for a potential pandemic. Lancet Infectious Diseases
4(8): 499-509. ISSN: 1473-3099.
Abstract: Sporadic human infection with avian influenza
viruses has raised concern that reassortment between human and avian subtypes
could generate viruses of pandemic potential. Vaccination is the principal
means to combat the impact of influenza. During an influenza pandemic the
immune status of the population would differ from that which exists during
interpandemic periods. An emerging pandemic virus will create a surge in
worldwide vaccine demand and new approaches in immunisation strategies may be
needed to ensure optimum protection of unprimed individuals when vaccine
antigen may be limited. The manufacture of vaccines from pathogenic avian
influenza viruses by traditional methods is not feasible for safety reasons as
well as technical issues. Strategies adopted to overcome these issues include
the use of reverse genetic systems to generate reassortant strains, the use of
baculovirus-expressed haemagglutinin or related non-pathogenic avian influenza
strains, and the use of adjuvants to enhance immunogenicity. In clinical
trials, conventional surface-antigen influenza virus vaccines produced from
avian viruses have proved poorly immunogenic in immunologically naive
populations. Adjuvanted or whole-virus preparations may improve immunogenicity
and allow sparing of antigen.
Descriptors: disease outbreaks prevention and control,
influenza immunology, influenza A virus, avian immunology, influenza vaccines
immunology, avian influenza immunology, poultry diseases immunology, influenza
prevention and control, influenza A virus, avian influenza genetics, influenza
vaccines therapeutic use, avian influenza prevention and control, poultry,
poultry diseases prevention and control, reassortant viruses immunology,
vaccination, vaccines, attenuated immunology, attenuated therapeutic use.
Stephenson, I.N.K.G., R. Gluck, R. Mischler, R.W.
Newman, A.M. Palache, N.Q. Verlander, F. Warburton, J.M. Wood, and M.C. Zambon
(2003). Safety and antigenicity of whole virus and subunit influenza A/Hong
Kong/1073/99 (H9nN2) vaccine in healthy adults: phase I randomised trial. Lancet
362(9400): 1959-1966. ISSN: 0099-5355.
NAL
Call Number: 448.8 L22
Descriptors: clinical immunology, humans, infection, vaccination,
clinical techniques, immune response.
Stohr, K. (2005). Avian influenza and
pandemics--research needs and opportunities. New England Journal of
Medicine 352(4): 405-7. ISSN:
1533-4406.
NAL
Call Number: 448.8 N442
Descriptors: disease outbreaks prevention and control,
influenza transmission, influenza A virus, avian influenza classification,
avian genetics, biomedical research, birds, disease transmission prevention and
control, influenza epidemiology, influenza virology, avian influenza transmission,
swine, zoonoses transmission.
Stohr, K. and M. Esveld (2004). Public health.
Will vaccines be available for the next influenza pandemic? Science
306(5705): 2195-6. ISSN: 1095-9203.
NAL
Call Number: 470 Sci2
Descriptors: disease outbreaks, influenza epidemiology,
influenza prevention and control, influenza vaccines supply and distribution,
clinical trials, drug industry, influenza virology, influenza A virus, avian
immunology, avian pathogenicity, human immunology, influenza vaccines administration
and dosage, influenza vaccines economics, international cooperation, population
surveillance, public policy, World Health Organization.
Suarez, D.L., M.L. Perdue, N. Cox, T. Rowe, C.
Bender, J. Huang, and D.E. Swayne (1998). Comparisons of highly virulent
H5N1 influenza A viruses isolated from humans and chickens from Hong Kong. Journal
of Virology 72(8): 6678-88. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: Genes of an influenza A (H5N1) virus from a
human in Hong Kong isolated in May 1997 were sequenced and found to be all
avian-like (K. Subbarao et al., Science 279:393-395, 1998). Gene sequences of
this human isolate were compared to those of a highly pathogenic chicken H5N1
influenza virus isolated from Hong Kong in April 1997. Sequence comparisons of
all eight RNA segments from the two viruses show greater than 99% sequence
identity between them. However, neither isolate's gene sequence was closely
(>95% sequence identity) related to any other gene sequences found in the
GenBank database. Phylogenetic analysis demonstrated that the nucleotide
sequences of at least four of the eight RNA segments clustered with Eurasian
origin avian influenza viruses. The hemagglutinin gene phylogenetic analysis
also included the sequences from an additional three human and two chicken H5N1
virus isolates from Hong Kong, and the isolates separated into two closely
related groups. However, no single amino acid change separated the chicken
origin and human origin isolates, but they all contained multiple basic amino
acids at the hemagglutinin cleavage site, which is associated with a highly
pathogenic phenotype in poultry. In experimental intravenous inoculation
studies with chickens, all seven viruses were highly pathogenic, killing most
birds within 24 h. All infected chickens had virtually identical pathologic
lesions, including moderate to severe diffuse edema and interstitial
pneumonitis. Viral nucleoprotein was most frequently demonstrated in vascular
endothelium, macrophages, heterophils, and cardiac myocytes. Asphyxiation from
pulmonary edema and generalized cardiovascular collapse were the most likely
pathogenic mechanisms responsible for illness and death. In summary, a small
number of changes in hemagglutinin gene sequences defined two closely related
subgroups, with both subgroups having human and chicken members, among the
seven viruses examined from Hong Kong, and all seven viruses were highly
pathogenic in chickens and caused similar lesions in experimental inoculations.
Descriptors: chickens virology, influenza virology,
influenza A virus avian genetics, human genetics, amino acid sequence, cell
line, chick embryo, dogs, hemagglutinin glycoproteins, influenza virus
genetics, Hong Kong epidemiology, influenza epidemiology, avian classification,
avian pathogenicity, human classification, human isolation and purification,
human pathogenicity, molecular sequence data, phylogeny, virulence.
Suarez, D.L., P.R. Woolcock, A.J. Bermudez, and D.A.
Senne (2002). Isolation from turkey breeder hens of a reassortant H1N2
influenza virus with swine, human, and avian lineage genes. Avian
Diseases 46(1): 111-121. ISSN:
0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: Type A influenza viruses can infect a wide
range of birds and mammals, but influenza in a particular species is usually
considered to be species specific. However, infection of turkeys with swine
H1N1 viruses has been documented on several occasions. This report documents
the isolation of an H1N2 influenza virus from a turkey breeder flock with a sudden
drop in egg production. Sequence analysis of the virus showed that it was a
complex reassortant virus with a mix of swine-, human-, and avian-origin
influenza genes. A swine influenza virus with a similar gene complement was
recently reported from pigs in Indiana. Isolation and identification of the
virus required the use of nonconventional diagnostic procedures. The virus was
isolated in embryonated chicken eggs by the yolk sac route of inoculation
rather than by the typical chorioallantoic sac route. Interpretation of
hemagglutination-inhibition test results required the use of turkey rather than
chicken red blood cells, and identification of the neuraminidase subtype
required the use of alternative reference sera in the neuraminidase-inhibition
test. This report provides additional evidence that influenza viruses can cross
species and cause a disease outbreak, and diagnosticians must be aware that the
variability of influenza viruses can complicate the isolation and
characterization of new isolates.
Descriptors: infection, molecular genetics, veterinary
medicine, hemagglutination inhibition test identification method, neuraminidase
inhibition test identification method, sequence analysis molecular genetic
method, yolk sac inoculation culture method, gene complement host specificity.
Subbarao, K. (2001). Influenza A infections: from
chickens to humans. Clinical Microbiology Newsletter 23(2):
9-13. ISSN: 0196-4399.
Descriptors: diagnosis, disease transmission,
epidemiology, outbreaks, poultry, avian influenza virus, humans, China, Hong
Kong.
Subbarao, K. and J. Katz (2000). Avian influenza
viruses infecting humans. Cellular and Molecular Life Sciences CMLS
57(12): 1770-84. ISSN: 1420-682X.
NAL
Call Number: QH301.C45
Abstract: Avian species, particularly waterfowl, are
the natural hosts of influenza A viruses. Influenza viruses bearing each of the
15 hemagglutinin and nine neuraminidase subtypes infect birds and serve as a
reservoir from which influenza viruses or genes are introduced into the human
population. Viruses with novel hemagglutinin genes derived from avian influenza
viruses, with or without other accompanying avian influenza virus genes, have
the potential for pandemic spread when the human population lacks protective
immunity against the new hemagglutinin. Avian influenza viruses were thought to
be limited in their ability to directly infect humans until 1997, when 18 human
infections with avian influenza H5N1 viruses occurred in Hong Kong. In 1999,
two human infections with avian influenza H9N2 viruses were also identified in
Hong Kong. These events established that avian viruses could infect humans
without acquiring human influenza genes by reassortment in an intermediate host
and highlighted challenges associated with the detection of human immune
responses to avian influenza viruses and the development of appropriate
vaccines.
Descriptors: influenza virology, influenza A virus avian
pathogenicity, antibodies, viral biosynthesis, birds, disease models, animal,
disease outbreaks, fowl plague epidemiology, Hong Kong epidemiology, immunity,
cellular, influenza epidemiology, influenza immunology, avian genetics, avian
immunology, influenza vaccine isolation and purification, mammals, models,
biological, phylogeny, species specificity, virulence.
Subbarao, K., A. Klimov, J. Katz, H. Regnery, W. Lim,
H. Hall, M. Perdue, D. Swayne, C.
Bender, J. Huang, M. Hemphill, T. Rowe, M. Shaw, X. Xu, K. Fukuda, and N. Cox
(1998). Characterization of an avian influenza A (H5N1) virus isolated from
a child with a fatal respiratory illness. Science 279(5349):
393-6. ISSN: 0036-8075.
NAL
Call Number: 470 Sci2
Abstract: An avian H5N1 influenza A virus (A/Hong
Kong/156/97) was isolated from a tracheal aspirate obtained from a 3-year-old
child in Hong Kong with a fatal illness consistent with influenza. Serologic
analysis indicated the presence of an H5 hemagglutinin. All eight RNA segments
were derived from an avian influenza A virus. The hemagglutinin contained
multiple basic amino acids adjacent to the cleavage site, a feature
characteristic of highly pathogenic avian influenza A viruses. The virus caused
87.5 to 100 percent mortality in experimentally inoculated White Plymouth Rock
and White Leghorn chickens. These results may have implications for global
influenza surveillance and planning for pandemic influenza.
Descriptors: hemagglutinin glycoproteins, influenza virus
genetics, influenza virology, influenza A virus avian genetics, avian
pathogenicity, amino acid sequence, cell line, chickens, child, preschool,
disease outbreaks, fatal outcome, fowl plague virology, genes viral,
hemagglutinin glycoproteins, influenza virus chemistry, Hong Kong epidemiology,
influenza epidemiology, avian isolation and purification, molecular sequence
data, neuraminidase genetics, phylogeny, virulence, virus replication.
Subbarao, K. and M.W. Shaw (2000). Molecular
aspects of avian influenza (H5N1) viruses isolated from humans. Reviews
in Medical Virology 10(5): 337-48.
ISSN: 1052-9276.
Descriptors: fowl plague transmission, influenza virology,
influenza A virus avian genetics, avian isolation and purification, birds, fowl
plague virology, genes viral, influenza diagnosis, avian classification, avian
pathogenicity.
Subbarao, K., R.G. Webster, Y. Kawaoka, and B.R.
Murphy (1995). Are there alternative avian influenza viruses for generation
of stable attenuated avian-human influenza A reassortant viruses? Virus
Research 39(2-3): 105-18. ISSN:
0168-1702.
NAL
Call Number: QR375.V6
Abstract: The present study evaluated gull influenza A
viruses as donors of attenuating genes for the production of live, attenuated
influenza A H1N1 and H3N2 avian-human (ah) reassortant viruses for use as
vaccines to prevent disease due to influenza A viruses in humans. The
previously evaluated duck influenza A viruses were abandoned as donors of
attenuating avian influenza virus genes because clinical evaluation of H1N1 and
H3N2 ah reassortant virus vaccines derived from duck viruses documented
residual virulence of H1N1 reassortants for seronegative infants and young
children. Gull influenza A viruses occupy an independent ecologic niche and are
rarely isolated from species other than gulls. The possibility of using gull
influenza A viruses as donors of internal gene segments in ah reassortant
viruses was evaluated in the present study using three different gull viruses
and three human influenza A viruses. Gull-human H3N2 reassortant influenza A
viruses with the desired 6-2 genotype (six internal avian influenza virus genes
and the two human influenza virus surface glycoprotein genes) were readily
generated and were found to be attenuated for squirrel monkeys and chimpanzees.
However, ah reassortant viruses with gull and human influenza A H1N1 genes were
difficult to generate, and reassortants that had the desired genotype of six
gull virus genes with human influenza A H1 and N1 genes were not isolated
despite repeated attempts. The gull PB2, NP and NS genes were not present in
any of the gull-human H1N1 reassortants generated. The under-representation of
these three gene segments suggests that reassortants bearing one or more of
these three gene segments might have reduced viability indicative of a
functional incompatibility in their gene products. The difficulties encountered
in the generation of a 6-2 gull-human H1N1 reassortant virus are sufficient to
conclude that the gull influenza A viruses tested would not be useful as donors
of sets of six internal genes to attenuate human influenza A viruses. This
study also identifies influenza virus gene segments that appear to be
incompatible for generation of reassortants. Elucidation of the molecular basis
of this restriction may provide information on intergenic interactions involved
in virion assembly or packaging.
Descriptors: influenza A virus avian genetics, human
genetics, reassortant viruses genetics, cell line, chick embryo, chickens,
dogs, genotype, Pan troglodytes, reassortant viruses isolation and
purification, reassortant viruses physiology, reproducibility of results,
saimiri, tissue culture, vaccines, attenuated genetics, vaccines, attenuated
isolation and purification, viral vaccines genetics, viral vaccines isolation
and purification, virus replication.
Suzuki, H. (2004). [Super pathogenic avian
influenza]. [Zasshi] Journal. Nihon Naika Gakkai 93(11):
2323-7. ISSN: 0021-5384.
Descriptors: chickens, influenza virology, avian influenza
A virus pathogenicity, avian influenza virology, poultry diseases virology, zoonoses
virology, acetamides therapeutic use, amantadine therapeutic use, antiviral
agents therapeutic use, disease outbreaks, influenza epidemiology, influenza
therapy, influenza transmission, influenza vaccines, avian influenza
epidemiology, avian influenza transmission, neuraminidase antagonists and
inhibitors, poultry diseases epidemiology, poultry diseases transmission,
sialic acids therapeutic use, zoonoses epidemiology, zoonoses transmission.
Swayne, D.E. (2000). Understanding the ecology and
epidemiology of avian influenza viruses: implications for zoonotic potential.
In: C. Brown and C. Bolin (editors), Emerging Diseases of Animals, ASM
Press: Washington, DC, p. 101-130. ISBN: 1555812015.
NAL
Call Number: SF781.E53 2000
Descriptors: Aves, virus transmission, avian influenza
viruses, ecology, epidemiology, zoonotic potential implications.
Syurin, V.N., N.G. Osidze, Z.Y. Chistova, and V.
Rodin Yu (1972). [Epizootiological potential of avian influenza virus.].
Veterinariia (8): 41-43.
NAL
Call Number: 41.8 V6426
Descriptors: avian influenza virus, poultry.
Takada, A., N. Kuboki, K. Okazaki, A. Ninomiya, H.
Tanaka, H. Ozaki, S. Itamura, H. Nishimura, M. Enami, M. Tashiro, K.F.
Shortridge, and H. Kida (1999). Avirulent Avian influenza virus as a vaccine
strain against a potential human pandemic. Journal of Virology
73(10): 8303-7. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: In the influenza H5N1 virus incident in Hong
Kong in 1997, viruses that are closely related to H5N1 viruses initially
isolated in a severe outbreak of avian influenza in chickens were isolated from
humans, signaling the possibility of an incipient pandemic. However, it was not
possible to prepare a vaccine against the virus in the conventional embryonated
egg system because of the lethality of the virus for chicken embryos and the
high level of biosafety therefore required for vaccine production. Alternative
approaches, including an avirulent H5N4 virus isolated from a migratory duck as
a surrogate virus, H5N1 virus as a reassortant with avian virus H3N1 and an
avirulent recombinant H5N1 virus generated by reverse genetics, have been
explored. All vaccines were formalin inactivated. Intraperitoneal immunization
of mice with each of vaccines elicited the production of hemagglutination-inhibiting
and virus-neutralizing antibodies, while intranasal vaccination without
adjuvant induced both mucosal and systemic antibody responses that protected
the mice from lethal H5N1 virus challenge. Surveillance of birds and animals, particularly
aquatic birds, for viruses to provide vaccine strains, especially surrogate
viruses, for a future pandemic is stressed.
Descriptors: influenza immunology, influenza A virus avian
immunology, influenza vaccine immunology, communicable disease control, disease
outbreaks, influenza prevention and control, influenza vaccine administration
and dosage, mice, vaccination.
Takahashi, T., Y. Suzuki, D. Nishinaka, N. Kawase, Y.
Kobayashi, K.I. Hidari, D. Miyamoto, C.T. Guo, K.F. Shortridge, and T. Suzuki
(2001). Duck and human pandemic influenza A viruses retain sialidase
activity under low pH conditions. Journal of Biochemistry 130(2):
279-83. ISSN: 0021-924X.
NAL
Call Number: 385 J822
Abstract: The majority of influenza A viruses isolated
from wild birds, but not humans, can replicate in the duck intestinal tract.
Here we demonstrate that all duck isolates tested universally retain sialidase
activities under low pH conditions independent of their neuraminidase (NA)
subtypes. In contrast, the sialidase activities of most isolates from humans
and pigs practically disappear below pH 4.5, with the exception of four human
pandemic viruses isolated in 1957 and 1968. Sequence comparisons among duck,
human, and swine N2 NA subtypes indicate that amino acids at positions 153,
253, 307, 329, 344, 347, 356, 368, 390, and 431 may be associated with the low
pH stability of duck and human pandemic N2 NAs. This finding suggests that the
low pH stability of duck influenza A virus NA may be a critical factor for replication
in the intestinal tract through the digestive tract of ducks, and that the
properties of NAs are important for understanding the epidemiology of the
influenza virus.
Descriptors: influenza virology, influenza A virus avian
enzymology, human enzymology, neuraminidase metabolism, ducks, enzyme
stability, hydrogen-ion concentration, influenza transmission, avian
physiology, human physiology, porcine enzymology, phylogeny, sequence analysis,
swine.
Tanaka, H., Park ChunHo, A. Ninomiya, H. Ozaki, A.
Takada, T. Umemura, and H. Kida (2003). Neurotropism of the 1997 Hong Kong
H5N1 influenza virus in mice. Veterinary Microbiology 95(1/2):
1-13. ISSN: 0378-1135.
NAL
Call Number: SF601.V44
Descriptors: disease transmission, encephalitis,
experimental infection, pathogenesis, pathogenicity, zoonoses, avian influenza
virus, influenza virus A, humans,
poultry, mice, China, Hong Kong.
Taubenberger, J.K., A.H. Reid, A.E. Krafft, K.E.
Bijwaard, and T.G. Fanning (1997). Initial genetic characterization of the
1918 "Spanish" influenza virus. Science 275(5307):
1793-6. ISSN: 0036-8075.
NAL
Call Number: 470 Sci2
Abstract: The "Spanish" influenza pandemic
killed at least 20 million people in 1918-1919, making it the worst infectious
pandemic in history. Understanding the origins of the 1918 virus and the basis
for its exceptional virulence may aid in the prediction of future influenza
pandemics. RNA from a victim of the 1918 pandemic was isolated from a
formalin-fixed, paraffin-embedded, lung tissue sample. Nine fragments of viral
RNA were sequenced from the coding regions of hemagglutinin, neuraminidase,
nucleoprotein, matrix protein 1, and matrix protein 2. The sequences are
consistent with a novel H1N1 influenza A virus that belongs to the subgroup of
strains that infect humans and swine, not the avian subgroup.
Descriptors: genes viral, influenza virology, influenza A
virus human genetics, porcine genetics, RNA viral genetics, algorithms, base
sequence, hemagglutinin glycoproteins, influenza virus genetics, history of
medicine, 20th century, influenza history, avian genetics, human
classification, human pathogenicity, porcine classification, porcine
pathogenicity, lung virology, molecular sequence data, neuraminidase genetics,
nucleoproteins genetics, phylogeny, polymerase chain reaction, viral core
proteins genetics, viral matrix proteins genetics, virulence.
Taubenberger, J.K. (2003 ). Fixed and frozen flu:
The 1918 influenza and lessons for the future. Avian Diseases
47(Special Issue): 789-791. ISSN:
0005-2086.
NAL
Call Number: 41.8 Av5
Descriptors: epidemiology, infection, Spanish influenza,
epidemiology, infectious disease, respiratory system disease, viral disease,
avian influenza, epidemiology, infectious disease, respiratory system disease,
viral disease, 1918 Spanish influenza pandemic virulence.
Taylor, H.R. and A.J. Turner (1977). A case report
of fowl plague keratoconjunctivitis. British Journal of Ophthalmology
61(2): 86-8. ISSN: 0007-1161.
Abstract: A case of human fowl plague
keratoconjunctivitis occurred after accidental laboratory exposure. The
conjunctivitis was characterised by follicle formation and a mucopurulent
discharge, and ran a self-limiting course over two weeks. The keratitis was of
an unusual type and consisted of small intraepithelial opacities, which
appeared after one week and resolved completely over the next three weeks. The
infection, confirmed by viral culture, was produced by Dutch strain (Hav 1 Neq
1) of fowl plague virus.
Descriptors: influenza A virus avian isolation and
purification, keratoconjunctivitis etiology, laboratory infection etiology,
adult, keratoconjunctivitis microbiology.
Thornley, M. (2004). Avian influenza flies across
Asia. Australian Veterinary Journal 82(1-2): 5. ISSN: 0005-0423.
NAL
Call Number: 41.8 Au72
Descriptors: chickens, avian influenza, epidemiology,
prevention and control, Asia epidemiology, Australia.
Tian, S.F., A.J. Buckler White, W.T. London, L.J.
Reck, R.M. Chanock, and B.R. Murphy (1985). Nucleoprotein and membrane
protein genes are associated with restriction of replication of influenza
A/Mallard/NY/78 virus and its reassortants in squirrel monkey respiratory
tract. Journal of Virology 53(3): 771-5. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: An avian influenza A virus,
A/Mallard/NY/6750/78(H2N2), was restricted in in replication in the respiratory
tract of squirrel monkeys. Avian-human influenza A reassortant viruses
possessing the six RNA segments coding for nonsurface proteins (i.e., internal
genes) of this avian virus were as restricted in replication in squirrel
monkeys as their avian influenza parent. These findings indicated that
restriction of replication of the avian influenza virus is a function of one or
more of its internal genes. For an investigation of which of the avian
influenza genes was responsible for restricted replication in the respiratory
tract of primates, reassortant viruses were produced that contained human
influenza virus surface antigens from the A/Udorn/72(H3N2) virus and one or
more of the internal genes derived from the avian influenza virus parent.
Avian-human reassortant influenza A viruses containing only the nucleoprotein
or matrix protein RNA segment from the avian influenza virus parent were as
restricted in their growth as an avian-human influenza reassortant virus
containing each of the six avian influenza internal genes. In addition, an
avian-human influenza reassortant virus possessing only the avian RNA 1 and nonstructural
genes (which by themselves do not specify restricted replication) manifested a
significant reduction of virus replication in squirrel monkey tracheas. Thus,
the avian nucleoprotein and matrix genes appear to play a major role in the
host range restriction exhibited by the A/Mallard/78 virus and its
reassortants, but the combination of RNA 1 and nonstructural genes also
contributes to restriction of replication.
Descriptors: genes viral, influenza A virus genetics,
nucleoproteins genetics, viral proteins genetics, virus replication, birds
microbiology, heat, influenza A virus physiology, RNA viral analysis, saimiri
microbiology, trachea microbiology, viral matrix proteins.
Tian, S.F., A.J. Buckler White, W.T. London, L.J.
Reck, R.M. Chanock, and B.R. Murphy (1986). [Nucleoprotein and membrane
protein genes responsible for restriction of replication of influenza
A/Mallard/NY/78 virus and its reassortants in the respiratory tract of squirrel
monkeys]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao Acta Academiae Medicinae
Sinicae 8(1): 1-6. ISSN: 1000-503X.
Descriptors: genes viral, influenza A virus avian
genetics, recombination, genetic, virus replication, avian physiology, membrane
proteins genetics, nucleoproteins genetics, respiratory system microbiology,
saimiri.
To, K.F., P.K. Chan, K.F. Chan, W.K. Lee, W.Y. Lam,
K.F. Wong, N.L. Tang, D.N. Tsang, R.Y. Sung, T.A. Buckley, J.S. Tam, and A.F.
Cheng (2001). Pathology of fatal human infection associated with avian
influenza A H5N1 virus. Journal of Medical Virology 63(3): 242-6
. ISSN: 0146-6615.
Abstract: Eighteen cases of human influenza A H5N1
infection were identified in Hong Kong from May to December 1997. Two of the
six fatal cases had undergone a full post-mortem which showed reactive
hemophagocytic syndrome as the most prominent feature. Other findings included
organizing diffuse alveolar damage with interstitial fibrosis, extensive
hepatic central lobular necrosis, acute renal tubular necrosis and lymphoid
depletion. Elevation of soluble interleukin-2 receptor, interleukin-6 and
interferon-gamma was demonstrated in both patients, whereas secondary bacterial
pneumonia was not observed. Virus detection using isolation, reverse
transcription-polymerase chain reaction and immunostaining were all negative.
It is postulated that in fatal human infections with this avian subtype,
initial virus replication in the respiratory tract triggers hypercytokinemia
complicated by the reactive hemophagocytic syndrome. These findings suggest
that the pathogenesis of influenza A H5N1 infection might be different from
that of the usual human subtypes H1-H3.
Descriptors: influenza pathology, influenza virology,
influenza A virus avian isolation and purification, adolescent, adult, bone
marrow pathology, cytokines blood, disease outbreaks, fatal outcome, Hong Kong
epidemiology, influenza epidemiology, lung pathology, lymphoid tissue
pathology, postmortem changes.
Tracey, J.P., R. Woods, D. Roshier, P. West, and G.R.
Saunders (2004). The role of wild birds in the transmission of avian
influenza for Australia: an ecological perspective. Emu 104(2):
109-124. ISSN: 0158-4197.
Descriptors: ecology, wild birds, vector biology, avian
influenza, transmission, Australia.
Trampuz, A., R.M. Prabhu, T.F. Smith, and L.M.
Baddour (2004). Avian influenza: a new pandemic threat? Mayo Clinic
Proceedings 79(4): 523-30. ISSN:
0025-6196.
NAL
Call Number: 448.8 M45
Abstract: In December 2003, the largest outbreak of
highly pathogenic avian influenza H5N1 occurred among poultry in 8 Asian
countries. A limited number of human H5N1 infections have been reported from
Vietnam and Thailand, with a mortality rate approaching 70%. Deaths have
occurred in otherwise healthy young individuals, which is reminiscent of the
1918 Spanish influenza pandemic. The main presenting features were fever,
pneumonitis, lymphopenia, and diarrhea. Notably, sore throat, conjunctivitis,
and coryza were absent. The H5N1 strains are resistant to amantadine and
rimantadine but are susceptible to neuraminidase inhibitors, which can be used
for treatment and prophylaxis. The widespread epidemic of avian influenza in
domestic birds increases the likelihood for mutational events and genetic
reassortment. The threat of a future pandemic from avian influenza is real.
Adequate surveillance, development of vaccines, outbreak preparedness, and
pandemic influenza planning are important. This article summarizes the current
knowledge on avian influenza, including the virology, epidemiology, diagnosis,
and management of this emerging disease.
Descriptors: communicable diseases, emerging epidemiology,
disease outbreaks statistics and numerical data, influenza A virus, avian
genetics, avian influenza pathogenicity, avian influenza epidemiology, poultry
diseases epidemiology, world health, amantadine therapeutic use, antiviral
agents therapeutic use, Asia epidemiology, communicable diseases, emerging
diagnosis, emerging prevention and control, emerging virology, disease
outbreaks prevention and control, drug resistance, multiple, viral, family
characteristics, forecasting, avian influenza diagnosis, avian influenza
prevention and control, avian influenza virology, mutation genetics,
neuraminidase antagonists and inhibitors, patient isolation, population
surveillance, poultry, poultry diseases diagnosis, poultry diseases prevention
and control, poultry diseases virology, recombination, genetics, rimantadine
therapeutic use, vaccination, zoonoses epidemiology, zoonoses virology.
Tran, T.H., T.L. Nguyen, T.D. Nguyen, T.S. Luong,
P.M. Pham, V.C. Nguyen, T.S. Pham, C.D. Vo, T.Q. Le, T.T. Ngo, B.K. Dao, P.P.
Le, T.T. Nguyen, T.L. Hoang, V.T. Cao, T.G. Le, D.T. Nguyen, H.N. Le, K.T.
Nguyen, H.S. Le, V.T. Le, D. Christiane, T.T. Tran, J. de Menno, C. Schultsz, P. Cheng, W. Lim,
P. Horby, J. Farrar, and World Health Organization International Avian
Influenza Investigative Team (2004). Avian influenza A (H5N1) in 10 patients
in Vietnam. New England Journal of Medicine 350(12): 1179-88. ISSN: 1533-4406.
NAL
Call Number: 448.8 N442
Descriptors: fowl plague transmission, influenza virology,
influenza A virus avian genetics, avian isolation and purification, adolescent,
adult, anti bacterial agents therapeutic use, antiviral agents therapeutic use,
chickens virology, child, preschool, ducks virology, influenza epidemiology,
influenza radiography, influenza therapy, lung radiography, RNA viral analysis,
reverse transcriptase polymerase chain reaction, treatment outcome, Vietnam
epidemiology.
Trapman, P., R. Meester, and H. Heesterbeek (2004). A
branching model for the spread of infectious animal diseases in varying
environments. Journal of Mathematical Biology 49(6): 553-76. ISSN: 0303-6812.
NAL
Call Number: QH323.5.J6
Abstract: This paper is concerned with a stochastic
model, describing outbreaks of infectious diseases that have potentially great
animal or human health consequences, and which can result in such severe
economic losses that immediate sets of measures need to be taken to curb the
spread. During an outbreak of such a disease, the environment that the
infectious agent experiences is therefore changing due to the subsequent
control measures taken. In our model, we introduce a general branching process
in a changing (but not random) environment. With this branching process, we
estimate the probability of extinction and the expected number of infected
individuals for different control measures. We also use this branching process
to calculate the generating function of the number of infected individuals at
any given moment. The model and methods are designed using important infections
of farmed animals, such as classical swine fever, foot-and-mouth disease and
avian influenza as motivating examples, but have a wider application, for
example to emerging human infections that lead to strict quarantine of cases
and suspected cases (e.g. SARS) and contact and movement restrictions.
Descriptors: classical swine fever epidemiology, classical
swine fever virus growth and development, veterinary disease outbreaks, biological
models, classical swine fever prevention and control, classical swine fever
transmission, epidemiologic methods, Netherlands epidemiology, stochastic
processes, swine.
Treanor, J.J., M.H. Snyder, W.T. London, and B.R.
Murphy (1989). The B allele of the NS gene of avian influenza viruses, but
not the A allele, attenuates a human influenza A virus for squirrel monkeys.
Virology 171(1): 1-9. ISSN:
0042-6822.
NAL
Call Number: 448.8 V81
Abstract: The nonstructural (NS) genes of avian
influenza A viruses have been divided into two groups on the basis of
nucleotide sequence homology, which we have referred to here as alleles A and
B. We sequenced the NS genes of eight additional avian influenza A viruses in
order to define the differences between these two alleles more thoroughly. Four
of the viruses had NS gene sequences which resembled that of A/FPV/Rostock/34
and belonged to allele A while the other four viruses had NS gene sequences
more similar to that of A/Duck/Alberta/76 and belonged to allele B. There was
approximately 90% sequence homology within alleles and 72% homology between
alleles. As previously reported the NS genes of human influenza A viruses
belong to allele A. We constructed single gene avian-human reassortant
influenza A viruses containing an allele A or B NS gene segment from an avian
influenza A virus and all other genes from a human influenza A virus and tested
these reassortants for their ability to grow in the respiratory tract of a
nonhuman primate. Reassortants containing an avian NS gene segment of allele B
were significantly restricted in growth in the respiratory tract of squirrel
monkeys while reassortants with an allele A NS gene segment were not. The
divergent evolution of the B NS allele in birds may have resulted in gene products
which do not function optimally in cooperation with genes from a human virus in
viral replication in primate respiratory epithelium.
Descriptors: capsid genetics, influenza A virus avian
genetics, human growth and development, viral core proteins genetics, alleles,
amino acid sequence, base sequence, genes viral, human genetics, molecular
sequence data, nasopharynx microbiology, saimiri microbiology, sequence
homology, nucleic acid, trachea microbiology, viral nonstructural proteins,
virus replication.
Treanor, J.J., E.L. Tierney, W.T. London, and B.R.
Murphy (1991). Characterization of the attenuating M and NP gene segments of
the avian influenza A/Mallard/78 virus during in vitro production of
avian-human reassortant vaccine viruses and after replication in humans and
primates. Vaccine 9(7): 495-501.
ISSN: 0264-410X.
NAL
Call Number: QR189.V32
Abstract: A unique requirement for live attenuated
reassortant influenza vaccines is the need to generate new reassortant vaccine
viruses with the appearance of each new antigenic variant. Thus, the
attenuation phenotype conferred by the attenuated donor influenza virus must
remain genetically stable during the generation of each new reassortant vaccine
virus. In this study we used nucleotide sequence analysis to evaluate the
genetic stability of the attenuating M and NP genes of the avian influenza
A/Mallard/NY/6750/78 attenuated donor virus during the in vitro generation and
subsequent in vivo replication of avian-human (AH) influenza A reassortant vaccine
viruses in monkeys and humans. Nucleotide sequence changes in the M and NP
genes occurred at a rate of approximately 0.61 substitutions/1000
nt/reassortant during in vitro generation of four AH reassortant viruses. Only
two nucleotide sequence changes occurred in the M and NP gene segments of four
isolates of H1N1 or H3N2 AH vaccine viruses following 6-8 days of replication
in seronegative children, and neither change affected amino acids previously
identified as playing a potential role in attenuation. In addition, there were
no changes in the nucleotide sequence of the M and NP genes of single gene AH
reassortant viruses following five serial passages in squirrel monkeys.
Finally, there was no change in the level or duration of replication of the
single gene reassortant viruses in the upper or lower respiratory tract of
monkeys following serial passage.(ABSTRACT TRUNCATED AT 250 WORDS)
Descriptors: influenza A virus avian genetics, influenza
vaccine genetics, nucleoproteins, viral core proteins genetics, viral matrix
proteins genetics, base sequence, cloning, molecular, avian pathogenicity,
avian physiology, human genetics, human pathogenicity, human physiology,
molecular sequence data, mutation
genetics, polymerase chain reaction, recombination, genetic physiology,
saimiri, vaccines, attenuated genetics, vaccines, synthetic genetics, virus
replication genetics.
Treanor, J.J., B.E. Wilkinson, F. Masseoud, J. Hu
Primmer, R. Battaglia, D. O'Brien, M. Wolff, G. Rabinovich, W. Blackwelder, and
J.M. Katz (2001). Safety and immunogenicity of a recombinant hemagglutinin
vaccine for H5 influenza in humans. Vaccine 19(13-14): 1732-7. ISSN: 0264-410X.
NAL
Call Number: QR189.V32
Abstract: Recent outbreaks of avian influenza in humans
have demonstrated the need for vaccines for influenza viruses with pandemic
potential. Recombinant hemagglutinins are an attractive option for such
vaccines because they do not require handling potentially highly pathogenic
influenza viruses for vaccine production. In order to evaluate the
immunogenicity, optimum dosing and timing of administration of a recombinant
baculovirus-expressed H5 HA (rH5) in humans, 147 healthy adults were assigned
randomly to receive intramuscular rH5 as two doses of 25, 45 or 90 microg each,
one dose of 90 microg followed by a dose of 10 microg, or two doses of placebo,
at intervals between doses of 21, 28 or 42 days. All doses of rH5 were well
tolerated. The rH5 vaccine was modestly immunogenic at high dose. Neutralizing
antibody responses to a titer of 1:80 or greater were seen in 23% (14/60) of
individuals after a single dose of 90 microg, and in 52% (15/29) after two
doses of 90 microg. Varying intervals between doses from 21 to 42 days had no
significant effect on antibody responses to vaccination. These results suggest
that baculovirus-expressed H5 HA can induce functional antibody in individuals
who have not had prior exposure to H5 viruses, but that further studies to
improve the immunogenicity of the vaccine are needed.
Descriptors: hemagglutinin glycoproteins, influenza virus
immunology, influenza A virus human immunology, influenza vaccine adverse
effects, influenza vaccine immunology, vaccines, synthetic adverse
effects, vaccines, synthetic immunology,
adult, antibodies, viral immunology, dose response relationship, immunologic,
enzyme linked immunosorbent assay, hemagglutinin glycoproteins, influenza virus
genetics, immunization schedule, kinetics, neutralization tests, vaccination.
Trinidad, J. (2004). Influenza Aviar: enfermedad
de variada severidad y consecuencias en las aves. [Avian influenza: disease of
varying severity and the consequences in birds]. Veterinaria Argentina 21(204):
287-289. ISSN: 0326-4629.
NAL
Call Number: SF604.V463
Descriptors: avian influenza virus, consequences, birds.
Tumova, B. and H.G. Pereira (1965). Genetic
interaction between influenza A viruses of human and animal origin. Virology
27(3): 253-61. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: orthomyxoviridae, ultraviolet rays, antigens,
birds, complement fixation tests, genetics, hemagglutination inhibition tests,
horses, influenza, influenza A virus avian, radiation effects, swine.
Tumova, B., E. Svandova, and G. Stumpa (1968). Findings
of antibodies to animal influenza viruses in human sera and their significance
for the study of interviral antigenic relationship. Journal of Hygiene,
Epidemiology, Microbiology, and Immunology 12(3): 284-95. ISSN: 0022-1732.
NAL
Call Number: 448.8 J826
Descriptors: antibodies analysis, antigens analysis,
orthomyxoviridae immunology, adult, age factors, aged, antigen antibody
reactions, depression, chemical, ducks, hemagglutination inhibition tests,
influenza A virus avian immunology, middle aged, neutralization tests, periodic
acid pharmacology, potassium pharmacology, turkeys.
Turner, A.J. (2004). The role of wild aquatic
birds in the epidemiology of avian influenza in Australia. Australian
Veterinary Journal 82(11): 713.
ISSN: 0005-0423.
NAL
Call Number: 41.8 Au72
Descriptors: epidemiological surveys, mutations,
outbreaks, pathogenicity, serological surveys, disease distribution, disease
prevalence, disease surveys, disease transmission, disease vectors, waterfowl,
wild birds, Anseriformes, avian influenza virus, Charadriiformes, ducks, fowl.
Ungchusak, K., P. Auewarakul, S.F. Dowell, R.
Kitphati, W. Auwanit, P. Puthavathana, M. Uiprasertkul, K. Boonnak, C.
Pittayawonganon, N.J. Cox, S.R. Zaki, P. Thawatsupha, M. Chittaganpitch, R.
Khontong, J.M. Simmerman, and S. Chunsutthiwat (2005). Probable
person-to-person transmission of avian influenza A (H5N1). New England
Journal of Medicine 352(4): 333-40.
ISSN: 1533-4406.
NAL
Call Number: 448.8 N442
Descriptors: disease transmission, vertical, influenza
transmission, influenza A virus, avian genetics, adult, child, fatal outcome,
influenza virology, avian influenza isolation and purification, avian influenza
transmission, lung radiography, phylogeny, poultry, reverse transcriptase
polymerase chain reaction, zoonoses transmission.
Uyeki, T.M., Y.H. Chong, J.M. Katz, W. Lim, Y.Y. Ho,
S.S. Wang, T.H. Tsang, W.W. Au, S.C. Chan, T. Rowe, J. Hu Primmer, J.C. Bell,
W.W. Thompson, C.B. Bridges, N.J. Cox, K.H. Mak, and K. Fukuda (2002). Lack
of evidence for human-to-human transmission of avian influenza A (H9N2) viruses
in Hong Kong, China 1999. Emerging Infectious Diseases 8(2):
154-9. ISSN: 1080-6040.
NAL
Call Number: RA648.5.E46
Abstract: In April 1999, isolation of avian influenza A
(H9N2) viruses from humans was confirmed for the first time. H9N2 viruses were
isolated from nasopharyngeal aspirate specimens collected from two children who
were hospitalized with uncomplicated, febrile, upper respiratory tract
illnesses in Hong Kong during March 1999. Novel influenza viruses have the
potential to initiate global pandemics if they are sufficiently transmissible
among humans. We conducted four retrospective cohort studies of persons exposed
to these two H9N2 patients to assess whether human-to-human transmission of
avian H9N2 viruses had occurred. No serologic evidence of H9N2 infection was
found in family members or health-care workers who had close contact with the
H9N2-infected children, suggesting that these H9N2 viruses were not easily
transmitted from person to person.
Descriptors: disease transmission, horizontal statistics
and numerical data, disease transmission, patient to professional statistics
and numerical data, fowl plague transmission, influenza A virus avian isolation
and purification, avian pathogenicity, antibodies, viral blood, birds, child,
preschool, cohort studies, fowl plague immunology, Hong Kong epidemiology,
infant, avian immunology, retrospective studies.
van Eijk, M., M.R. White, J.J. Batenburg, A.B.
Vaandrager, L.M. van Golde, H.P. Haagsman, and K.L. Hartshorn (2004). Interactions
of influenza A virus with sialic acids present on porcine surfactant protein D.
American Journal of Respiratory Cell and Molecular Biology 30(6):
871-9. ISSN: 1044-1549.
Abstract: Pigs can be infected with both human and
avian influenza A virus (IAV) strains and are therefore considered to be
important intermediates in the emergence of new IAV strains due to mixing of
viral genes derived from human, avian, or porcine influenza viruses. These
reassortant strains may have potential to cause pandemic influenza outbreaks in
humans. The innate immune response against IAV plays a significant role in
containment of IAV in the airways. We studied the interactions of IAV with
porcine surfactant protein D (pSP-D), an important component of this first line
defense system. Hemagglutination inhibition analysis shows that the distinct
interactions of pSP-D with IAV mediated by the N-linked carbohydrate moiety in
the carbohydrate recognition domain of pSP-D depend on the terminal sialic
acids (SAs) present on this carbohydrate. Analysis by both lectin staining and
by cleavage with linkage-specific sialidases shows that the carbohydrate of
pSP-D is exclusively sialylated with alpha(2,6)-linked SAs, in contrast to
surfactant protein A, which contains both alpha(2,3)- and alpha(2,6)-linked SAs
on its N-linked carbohydrate. Enzymatic modification of the SA-linkages present
on pSP-D demonstrates that the type of SA-linkage is important for its
hemagglutination-inhibitory activity, and correlates with receptor-binding
specificity of the IAV strains. The SAs present on pSP-D appear especially
important for interactions with poorly glycosylated IAV strains. It remains to
be elucidated to what extent the unique sialylation profile of pSP-D is
involved in host range control of IAV in pigs, and whether it facilitates
adaptation of avian or human IAV strains that can contribute to the production
of reassortant strains in pigs.
Descriptors: influenza A virus metabolism, pulmonary
surfactant associated protein D chemistry, sialic acids metabolism, swine,
carbohydrate conformation, carbohydrate sequence, chickens, hemagglutination
inhibition tests, molecular sequence data, molecular structure, neuraminidase
metabolism, pulmonary surfactant associated protein A chemistry, pulmonary
surfactant associated protein A metabolism, pulmonary surfactant associated
protein D metabolism, pulmonary surfactants chemistry, receptors, cell surface,
sialic acids chemistry.
van Rooijen, J. (2004). Veterinair vooroordeel.
[Veterinary pre-judgement]. Tijdschrift Voor Diergeneeskunde
129(11): 381-2. ISSN: 0040-7453.
NAL
Call Number: 41.8 T431
Descriptors: animal husbandry methods, avian influenza
prevention and control, poultry diseases prevention and control, animal
husbandry standards, hygiene, avian influenza transmission, poultry, poultry
diseases transmission, zoonoses.
van Veen, L. (2004). Verslag symposium aviaire
influenza 'Dierenarts vogelvrij door vogelgriep?' [Report of the symposium on
avian influenza. 'Veterinarians bird free due to avian influenza?'. Tijdschrift
Voor Diergeneeskunde 129(21): 733-4.
ISSN: 0040-7453.
NAL
Call Number: 41.8 T431
Descriptors: disease outbreaks veterinary, avian
influenza, prevention and control, avian influenza transmission, public health,
zoonoses, birds, disease outbreaks prevention and control, feces virology,
avian imortality, risk factors, vaccination veterinary.
Vogel, G. (1998). Sequence offers clues to deadly
flu. Science 279(5349): 324.
ISSN: 0036-8075.
NAL
Call Number: 470 Sci2
Descriptors: hemagglutinin glycoproteins, influenza virus
genetics, influenza virology, influenza A virus avian genetics, avian
pathogenicity, chickens, child, preschool, disease outbreaks, fowl plague
virology, genes viral, hemagglutinin glycoproteins, influenza virus chemistry,
Hong Kong epidemiology, influenza epidemiology, influenza transmission, avian
physiology, sequence analysis, DNA, virus replication.
Von Hoyningen Huene, V., C. Scholtissek, and V. Von
Hoyningen Huene (1983). Low genetic mixing between avian influenza viruses
of different geographic regions; brief report. Archives of Virology
76(1): 63-67. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Descriptors: RNA, epidemiology, avian influenza virus,
genetic mixing, report.
Walli, T.K. and Keshab Barman (2004). Prevention
and containment of transmittable diseases from livestock to man - a global challenge.
Indian Dairyman 56(2): 37-43.
ISSN: 0019-4603.
NAL
Call Number: 44.8 In282
Descriptors: bovine spongiform encephalopathy, avian
influenza virus, Coronavirus, disease control, disease distribution, disease
prevalence, disease prevention, epidemiology, livestock, zoonoses, human,
prions.
Ward, P., I. Small, J. Smith, P. Suter, and R.
Dutkowski (2005). Oseltamivir (Tamiflu(R)) and its potential for use in the
event of an influenza pandemic. Journal of Antimicrobial Chemotherapy
55(Suppl. 1): i5-i21. ISSN: 0305-7453.
NAL
Call Number: RM260.J6
Abstract: Recent cross species transmission of avian
influenza has highlighted the threat of pandemic influenza. Oseltamivir
(Tamiflu((R) has been shown to be effective in the treatment and prevention of
epidemic influenza infection in adults, adolescents and children (>/= 1
year). Although oseltamivir has not been approved for prophylactic use in
children, it has been shown to be effective. Oseltamivir is also active against
avian influenza virus strains. Evidence suggests that lower doses or shorter
durations of treatment/chemoprophylaxis other than those approved may not be
effective and may contribute to emergence of viral resistance. Safety data from
dose ranging studies show that 5 day courses of 150 mg twice daily for
treatment and 6 week courses of 75 mg twice daily for prophylaxis were as well
tolerated as the approved dose regimens. The use of oseltamivir in a pandemic
is influenced by the goals of the pandemic plan developed by the responsible Government
and Health Authority. To optimize use of antiviral medications, processes will
be needed to collect, collate and report outcome data from treated patients
and/or from use for chemoprophylaxis of pandemic influenza during the
first-wave outbreaks. If oseltamivir is included in a national or regional
pandemic plan, stockpiling of the material, either in the form of capsules or
the bulk active pharmaceutical ingredient will be necessary. In the absence of
a stockpile, there is no guarantee that an adequate supply of oseltamivir will
be available.
Descriptors: pharmacology, infection, pulmonary medicine,
human medicine, oseltamivir, Tamiflu, adults, adolescents, children, pandemic
influenza.
Watts, J. (2004). Asian nations step up action to
curb spread of avian influenza. Outbreak is spreading at an unprecendented
speed, WHO says, and nowhere can be considered safe. Lancet 363(9406): 373. ISSN: 1474-547X.
NAL
Call Number: 448.8 L22
Descriptors: chickens, disease outbreaks veterinary, influenza
epidemiology, influenza A virus, avian, influenza, avian epidemiology,
southastern Asia epidemiology, child, influenza prevention and control,
influenza virology, avian influenza prevention and control, avian influenza
transmission, world health organization.
Webby, R.J., D.R. Perez, J.S. Coleman, Y. Guan, J.H.
Knight, E.A. Govorkova, L.R. McClain Moss, J.S. Peiris, J.E. Rehg, E.I.
Tuomanen, and R.G. Webster (2004). Responsiveness to a pandemic alert: use
of reverse genetics for rapid development of influenza vaccines. Lancet 363(9415): 1099-103. ISSN: 1474-547X.
NAL
Call Number: 448.8 L22
Abstract: BACKGROUND: In response to the emergence of
severe infection capable of rapid global spread, WHO will issue a pandemic
alert. Such alerts are rare; however, on Feb 19, 2003, a pandemic alert was
issued in response to human infections caused by an avian H5N1 influenza virus,
A/Hong Kong/213/03. H5N1 had been noted once before in human beings in 1997 and
killed a third (6/18) of infected people. The 2003 variant seemed to have been
transmitted directly from birds to human beings and caused fatal pneumonia in
one of two infected individuals. Candidate vaccines were sought, but no
avirulent viruses antigenically similar to the pathogen were available, and the
isolate killed embryonated chicken eggs. Since traditional strategies of
vaccine production were not viable, we sought to produce a candidate reference
virus using reverse genetics. METHODS: We removed the polybasic aminoacids that
are associated with high virulence from the haemagglutinin cleavage site of
A/Hong Kong/213/03 using influenza reverse genetics techniques. A reference
vaccine virus was then produced on an A/Puerto Rico/8/34 (PR8) backbone on
WHO-approved Vero cells. We assessed this reference virus for pathogenicity in
in-vivo and in-vitro assays. FINDINGS: A reference vaccine virus was produced
in Good Manufacturing Practice (GMP)-grade facilities in less than 4 weeks from
the time of virus isolation. This virus proved to be non-pathogenic in chickens
and ferrets and was shown to be stable after multiple passages in embryonated
chicken eggs. INTERPRETATION: The ability to produce a candidate reference
virus in such a short period of time sets a new standard for rapid response to
emerging infectious disease threats and clearly shows the usefulness of reverse
genetics for influenza vaccine development. The same technologies and
procedures are currently being used to create reference vaccine viruses against
the 2004 H5N1 viruses circulating in Asia.
Descriptors: disease outbreaks prevention and control,
influenza vaccines immunology, orthomyxoviridae immunology, orthomyxoviridae
infections prevention and control, antibodies, viral immunology, Asia
epidemiology, birds, communicable disease control methods, drug design, genetic
engineering, Hong Kong epidemiology, influenza A virus, avian immunology, human
immunology, avian influenza prevention and control, avian influenza virology,
orthomyxoviridae chemistry, orthomyxoviridae growth and development,
orthomyxoviridae infections immunology, orthomyxoviridae infections virology,
plasmids immunology, poultry diseases immunology, poultry diseases prevention
and control, poultry diseases virology, reassortant viruses chemistry,
reassortant viruses growth and development, reassortant viruses immunology,
transformation, genetic immunology, virulence factors isolation and
purification.
Webby, R.J., S.L. Swenson, S.L. Krauss, P.J. Gerrish,
S.M. Goyal, and R.G. Webster (2000). Evolution of swine H3N2 influenza
viruses in the United States. Journal of Virology 74(18):
8243-51. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: During 1998, severe outbreaks of influenza
were observed in four swine herds in the United States. This event was unique
because the causative agents, H3N2 influenza viruses, are infrequently isolated
from swine in North America. Two antigenically distinct reassortant viruses
(H3N2) were isolated from infected animals: a double-reassortant virus
containing genes similar to those of human and swine viruses, and a
triple-reassortant virus containing genes similar to those of human, swine, and
avian influenza viruses (N. N. Zhou, D. A. Senne, J. S. Landgraf, S. L.
Swenson, G. Erickson, K. Rossow, L. Liu, K.-J. Yoon, S. Krauss, and R. G.
Webster, J. Virol. 73:8851-8856, 1999). Because the U.S. pig population was
essentially naive in regard to H3N2 viruses, it was important to determine the
extent of viral spread. Hemagglutination inhibition (HI) assays of 4, 382 serum
samples from swine in 23 states indicated that 28.3% of these animals had been
exposed to classical swine-like H1N1 viruses and 20.5% had been exposed to the
triple-reassortant-like H3N2 viruses. The HI data suggested that viruses
antigenically related to the double-reassortant H3N2 virus have not become
widespread in the U.S. swine population. The seroreactivity levels in swine
serum samples and the nucleotide sequences of six additional 1999 isolates, all
of which were of the triple-reassortant genotype, suggested that H3N2 viruses
containing avian PA and PB2 genes had spread throughout much of the country.
These avian-like genes cluster with genes from North American avian viruses.
The worldwide predominance of swine viruses containing an avian-like internal
gene component suggests that these genes may confer a selective advantage in
pigs. Analysis of the 1999 swine H3N2 isolates showed that the internal gene
complex of the triple-reassortant viruses was associated with three recent
phylogenetically distinct human-like hemagglutinin (HA) molecules. Acquisition
of HA genes from the human virus reservoir will significantly affect the
efficacy of the current swine H3N2 vaccines. This finding supports continued
surveillance of U.S. swine populations for influenza virus activity.
Descriptors: influenza veterinary, influenza A virus,
porcine genetics, swine diseases virology, antigenic variation, cross
reactions, hemagglutination, viral, hemagglutinin glycoproteins, influenza virus
genetics, influenza epidemiology, influenza virology, avian genetics, human
genetics, porcine isolation and purification, phylogeny, reverse transcriptase
polymerase chain reaction, sequence homology, nucleic acid, seroepidemiologic
studies, swine, swine diseases epidemiology, United States epidemiology.
Webby, R.J. and R.G. Webster (2001). Emergence of
influenza A viruses. Philosophical Transactions of the Royal Society of
London. Series B Biological Sciences 356(1416): 1817-1828. ISSN: 0962-8436.
NAL
Call Number: 501 L84Pb
Abstract: Pandemic influenza in humans is a zoonotic
disease caused by the transfer of influenza A viruses or virus gene segments
from animal reservoirs. Influenza A viruses have been isolated from avian and
mammalian hosts, although the primary reservoirs are the aquatic bird
populations of the world. In the aquatic birds, influenza is asymptomatic, and
the viruses are in evolutionary stasis. The aquatic bird viruses do not
replicate well in humans, and these viruses need to reassort or adapt in an
intermediate host before they emerge in human populations. Pigs can serve as a
host for avian and human viruses and are logical candidates for the role of
intermediate host. The transmission of avian H5N1 and H9N2 viruses directly to humans
during the late 1990s showed that land-based poultry also can serve between
aquatic birds and humans as intermediate hosts of influenza viruses. That these
transmission events took place in Hong Kong and China adds further support to
the hypothesis that Asia is an epicentre for influenza and stresses the
importance of surveillance of pigs and live-bird markets in this area.
Descriptors: epidemiology, evolution and adaptation,
infection, vector biology, avian influenza, viral disease, pandemic influenza,
epidemiology, respiratory system disease, viral disease, evolutionary stasis,
viral transmission.
Webby, R.J. and R.G. Webster (2003). Are we ready
for pandemic influenza? Science 302(5650): 1519-1522. ISSN: 0036-8075.
NAL
Call Number: 470 Sci2
Descriptors: infection, public health, influenza,
monkeypox, severe acute respiratory syndrome, WHO, World Health Organization,
avian to human transmission, bioterrorism, influenza surveillance, pandemic
preparedness, zoonoses.
Webster, R.G. (1997). Influenza virus:
transmission between species and relevance to emergence of the next human
pandemic. Archives of Virology. Supplementum 13: 105-13. ISSN: 0939-1983.
NAL
Call Number: QR355.A72 no.13
Abstract: Although influenza viruses are not spread
from human to human through the conventional food chain, this is not
necessarily the case for the transmission of the precursors of the human
pandemic influenza viruses. Aquatic birds of the world are the reservoirs for
all influenza A viruses; the virus is spread by fecal-oral transmission in
untreated water. Influenza A viruses are frequently transmitted to domestic
poultry and two of the 15 subtypes H5 and H7 can become highly pathogenic and
have the capacity to decimate commercial poultry flocks. Less frequently, avian
influenza viruses are transmitted between species-to pigs, horses and sea
mammals. This transmission involves mutational, reassortant or recombinational
events and can occur through fecal contamination of unprocessed avian protein
or through the water. The transmission of avian influenza viruses or virus
genes to humans is postulated to occur through pigs that act as the
intermediate host. This involves either multiple mutational or reassortant
events and is believed to occur by airborne transmission. Once avian influenza
viruses are established in mammals, they are transmitted from animal to animal
by the respiratory airborne route. The transmission of avian influenza virus
from their reservoir in wild aquatic birds to domestic poultry and to mammalian
species including humans can be prevented by treatment of the water supply and
of avian protein sources with disinfectants or by heating. Agricultural
authorities have recommended the separation of wild aquatic and domestic
poultry and of pig and poultry farming. It is theoretically possible to reduce
the possibility of the next pandemic of influenza in humans by changes in
agricultural practices so that ducks are separated from pigs and people.
Descriptors: birds virology, influenza epidemiology, influenza
transmission, influenza A virus avian, zoonoses virology, disease reservoirs,
fowl plague transmission, fowl plague virology, influenza prevention and
control, influenza veterinary.
Webster, R.G. (2004). Wet markets--a continuing
source of severe acute respiratory syndrome and influenza? Lancet 363(9404): 234-6. ISSN: 1474-547X.
NAL
Call Number: 448.8 L22
Abstract: CONTEXT: Live-animal markets (wet markets)
provide a source of vertebrate and invertebrate animals for customers in
tropical and subtropical regions of the world. Wet markets sell live poultry,
fish, reptiles, and mammals of every kind. Live-poultry markets (mostly
chicken, pigeon, quail, ducks, geese, and a wide range of exotic wild-caught
and farm-raised fowl) are usually separated from markets selling fish or
red-meat animals, but the stalls can be near each other with no physical
separation. Despite the widespread availability of affordable refrigeration,
many Asian people prefer live animals for fresh produce. Wet markets are widespread
in Asian countries and in countries where Asian people have migrated.
Live-poultry markets were the source of the H5N1 bird-influenza virus that
transmitted to and killed six of 18 people in Hong Kong. STARTING POINT: Yi
Guan and colleagues (Science 2003; 302: 276-78) recently reported the isolation
of severe acute respiratory syndrome (SARS) coronavirus (CoV) from Himalayan
palm civets (Paguna larvata) in wet markets in Shenzen, southern China.
These researchers also found serological evidence of infection in raccoon dogs
(Nyctereutes procuyoinboides). Serological evidence for SARS CoV in
human beings working in these markets, taken together with the earliest cases
of SARS in restaurant workers, supports the contention of a potential zoonotic
origin for SARS. WHERE NEXT? Will SARS reappear? This question confronts
public-health officials worldwide, particularly infectious disease personnel in
those regions of the world most affected by the disease and the economic burden
of SARS, including China, Taiwan, and Canada. Will the virus re-emerge from wet
markets or from laboratories working with SARS CoV, or are asymptomatic
infections ongoing in human beings? Similar questions can be asked about a
pandemic of influenza that is probably imminent. Knowledge of the ecology of
influenza in wet markets can be used as an early-warning system to detect the
reappearance of SARS or pandemic influenza.
Descriptors: food industry methods, influenza
epidemiology, severe acute respiratory syndrome epidemiology, zoonoses
transmission, communicable diseases, emerging epidemiology, communicable
diseases, emerging transmission, communicable diseases, emerging veterinary,
disease outbreaks statistics and numerical data, disease reservoirs veterinary,
disease vectors, Hong Kong epidemiology, influenza transmission, influenza
veterinary, influenza A virus avian isolation and purification, poultry
diseases epidemiology, poultry diseases transmission, severe acute respiratory
syndrome transmission, severe acute respiratory syndrome veterinary, zoonoses
epidemiology, zoonoses virology.
Webster, R.G. and C.H. Campbell (1972). The in
vivo production of "new" influenza A viruses. II. In vivo isolation
of "new" viruses. Virology 48(2): 528-36. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: orthomyxoviridae isolation and purification,
recombination, genetic, antigens, heterophile, chickens, epitopes, genetics,
microbial, hemagglutination inhibition tests, hemagglutinins viral analysis,
hybridization, genetic, immunization, influenza A virus avian enzymology, avian
immunology, lung, neuraminidase, neutralization tests, orthomyxoviridae
enzymology, orthomyxoviridae immunology, tissue extracts, turkeys, viral
vaccines.
Webster, R.G., C.H. Campbell, and A. Granoff (1971). The
"in vivo" production of "new" influenza A viruses. I.
Genetic recombination between avian and mammalian influenza viruses. Virology
44(2): 317-28. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: orthomyxoviridae enzymology, orthomyxoviridae
growth and development, orthomyxoviridae immunology, orthomyxoviridae isolation
and purification, orthomyxoviridae pathogenicity, recombination, genetic,
antigens analysis, centrifugation, density gradient, chick embryo, fetal
membranes, fibroblasts, hemagglutination inhibition tests, hemagglutination
tests, hemagglutinins viral analysis, hybridization, genetic, immune sera,
influenza microbiology, influenza A virus avian enzymology, avian growth and
development, avian immunology, avian pathogenicity, lung microbiology,
neuraminidase analysis, rabbits, sucrose, swine, tissue culture, turkeys,
virulence, virus replication.
Webster, R.G., V.S. Hinshaw, W.J. Bean, and G. Sriram
(1980). Influenza viruses: transmission between species. Philosophical
Transactions of the Royal Society of London. Series B Biological Sciences
288(1029): 439-47. ISSN: 0962-8436.
NAL
Call Number: 501 L84Pb
Abstract: The only direct evidence for transmission of
influenza viruses between species comes from studies on swine influenza
viruses. Antigenically and genetically identical Hsw1N1 influenza viruses were
isolated from pigs and man on the same farm in Wisconsin, U.S.A. The isolation
of H3N2 influenza viruses from a wide range of lower animals and birds suggests
that influenza viruses of man can spread to the lower orders. Under some
conditions the H3N2 viruses can persist for a number of years in some species.
The isolation, from aquatic birds, of a large number of influenza A viruses
that possess surface proteins antigenically similar to the viruses isolated
from man, pigs and horses provides indirect evidence for inter-species
transmission. There is now a considerable body of evidence which suggests that
influenza viruses of lower animals and birds may play a role in the origin of
some of the pandemic strains of influenza A viruses. There is no direct
evidence that the influenza viruses in aquatic birds are transmitted to man,
but they may serve as a genetic pool from which some genes may be introduced
into humans by recombination. Preliminary evidence suggests that the molecular
basis of host range and virulence may be related to the RNA segments coding for
one of the polymerase proteins (P3) and for the nucleoprotein (NP).
Descriptors: influenza transmission, influenza A virus
genetics, orthomyxoviridae infections veterinary, birds microbiology, ducks
microbiology, fowl plague transmission, genes viral, influenza A virus avian
genetics, mammals microbiology, RNA viral genetics, recombination, genetic,
species specificity.
Webster, R.G., V.S. Hinshaw, W.J. Bean, K.L. Van
Wyke, J.R. Geraci, D.J. St Aubin, and G. Petursson (1981). Characterization
of an influenza A virus from seals. Virology 113(2): 712-24. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Descriptors: influenza A virus physiology,
orthomyxoviridae infections veterinary, pinnipedia microbiology, seals
microbiology, antigens, viral analysis, birds microbiology, conjunctivitis
etiology, genes viral, influenza A virus avian immunology, influenza A virus
isolation and purification, mammals microbiology, orthomyxoviridae infections
microbiology, RNA viral genetics, virus replication.
Webster, R.G., V.S. Hinshaw, W.J.J. Bean, B. Turner,
and K.F. Shortridge (1977). Influenza viruses from avian and porcine sources
and their possible role in the origin of human pandemic strains. Developments
in Biological Standardization 39: 461-8.
ISSN: 0301-5149.
NAL
Call Number: QR180.3.D4
Abstract: Studies on influenza viruses from feral ducks
trapped in Canada in August 1976, gave a 26% isolation rate from cloacal
samples of juvenile birds. Several different influenza A viruses were isolated,
some of which possessed novel hemagglutinin and/or neuraminidase antigens.
Influenza A viruses isolated from the rectum of feral ducks replicate in the
upper respiratory tract and also in the intestinal tract of feral and domestic
ducks. Representative human influenza viruses of the H0N1, H3N2 and Hsw1 N1
subtypes replicate in the upper respiratory tract of ducks but not in the
intestinal tract. The A/Hong Kong/68 [H3N2] influenza virus that has not been
isolated from man for several years was recently isolated from pigs originating
from The People's Republic of China. A/Victoria/3/75-like influenza viruses
that are currently circulating in man were also isolated from pigs. Both the
A/Hong Kong/68 and the A/Victoria/75-like viruses transmitted readily from pig
to pig in experimental studies. The susceptibility of ducks and pigs to
infection with human influenza viruses suggests that these animals may play an
important role in the ecology of influenza A viruses.
Descriptors: influenza etiology, influenza A virus avian
immunology, avian isolation and purification, porcine immunology, porcine
isolation and purification, influenza A virus isolation and purification,
antibodies, viral, cloaca microbiology, disease outbreaks, ducks microbiology,
hemagglutinins viral isolation and purification, swine microbiology, virus
replication.
Webster, R.G. and D.J. Hulse (2004). Microbial
adaptation and change: avian influenza. Revue Scientifique Et Technique
Office International Des Epizooties 23(2): 453-65. ISSN: 0253-1933.
NAL
Call Number: SF781.R4
Abstract: The evolution of influenza is a continuing
process involving viral and host factors. The increasing frequency of emergence
of the highly pathogenic H5N1, H7N3 and H7N7 influenza viruses and the
panzootic spread of H9N2 influenza virus, all of which can be potentially
transmitted to humans, are of great concern to both veterinary and human public
health officials. The question is how soon the next pandemic will emerge. A
convergence of factors, including the population densities of poultry, pigs and
humans, are likely factors affecting the evolution of the virus. Highly
concentrated poultry and pig farming, in conjunction with traditional live
animal or 'wet' markets, provide optimal conditions for increased mutation,
reassortment and recombination of influenza viruses. Strategies to reduce the
evolution of influenza and the emergence of pandemics include the separation of
species, increased biosecurity, the development of new vaccine strategies and
better basic knowledge of the virus. More effective co-operation between
scientists and veterinary and public health officials is required to achieve
these goals.
Descriptors: epidemiology, evolution and adaptation,
infection, public health, poultry, host disease vector, avian influenza virus,
drug therapy, etiology, immunology, prevention and control, transmission,
influenza, human, veterinary medicine, medical sciences.
Webster, R.G., Y. Kawaoka, and W.J. Bean (1989). What
is the potential of avirulent influenza viruses to complement a cleavable hemagglutinin
and generate virulent strains? Virology 171(2): 484-92. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: A large pool of avirulent influenza viruses
are maintained in the wild ducks and shorebirds of the world, but we know
little about their potential to become virulent. It is well established that
the hemagglutinin (HA) is pivitol in determining virulence and that a
constellation of other genes is also necessary (R. Rott, M. Orlich, and C.
Scholtissek, 1976, J. Virol. 19, 54-60). The question we are asking here is the
ability of avirulent influenza viruses to provide the gene constellation that
will complement the HA from a highly virulent virus and for the reassortant to
be virulent. Reassortant influenza viruses were prepared between ultraviolet
treated A/Chicken/Pennsylvania/1370/83 (H5N2) [Ck/Penn] and influenza viruses
from natural reservoirs. These viruses included examples of the predominant
subtypes in wild ducks, shorebirds, and domestic poultry. Attention was given
to the influenza viruses from live poultry markets, for it is possible that
these establishments may be important in mixing of influenza genes from
different species and the possible transmission to domestic and mammalian
species. The reassortants were genotyped by partial sequencing of each gene and
were tested for virulence in chickens. Each of the reassortants contained the
hemagglutinin and matrix (M) genes from Ck/Penn and a majority of genes from
the viruses from natural reservoirs indicating a preferential association
between the HA and M genes. The reassortants containing multiple genes from
wild ducks and a cleavable HA were avirulent indicating that the gene pool in
ducks may not have a high potential to provide genes that are potentially
virulent. In contrast, a disproportionate number of viruses from shorebirds and
all avirulent H5N2 influenza viruses from city markets provided a gene
constellation that in association with cleavable H5 HA were highly virulent in
chickens. An evolutionary tree based on oligonucleotide mapping established
that the H5N2 influenza viruses from birds in city markets are closely related.
Descriptors: hemagglutinins viral genetics, influenza A
virus avian pathogenicity, poultry diseases microbiology, animals, wild
microbiology, antibodies, monoclonal, birds microbiology, disease reservoirs, genes viral, hn protein,
hemagglutinins viral immunology, avian genetics, oligonucleotides analysis,
poultry microbiology, viral envelope proteins genetics, viral envelope proteins
immunology, viral matrix proteins genetics, virus replication.
Webster, R.G. (2001). A molecular whodunit. Science
293(5536): 1773-1775. ISSN: 0036-8075.
NAL
Call Number: 470 Sci2
Descriptors: molecular genetics, infection, epidemiology,
Spanish flu, viral disease, influenza, respiratory system disease, viral
disease, influenza virulence virology world population growth.
Webster, R.G., G.B. Sharp, and E.C.J. Claas (1995). Interspecies
Transmission of Influenza Viruses. American Journal of Respiratory and
Critical Care Medicine 152(4, Pt. 2): S25-S30. ISSN: 1073-449X.
Abstract: In this report we examine the hypothesis that
aquatic birds are the primordial source of all influenza viruses in other
species. Two partly overlapping reservoirs of influenza A viruses exist in
migrating waterfowl and shorebirds throughout the world. These species harbor
influenza viruses of all the known hemagglutinin and neuraminidase subtypes. In
contrast to the rapid, progressive changes in both the nucleotide and amino
acid sequences of mammalian virus gene lineages, avian virus genes show far
less variation and, in most cases, appear to be in evolutionary stasis. There
are periodic exchanges of influenza virus genes or whole viruses between
species, giving rise to pandemics of disease in humans, lower animals, and
birds. The periodic exchange of influenza viruses between species has been
illustrated by the appearance of new pandemic influenza viruses in humans,
including the Spanish influenza of 1918, the Asian influenza of 1957, and the
Hong Kong influenza of 1968. Transmission of avian influenza viruses to swine
in Europe in 1979 has resulted in the appearance of human-avian reassortant
influenza viruses in pigs in Italy and in children in the Netherlands. These
studies provide evidence supporting the possibility that pigs serve as a mixing
vessel for reassortment between influenza viruses in mammalian and avian hosts
and raise the question of whether the avian influenza viruses now circulating
in European swine are the precursors of the next human pandemic virus.
Descriptors: epidemiology, genetics, infection,
microbiology, vector biology, veterinary medicine, epidemiology genetics
vectors.
Weiss, J. (2004). Vogelgrippe -- Ubertragungsrate
auf den Menschen hoher als angenommen. [Bird flu - transmission rate to people
higher than supposed]. Pneumologie 58(11): 763. ISSN: 0934-8387.
Descriptors: influenza, avian transmission, zoonoses,
incidence, poultry.
Weiss, R.A. and A.J. McMichael (2004). Social and
environmental risk factors in the emergence of infectious diseases. Nature
Medicine 10(12 Suppl.): S70-6. ISSN:
1078-8956.
Abstract: Fifty years ago, the age-old scourge of
infectious disease was receding in the developed world in response to improved
public health measures, while the advent of antibiotics, better vaccines,
insecticides and improved surveillance held the promise of eradicating residual
problems. By the late twentieth century, however, an increase in the emergence
and re-emergence of infectious diseases was evident in many parts of the world.
This upturn looms as the fourth major transition in human-microbe relationships
since the advent of agriculture around 10,000 years ago. About 30 new diseases
have been identified, including Legionnaires' disease, human immunodeficiency
virus (HIV)/acquired immune deficiency syndrome (AIDS), hepatitis C, bovine
spongiform encephalopathy (BSE)/variant Creutzfeldt-Jakob disease (vCJD), Nipah
virus, several viral hemorrhagic fevers and, most recently, severe acute
respiratory syndrome (SARS) and avian influenza. The emergence of these
diseases, and resurgence of old ones like tuberculosis and cholera, reflects
various changes in human ecology: rural-to-urban migration resulting in
high-density peri-urban slums; increasing long-distance mobility and trade; the
social disruption of war and conflict; changes in personal behavior; and,
increasingly, human-induced global changes, including widespread forest
clearance and climate change. Political ignorance, denial and obduracy (as with
HIV/AIDS) further compound the risks. The use and misuse of medical technology
also pose risks, such as drug-resistant microbes and contaminated equipment or
biological medicines. A better understanding of the evolving social dynamics of
emerging infectious diseases ought to help us to anticipate and hopefully
ameliorate current and future risks.
Descriptors: communicable diseases diagnosis, communicable
diseases etiology, cardiovascular diseases diagnosis, cardiovascular diseases
etiology, communicable disease control, communicable diseases, emerging,
demography, disease outbreaks, health, international cooperation, neoplasms
diagnosis, neoplasms etiology, public health, risk, risk factors, time factors,
world health.
Weiss, R.A. (2001). The Leeuwenhoek Lecture 2001.
Animal origins of human infectious disease. Philosophical Transactions
of the Royal Society of London. Series B Biological Sciences 356(1410):
957-977. ISSN: 0962-8436.
NAL
Call Number: 501 L84Pb
Abstract: Since time immemorial animals have been a
major source of human infectious disease. Certain infections like rabies are
recognized as zoonoses caused in each case by direct animal-to-human
transmission. Others like measles became independently sustained with the human
population so that the causative virus has diverged from its animal progenitor.
Recent examples of direct zoonoses are variant Creutzfeldt-Jakob disease
arising from bovine spongiform encephalopathy, and the H5N1 avian influenza
outbreak in Hong Kong. Epidemics of recent animal origin are the 1918-1919
influenza pandemic, and acquired immune deficiency syndrome caused by human
immunodeficiency virus (HIV). Some retroviruses jump into and out of the
chromosomal DNA of the host germline, so that they oscillate between being
inherited Mendelian traits or infectious agents in different species. Will new
procedures like animal-to-human transplants unleash further infections? Do
microbes become more virulent upon cross-species transfer? Are animal microbes
a threat as biological weapons? Will the vast reservoir of immunodeficient
hosts due to the HIV pandemic provide conditions permissive for sporadic
zoonoses to take off as human-to-human transmissible diseases? Do human infections
now pose a threat to endangered primates? These questions are addressed in this
lecture.
Descriptors: infection, Creutzfeldt Jakob disease,
behavioral and mental disorders, nervous system disease, prion disease,
acquired immunodeficiency syndrome (AIDS), immune system disease, viral
disease, bovine spongiform encephalopathy, nervous system disease, prion
disease, influenza, respiratory system disease, viral disease, measles, viral
disease, plague, bacterial disease, smallpox, viral disease, typhus, bacterial
disease, yellow fever, viral disease, animal to human transmission, zoonosis.
Widjaja, L., S.L. Krauss, R.J. Webby, T. Xie, and
R.G. Webster (2004). Matrix gene of influenza a viruses isolated from wild
aquatic birds: ecology and emergence of influenza A viruses. Journal of
Virology 78(16): 8771-9. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: Wild aquatic birds are the primary reservoir
of influenza A viruses, but little is known about the viruses' gene pool in
wild birds. Therefore, we investigated the ecology and emergence of influenza
viruses by conducting phylogenetic analysis of 70 matrix (M) genes of influenza
viruses isolated from shorebirds and gulls in the Delaware Bay region and from
ducks in Alberta, Canada, during >18 years of surveillance. In our analysis,
we included 61 published M genes of isolates from various hosts. We showed that
M genes of Canadian duck viruses and those of shorebird and gull viruses in the
Delaware Bay shared ancestors with the M genes of North American poultry
viruses. We found that North American and Eurasian avian-like lineages are
divided into sublineages, indicating that multiple branches of virus evolution
may be maintained in wild aquatic birds. The presence of non-H13 gull viruses
in the gull-like lineage and of H13 gull viruses in other avian lineages
suggested that gulls' M genes do not preferentially associate with the H13
subtype or segregate into a distinct lineage. Some North American avian
influenza viruses contained M genes closely related to those of Eurasian avian
viruses. Therefore, there may be interregional mixing of the two clades.
Reassortment of shorebird M and HA genes was evident, but there was no
correlation among the HA or NA subtype, M gene sequence, and isolation time. Overall,
these results support the hypothesis that influenza viruses in wild waterfowl
contain distinguishable lineages of M genes.
Descriptors: animals, wild virology, birds virology,
ecology, evolution, molecular, influenza A virus, avian genetics, viral matrix
proteins genetics, ducks virology, avian classification, avian isolation and
purification, molecular sequence data, phylogeny, sequence analysis, DNA.
Wilpshaar, H., M.P.M. Meuwissen, F.H.M. Tomassen,
M.C.M. Mourits, M.A.P.M. van Asseldonk and
R.B.M. Huirne (2003). Economic decision-making to prevent the spread
of infectious animal diseases. In: Compendium of Technical Items
Presented to the International Committee or to Regional Commissions 2001-2002,
p. 337-388. ISBN: 9290446145.
Descriptors: animal diseases, disease control, disease
transmission, decision making, economic analysis, losses, epidemiology, foot
and mouth disease, Aphthovirus, avian influenza virus, swine fever virus.
Wilson, D.D., E.T. Schmidtmann, R.D. Richard, R.D.
Lehman, T.D. St George, B.H. Kay (ed.), and J. Blok. (1986). Isolation of
avian influenza from insects. In: Arbovirus research in Australia.
Proceedings Fourth Symposium, Brisbane, Australia, p. 221-226.
NAL
Call Number:
RC114.5.A7
Descriptors: epidemiology, disease vectors,
avian influenza virus, insects, Coleoptera, Diptera, Musca domestica, Hydrotaea
aenescens, Coproica hirtula, Alphitobius diaperinus, Dermestes
maculatus.
Witt, C.J. and J.L. Malone (2005). A
veterinarian's experience of the spring 2004 avian influenza outbreak in Laos.
Lancet Infectious Diseases 5(3): 143-5.
ISSN: 1473-3099.
Descriptors: avian influenza, epidemiology, outbreaks
prevention, control, mortality, transmission, Laos, poultry, rural health,
veterinarians, zoonoses, emerging infectious diseases.
Wolf, H.H., O. Werner, L.P. Mueller, H.J. Holzhausen,
and H.J. Schmoll (2001). Lymphadenopathy and cerebral infection in a 20 year
old patient presenting antibodies to the avian influenza H4 subtype. Blood
98(11, Pt. 1): 505a. ISSN: 0006-4971.
NAL
Call Number: RB145.A21B57
Abstract: Lymphadenopathy may appear as a common
symptom of infectious or malignant diseases. We report a 20 year old male
patient, worker in an avian slaughter house, who presented with axillary,
infraclavicular, and inguinal lymphadenopathy, splenomegaly, granulocytopenia
(0.9 Gpt/l), and monocytosis (17% out of 2.9 Gpt/l leukocytes).
Thrombocytopenia (39 Gpt/l) was found to be caused by HLA-antibodies and
antiplatelet autoantibodies. There were no clinical signs of infection,
pneumonia nor B symptoms. Lymphadenectomy 27 months ago had revealed chronic
non-granulomatous lymphadenitis and follicular hyperplasia, no malignancy.
Previous histologic findings had been confirmed by second biopsy of recurrent
axillary lymphomas. No infectious agent had been identified so far, broad
serologic and immunological testings had been negative. Bone marrow biopsy
revealed normal hematopoiesis. The patient was admitted to neurologic
department due to seizures 27 months after onset of lymphadenopathy.
Cerebrospinal fluid revealed lymphocytic pleocytosis, no malignant cells,
microbiological and serological testings were negative. MRI of the cerebrum was
without any pathologic finding. Due to a 4 months prednisolone therapy,
lymphadenopathy resolved and platelet count normalized, but seizures reappeared
after stop of steroid therapy. Broad infectiologic screening was negative
including human influenza virus antibodies, but hemagglutination inhibition
test (HI-test) revealed low concentrations of anti avian influenza virus
A/Duck/Ukraine/1/63 (H3N8) antibodies. HI-test was strongly reactive (1:128) to
avian A/duck/Czech/56 (H4N6) with slight titer reduction after a 2 months
interval. Human infections may be caused by the H1, H2, or H3 influenza subtype
in combination with various neuraminidases. Therefore, HI-titer to avian
influenza H3N8 could indicate cross-reactivity to human viruses. Singular
reports of infection in humans with H5, H7, as well as H9 subtype reflect
typical symptoms of influenza or pneumonia. However, there are no reports so
far concerning detection of avian H4 antibodies in humans. Furthermore, during
the year 2000 there was not even a single proof of anti avian H4 antibodies out
of almost 180 000 birds screened in Germany. We conclude that chronic
lymphadenopathy, non-specific symptoms and cerebral infection in our patient
might be related to atypical avian influenza. To our knowledge this should be a
rare, if not the first report on detection of anti avian influenza H4 antibodies
in humans.
Descriptors: clinical immunology, infection, neurology,
cerebral infection, infectious disease, nervous system disease,
granulocytopenia, blood and lymphatic disease, immune system disease,
lymphadenopathy, blood and lymphatic disease, immune system disease,
monocytosis, blood and lymphatic disease, seizures, nervous system disease,
splenomegaly, blood and lymphatic disease, thrombocytopenia, blood and
lymphatic disease, meeting abstract, meeting poster.
Wood, G.W., J. Banks, I.H. Brown, I. Strong, and D.J.
Alexander (1997). The nucleotide sequence of the HA1 of the haemagglutinin
of an H1 avian influenza virus isolate from turkeys in Germany provides
additional evidence suggesting recent transmission from pigs. Avian
Pathology 26(2): 347-355. ISSN:
0307-9457.
NAL
Call Number: SF995.A1A9
Abstract: The nucleotide sequence encoding the HA1
portion of the haemagglutinin gene of the influenza virus
A/turkey/Germany/2482/90, isolated from birds kept in an area of many pig
farms, was determined and compared with those of recent avian and swine
influenza isolates. It was found to be closest to the 'avian-like' swine H1N1
influenza viruses that have been reported in Europe since the early 1980s and
may represent good evidence for transmission of these viruses back to birds
after they have become established in pigs.
Descriptors: animal husbandry, genetics, infection,
methods and techniques, microbiology, veterinary medicine, avian influenza
virus Ha1, nucleotide sequence, hemagglutinin gene H1 isolate, infection,
molecular genetics, pathogen, swine farm proximity, viral transmission.
Wood, J.M., K.G. Nicholson, I. Stephenson, M. Zambon,
R.W. Newman, D.L. Major, and A. Podda (2002). Experience with the clinical
development of influenza vaccines for potential pandemics. Medical
Microbiology and Immunology 191(3-4): 197-201. ISSN: 0300-8584.
Abstract: During normal interpandemic influenza
seasons, immune responses to vaccines are quite predictable and meet the
licensing criteria of the European Union (EU) Committee for Proprietary
Medicinal Products (CPMP). In a pandemic situation, large sections, if not all
of the community will be immunologically naive and therefore new immunisation
strategies will be needed. In 1976 and 1977 H1N1 vaccines were prepared and
tested clinically. To stimulate 'protective' antibody responses, two doses of
vaccine were needed in people below the age of 24 years (no previous experience
of H1N1 virus), whereas one conventional dose was adequate in older people. In
1997, the highly pathogenic avian influenza H5N1 virus caused widespread
concern when it infected man, with lethal effects. Due to safety concerns it
was necessary to adopt new strategies for vaccine development and one such
strategy was to produce vaccine from an avirulent H5N3 virus,
A/Duck/Singapore-Q/F119-2/97. Clinical trials of a subunit vaccine prepared
from A/Duck/Sing/97 virus revealed that even two doses of twice the normal
vaccine concentration (i.e. 30 mug haemagglutinin) were poorly immunogenic,
whereas an H5N3 vaccine adjuvanted with microfluidised emulsion (MF) 59
stimulated antibody levels that complied with CPMP criteria after two half
strength doses (i.e. 7.5 mug haemagglutinin).
Descriptors: clinical immunology, epidemiology, infection,
pharmacology, public health, pulmonary medicine, influenza, immunology,
prevention and control, respiratory system disease, viral disease, pandemic
prevention, vaccine development.
Wood, J.M. (2001). Developing vaccines against
pandemic influenza. Philosophical Transactions of the Royal Society of
London. Series B Biological Sciences 356(1416): 1953-1960. ISSN: 0962-8436.
NAL
Call Number: 501 L84Pb
Abstract: Pandemic influenza presents special problems
for vaccine development. There must be a balance between rapid availability of
vaccine and the safeguards to ensure safety, quality and efficacy of vaccine.
Vaccine was developed for the pandemics of 1957, 1968, 1977 and for the
pandemic alert of 1976. This experience is compared with that gained in
developing vaccines for a possible H5N1 pandemic in 1997-1998. Our ability to
mass produce influenza vaccines against a pandemic threat was well illustrated
by the production of over 150 million doses of 'swine flu' vaccine in the USA
within a 3 month period in 1976. However, there is cause for concern that the
lead time to begin vaccine production is likely to be about 7-8 months.
Attempts to reduce this time should receive urgent attention. Immunogenicity of
vaccines in pandemic situations is compared over the period 1968-1998. A
consistent feature of the vaccine trials is the demonstration that one
conventional 15 mug haemagglutinin dose of vaccine is not sufficiently
immunogenic in naive individuals. Much larger doses or two lower doses are
needed to induce satisfactory immunity. There is some evidence that whole-virus
vaccines are more immunogenic than split or subunit vaccines, but this needs
substantiating by further studies. H5 vaccines appeared to be particularly poor
immunogens and there is evidence that an adjuvant may be needed. Prospects for
improving the development of pandemic vaccines are discussed.
Descriptors: clinical immunology, epidemiology, infection,
pharmacology, avian influenza, viral disease, pandemic influenza infection,
prevention and control, respiratory system disease, viral disease, 1997-1998
pandemic, vaccine development.
Woolcock, P.R., H.L. Shivaprasad, and R.M. De (2000).
Isolation of avian influenza virus (H10N7) from an emu (Dromaius
novaehollandiae) with conjunctivitis and respiratory disease. Avian
Diseases 44(3): 737-744. ISSN:
0005-2086.
NAL
Call Number: 41.8 Av5
Abstract: Avian influenza virus was isolated from the
conjunctiva of a male emu chick. Clinical observations included ocular discharge,
dyspnea, and mild respiratory signs. Lesions included conjunctivitis,
tracheitis, bronchopneumonia, and airsacculitis. Escherichia coli was
isolated from the conjunctiva and the sinus, and Staphylococcus sp. was
isolated from the conjunctiva. Influenza A viral nucleoprotein was detected
immunohistochemically in epithelial cells of the bronchi, lung parenchyma and
tracheal mucosa, and mononuclear inflammatory cells within the exudate of the
bronchial lumen; conjunctiva, air sacs, kidney, intestine, and liver were
negative for the viral nucleoprotein. The isolated influenza virus was typed as
H10N7 and was determined to be nonpathogenic for chickens.
Descriptors: veterinary medicine, respiratory system,
sense organs, virology, airsacculitis, respiratory system disease,
bronchopneumonia, respiratory system disease, conjunctivitis, eye disease,
dyspnea, respiratory system disease, ocular discharge, eye disease, respiratory
disease, respiratory system disease, tracheitis, respiratory system disease, case
study.
World Health Organization (2004). Avian influenza
A(H5N1) in humans and poultry, Vietnam. Weekly Epidemiological Record;
Releve Epidemiologique Hebdomadaire 79(3): 13-4. ISSN: 0049-8114.
Descriptors: avian influenza, humans, poultry, WHO, weekly
record.
World Health Organization (2004). Development of a
vaccine effective against avian influenza H5N1 infection in humans. Weekly
Epidemiological Record Releve Epidemiologique Hebdomadaire 79(4):
25-6. ISSN: 0049-8114.
Descriptors: influenza prevention and control, influenza A
virus avian immunology, influenza vaccine, birds virology, influenza
epidemiology, avian genetics, sentinel surveillance, vaccination, Vietnam.
Wright, S.M., Y. Kawaoka, G.B. Sharp, D.A. Senne, and
R.G. Webster (1992). Interspecies transmission and reassortment of influenza
A viruses in pigs and turkeys in the United States. American Journal of
Epidemiology 136(4): 488-97. ISSN:
0002-9262.
NAL
Call Number: 449.8 Am3
Abstract: Genetic reassortment between influenza A viruses
in humans and in animals and birds has been implicated in the appearance of new
pandemics of human influenza. To determine whether such reassortment has
occurred in the United States, the authors compared the genetic origins of gene
segments of 73 swine influenza virus isolates (1976-1990), representing 11
states, and 11 turkey virus isolates (1980-1989), representing eight states.
The host origin of gene segments encoding the internal proteins of H1N1 swine
and turkey influenza viruses was identified by developing a dot-blot assay. All
gene segments of swine influenza viruses were characteristic of influenza virus
genes from that species, indicating that pigs may not be frequent participants
in interspecies genetic exchange and reassortment of influenza viruses in the
United States. In contrast, 73% of the turkey influenza virus isolates
contained genes of swine origin. One turkey isolate was a reassortant having
three genes characteristic of avian influenza virus and three of swine origin.
These findings document a high degree of genetic exchange and reassortment of
influenza A viruses in domestic turkeys in the United States. The molecular
biologic techniques used by the authors should aid future epidemiologic studies
of influenza pandemics.
Descriptors: disease vectors, influenza transmission,
influenza A virus, porcine genetics, reassortant viruses genetics, swine
microbiology, turkeys microbiology, immunoblotting, influenza microbiology,
human genetics, polymerase chain reaction, United States.
Xu, X., Subbarao, N.J. Cox, and Y. Guo (1999). Genetic characterization of the pathogenic
influenza A/Goose/Guangdong/1/96 (H5N1) virus: similarity of its hemagglutinin
gene to those of H5N1 viruses from the 1997 outbreaks in Hong Kong. Virology
261(1): 15-9. ISSN: 0042-6822.
NAL
Call Number: 448.8 V81
Abstract: Analysis of the sequences of all eight RNA
segments of the influenza A/Goose/Guangdong/1/96 (H5N1) virus, isolated from a
sick goose during an outbreak in Guangdong province, China, in 1996, revealed
that the hemagglutinin (HA) gene of the virus was genetically similar to those
of the H5N1 viruses isolated in Hong Kong in 1997. However, the remaining genes
showed greater similarity to other avian influenza viruses. Notably, the
neuraminidase gene did no have the 19-amino-acid deletion in the stalk region
seen in the H5N1 Hong Kong viruses and the NS gene belonged to allele B, while
that of the H5N1 Hong Kong viruses belonged to allele A. These data suggest
that the H5N1 viruses isolated from the Hong Kong outbreaks derived their HA
genes from a virus similar to the A/Goose/Guangdong/1/96 virus or shared a
progenitor with this goose pathogen.
Descriptors: geese virology, hemagglutinin glycoproteins,
influenza virus genetics, influenza virology, influenza A virus avian genetics,
human genetics, chickens virology, DNA, viral chemistry, DNA, viral genetics,
disease outbreaks, fowl plague epidemiology, fowl plague virology, genes viral,
Hong Kong epidemiology, influenza epidemiology, avian classification, avian
isolation and purification, human classification, molecular sequence data,
neuraminidase genetics, phylogeny, sequence analysis, DNA, viral nonstructural
proteins genetics.
Yagyu, K., R. Yanagawa, Y. Matsuura, and H. Noda
(1981). Contact infection of mink with influenza A viruses of avian and
mammalian origin. Archives of Virology 68(2): 143-5. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Descriptors: fowl plague transmission, mink microbiology,
orthomyxoviridae infections transmission, influenza A virus avian growth and
development, human growth and development, porcine growth and development,
influenza A virus growth and development, species specificity.
Yamada, A., L.E. Brown, and R.G. Webster (1985). Antigenic
analysis of H2 influenza virus haemagglutinin with monoclonal antibodies. Vaccine
3(3 Suppl.): 195-8. ISSN: 0264-410X.
NAL
Call Number: QR189.V32
Abstract: Antigenic analysis of human and avian H2
influenza virus was carried out with monoclonal antibodies to the HA molecules
of H2 influenza viruses isolated in the early stage of an H2 pandemic. The
study revealed antigenic differences between inhibitor sensitive (Japan+/57,
RI+57) and inhibitor resistant strains (Japan-/57, Ri-/57). This indicates that
the receptor-binding specificity of the haemagglutinin can markedly influence
the antigenic analysis obtained with monoclonal antibodies in HI test. Minor
antigenic differences (microheterogeneity) could be detected between different
H2 influenza viruses isolated in 1957. Minor antigenic variation continued in
the H2 viruses until 1961, but significant antigenic drift occurred in 1962 so
that viruses isolated after that date reacted with few monoclonal antibodies.
Analysis of avian H2 influenza viruses suggested antigenic differences between
the different avian H2 haemagglutinin, but no correlation between the year of
isolation and the progressive antigenic drift similar to that seen in the human
strains was found.
Descriptors: antigens, viral immunology, hemagglutinins
viral immunology, influenza A virus avian immunology, human immunology,
antibodies, monoclonal immunology, antigens, viral genetics, genes viral,
hemagglutinins viral genetics, avian genetics, human genetics, variation
genetics.
Yang, Y.H. (2004). [Pay enough attention to human
infection with avian influenza virus]. Zhonghua Er Ke Za Zhi 42(4):
246-7. ISSN: 0578-1310.
Descriptors: influenza prevention and control, avian influenza
A virus classification, avian influenza prevention and control, birds, China,
Hong Kong, influenza etiology, avian influenza A virus pathogenicity, avian
influenza virus complications, prognosis, World Health Organization.
Yao, Y., L.J. Mingay, J.W. McCauley, and W.S. Barclay
(2001). Sequences in influenza A virus PB2 protein that determine productive
infection for an avian influenza virus in mouse and human cell lines. Journal
of Virology 75(11): 5410-5. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: Reverse genetics was used to analyze the host
range of two avian influenza viruses which differ in their ability to replicate
in mouse and human cells in culture. Engineered viruses carrying sequences
encoding amino acids 362 to 581 of PB2 from a host range variant productively
infect mouse and human cells.
Descriptors: influenza A virus avian genetics, viral
proteins genetics, cell line, genes viral, avian chemistry, avian
pathogenicity, mice, sequence analysis, protein, species specificity, transfection.
Yasuda, J., K.F. Shortridge, Y. Shimizu, and H. Kida
(1991). Molecular evidence for a role of domestic ducks in the introduction
of avian H3 influenza viruses to pigs in southern China, where the A/Hong
Kong/68 (H3N2) strain emerged. Journal of General Virology 72(Pt.
8): 2007-10. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: The haemagglutinins (HAs) of five H3
influenza A viruses isolated from domestic ducks and one from a goose in
southern China were analysed antigenically and genetically. The patterns of
reactivity of two of the duck viruses and the goose virus with a panel of
monoclonal antibodies to 10 different epitopes on the H3 HA were similar to
those of influenza viruses isolated from wild ducks and pigs, as well as those
of the earliest human H3 viruses. The other three isolates from domestic ducks
were different from each other and from these viruses antigenically. Sequence
analysis revealed that the HA genes of the two duck viruses and the goose virus
were closely related to those of isolates from wild ducks and pigs; the
identities between the deduced amino acid sequence of the HA of one of the
isolates from domestic ducks and those of isolates from a wild duck and a pig
were 98.7% and 99.5%, respectively. The antigenic and genetic similarity
between these H3 HAs suggests that in southern China, the hypothetical
influenza epicentre, domestic ducks may have played a role in the introduction
of avian influenza viruses to pigs from feral ducks. The findings also support
the hypothesis that the pig was a 'mixing vessel', producing a new human
pandemic strain, A/Hong Kong/68 (H3N2), by genetic reassortment.
Descriptors: ducks microbiology, influenza microbiology,
influenza A virus avian immunology, human immunology, amino acid sequence,
antibodies, monoclonal immunology, base sequence, China, DNA, viral, geese
microbiology, hemagglutinins viral genetics, hemagglutinins viral immunology,
influenza transmission, avian genetics, human genetics, molecular sequence
data, sequence alignment, swine microbiology.
Yuen, K.Y., P.K. Chan, M. Peiris, D.N. Tsang, T.L.
Que, K.F. Shortridge, P.T. Cheung, W.K. To, E.T. Ho, R. Sung, and A.F. Cheng (1998). Clinical
features and rapid viral diagnosis of human disease associated with avian influenza
A H5N1 virus. Lancet 351(9101): 467-71. ISSN: 0140-6736.
NAL
Call Number: 448.8 L22
Abstract: BACKGROUND: Human infection with an avian
influenza A virus (subtype H5N1) was reported recently in Hong Kong. We
describe the clinical presentation of the first 12 patients and options for
rapid viral diagnosis. METHODS: Case notes of 12 patients with
virus-culture-confirmed influenza A H5N1 infection were analysed. The clinical
presentation and risk factors associated with severe disease were defined and
the results of methods for rapid virus diagnosis were compared. FINDINGS:
Patients ranged from 1 to 60 years of age. Clinical presentation was that of an
influenza-like illness with evidence of pneumonia in seven patients. All seven
patients older than 13 years had severe disease (four deaths), whereas children
5 years or younger had mild symptoms with the exception of one who died with
Reye's syndrome associated with intake of aspirin. Gastrointestinal
manifestations, raised liver enzymes, renal failure unrelated to
rhabdomyolysis, and pancytopenia were unusually prominent. Factors associated
with severe disease included older age, delay in hospitalisation,
lower-respiratory-tract involvement, and a low total peripheral white blood
cell count or lymphopenia at admission. An H5-specific reverse-transcription
PCR assay (RT-PCR) was useful for rapid detection of virus directly in
respiratory specimens. A commercially available enzyme immunoassay was more
sensitive than direct immunofluorescence for rapid viral diagnosis. Direct
immunofluorescence with an H5-specific monoclonal antibody pool was useful for
rapid exclusion of H5-subtype infection. INTERPRETATION: Avian Influenza A H5N1
virus causes human influenza-like illness with a high rate of complications in
adults admitted to hospital. Rapid H5-subtype-specific laboratory diagnosis can
be made by RT-PCR applied directly to clinical specimens.
Descriptors: disease outbreaks, influenza diagnosis,
influenza virology, influenza A virus avian isolation and purification, adult,
child, preschool, fluorescent antibody technique, direct, fowl plague
transmission, Hong Kong epidemiology, immunoenzyme techniques, infant, influenza epidemiology, influenza
transmission, middle aged, polymerase chain reaction methods, risk factors,
time factors.
Zakstel'skaia, L.I.A., S.F. Shenderovich, M.A.
Iakhno, V.A. Isachenko, and V.M. Zhdanov (1980). Issledovanie antigennoi
obshchnosti gemaggliutininov virusov grippa A cheloveka i zhivotnykh metodom
immunoadsorbtsii. [Antigenic similarity of the hemagglutinins of human and
animal influenza A viruses studied by immunoadsorption]. Voprosy
Virusologii 3: 287-90. ISSN:
0507-4088.
NAL
Call Number: 448.8 P942
Abstract: Antigenic relationships between human
influenza A viruses containing hemagglutinins of HO and H1 subtypes and animal
and avian influenza viruses Hsw1 and Hav5 were studied by immunoadsorption
using inorganic base of the sorbent. Direct and indirect relations due to the
presence in hemagglutinin of common antigenic determinants and hapten groups
were revealed. The strains representing drift variations within one subtype
differed by the spectrum of hapten determinants typical of other subtypes. No
common determinant typical for all members of this group was isolated.
Descriptors: antigens, viral analysis, hemagglutinins
viral analysis, influenza A virus avian immunology, human immunology, porcine
immunology, influenza A virus
immunology, epitopes analysis, hemagglutination inhibition tests, immunosorbent
techniques.
Zakstelskaya, L.Y., S.S. Yamnikova, V.P. Yuferov,
and I.G. Kharitonenkov (1975). Shtammovye razlichiya v elektroforeticheskoi
podvizhnosti belkovykh kamponentov virusov grippa tipa A cheloveka i ptits.
[Strain variations in electrophoretic mobility of protein components of a human
and avian influenza A viruses]. Sbornik Trudov Institut Virusologii
Imeni D.I. Ivanovskogo, "Ekologiya Virusov" 3: 38-43.
Descriptors: avian influenza A virus, strain variations,
human, protein components.
Zambon, M. (2004). The inexact science of
influenza prediction. Lancet 363(9409): 582-3. ISSN: 1474-547X.
NAL
Call Number: 448.8 L22
Descriptors: influenza epidemiology, influenza
transmission, disease outbreaks statistics and numerical data, influenza
virology, influenza A virus, avian genetics, avian growth and development,
human genetics, human growth and development, population surveillance, poultry
diseases epidemiology, poultry diseases transmission, poultry diseases
virology, probability, virus replication, zoonoses epidemiology, zoonoses
transmission.
Zambon, M.C. (2001). The pathogenesis of influenza
in humans. Reviews in Medical Virology 11(4): 227-41. ISSN: 1052-9276.
Descriptors: antigenic variation physiology, influenza
virology, orthomyxoviridae pathogenicity, orthomyxoviridae physiology,
antigenic variation genetics, birds virology, disease reservoirs, evolution,
molecular, hemagglutinin glycoproteins, influenza virus chemistry,
hemagglutinin glycoproteins, influenza virus genetics, hemagglutinin glycoproteins,
influenza virus metabolism, influenza epidemiology, influenza transmission,
neuraminidase genetics, neuraminidase metabolism, orthomyxoviridae enzymology,
orthomyxoviridae genetics.
Zhao, C.A. and Y.H. Yang (2004). [Present status
of studies on avian influenza and human infection with avian influenza virus].
Zhonghua Er Ke Za Zhi 42(4): 310-1.
ISSN: 0578-1310.
Descriptors: influenza prevention and control, avian
influenza A virus pathogenicity, avian influenza prevention and control, birds,
influenza etiology, avian influenza A virus classification, avian influenza
complications, avian influenza virology.
Zhirnov, O. and A.G. Bukrinskaya (1984). Nucleoproteins
of animal influenza viruses, in contrast to those of human strains, are not
cleaved in infected cells. Journal of General Virology 65(Pt. 6):
1127-34. ISSN: 0022-1317.
NAL
Call Number: QR360.A1J6
Abstract: We previously reported that nucleoproteins
(NPs) of human influenza viruses are cleaved in infected cells and, as a
result, two forms of NP, uncleaved (mol. wt. 56000) and cleaved (mol. wt.
53000) were accumulated late in infection. Here, we report that NPs of animal
influenza viruses of non-human origin (isolated from pigs, equids, seals,
whales, birds) exhibited proteolytic resistance in infected cells and did not
undergo a change in mol. wt. in the course of infection. The resistance of the
animal virus NPs to proteolytic cleavage was shown to be a virus-specific
property and not the consequence of a low level of proteolysis in infected
cells. Influenza A/H3N2 viruses isolated from swine in Hong Kong in 1976 were
found to have a cleavable NP like that of 'human' viruses, supporting the
hypothesis concerning the 'human' origin of these strains. The NP of human
influenza virus (A/Aichi/2/68) adapted to an animal host (mouse) retained
susceptibility to limited intracellular proteolysis. Thus, NP resistance to
cleavage seems to be a stable viral characteristic enabling the NP56 ---- NP53
modification to be used as an indication of the origin of influenza viruses.
Descriptors: influenza microbiology, influenza A virus
human metabolism, nucleoproteins metabolism, orthomyxoviridae metabolism, viral
proteins metabolism, chick embryo, influenza metabolism, avian metabolism,
porcine metabolism, peptide hydrolases metabolism, peptides analysis, peptides
metabolism, virus cultivation.
Zhong, N.S. (2004). [Taking precautions,
strengthen the prevention and management of avian influenza in human beings].
Zhonghua Jie He He Hu Xi Za Zhi;
Zhonghua Jiehe He Huxi Zazhi; Chinese Journal of Tuberculosis and Respiratory
Diseases 27(4): 217. ISSN:
1001-0939.
Descriptors: influenza prevention and control, avian
influenza A virus isolation and purification, avian influenza transmission,
zoonoses transmission, influenza transmission, influenza veterinary, avian
influenza A virus pathogenicity, poultry.
Zhou, N., S. He, T. Zhang, W. Zou, L. Shu, G.B.
Sharp, and R.G. Webster (1996). Influenza infection in humans and pigs in
southeastern China. Archives of Virology 141(3-4): 649-661. ISSN: 0304-8608.
NAL
Call Number: 448.3 Ar23
Abstract: The three last pandemic strains of influenza
A virus -Asian/57, Hong Kong/68 and Russian/77 - are believed to have
originated in China. The strains responsible for the 1957 and 1968 human
pandemics were reassortants incorporating both human and avian influenza
viruses, which may have arisen in pigs. We therefore undertook a
population-based study in the Nanchang region of Central China to establish the
prevalence, types and seasonal pattern of human influenza infection and to
screen serum samples from animals and humans for evidence of interspecies
transmission of influenza viruses. Two definite influenza seasons were
demonstrated, one extending from November to March and the other July to
September. The profile of antibodies to commonly circulating human influenza
viruses was no different in Nanchang and neighboring rural communities than in
Memphis, Tennessee, USA. In particular, Chinese women who raised pigs in their
homes were no more likely to have been exposed to influenza virus than were
subjects who seldom or never had contact with pigs. However, we did obtain
evidence using isolated H7 protein in an enzyme-linked immunoabsorbent assay
for infection of pig farmers by an avian H7 influenza virus suggesting that
influenza A viruses may have been transmitted directly from ducks to humans.
The results of the serological survey also indicated that pigs in or near
Nanchang were infected by human H1N1 and H3N2 influenza viruses, but not with
typical swine viruses. We found no serological evidence for H2 influenza
viruses in humans after 1968.
Descriptors: animal husbandry, climatology, epidemiology,
infection, public health, vector biology, veterinary medicine, disease
transmission epidemiology interspecies transmission seasonal infection.
Zhou, N.N., D.A. Senne, J.S. Landgraf, S.L. Swenson,
G. Erickson, K. Rossow, L. Liu, K. Yoon, S. Krauss, and R.G. Webster (1999). Genetic reassortment
of avian, swine, and human influenza A viruses in American pigs. Journal
of Virology 73(10): 8851-6. ISSN:
0022-538X.
NAL
Call Number: QR360.J6
Abstract: In late summer through early winter of 1998,
there were several outbreaks of respiratory disease in the swine herds of North
Carolina, Texas, Minnesota, and Iowa. Four viral isolates from outbreaks in
different states were analyzed genetically. Genotyping and phylogenetic
analyses demonstrated that the four swine viruses had emerged through two
different pathways. The North Carolina isolate is the product of genetic
reassortment between H3N2 human and classic swine H1N1 influenza viruses, while
the others arose from reassortment of human H3N2, classic swine H1N1, and avian
viral genes. The hemagglutinin genes of the four isolates were all derived from
the human H3N2 virus circulating in 1995. It remains to be determined if either
of these recently emerged viruses will become established in the pigs in North
America and whether they will become an economic burden.
Descriptors: genome, viral, influenza A virus avian
genetics, human genetics, porcine genetics, reassortant viruses, amino acid
sequence, birds virology, molecular sequence data, swine virology.
Zhou, N.N., K.F. Shortridge, E.C. Claas, S.L. Krauss,
and R.G. Webster (1999). Rapid evolution of H5N1 influenza viruses in
chickens in Hong Kong. Journal of Virology 73(4): 3366-74. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: The H5N1 avian influenza virus that killed 6
of 18 persons infected in Hong Kong in 1997 was transmitted directly from
poultry to humans. Viral isolates from this outbreak may provide molecular
clues to zoonotic transfer. Here we demonstrate that the H5N1 viruses
circulating in poultry comprised two distinguishable phylogenetic lineages in
all genes that were in very rapid evolution. When introduced into new hosts,
influenza viruses usually undergo rapid alteration of their surface
glycoproteins, especially in the hemagglutinin (HA). Surprisingly, these H5N1
isolates had a large proportion of amino acid changes in all gene products
except in the HA. These viruses maybe reassortants each of whose HA gene is
well adapted to domestic poultry while the rest of the genome arises from a different
source. The consensus amino acid sequences of "internal" virion
proteins reveal amino acids previously found in human strains. These
human-specific amino acids may be important factors in zoonotic transmission.
Descriptors: fowl plague virology, genes viral, genome,
viral, influenza A virus avian genetics, amino acid sequence, chickens,
evolution, molecular, fowl plague epidemiology, fowl plague transmission,
hemagglutinins genetics, Hong Kong epidemiology, molecular sequence data,
sequence alignment.
Zilske, E., R. Sinnecker, and H. Sinnecker (1981). Neuraminidasehemmende
Antikorper gegen aviare Influenzabirus- Subtypen in Humanseren.
[Neuraminidase-Inhibiting Antibodies to Avian Influenza Virus Subtypes in Human
Sera (author's transl)]. Zentralblatt Fur Bakteriologie, Mikrobiologie
Und Hygiene. 1. Abt. Originale A, Medizinische Mikrobiologie,
Infektionskrankheiten Und Parasitologie
International Journal of Microbiology and Hygiene. A 250(1-2):
34-41. ISSN: 0174-3031.
NAL
Call Number: 448.3 C33 (1)
Abstract: 400 human sera were tested both in
hemagglutination inhibition (HI) and neuraminidase inhibition (NI) tests for
antibodies to avian and animal influenza virus subtypes. In the H1 test we only
found antibodies to the avian subtype Hav 7 and the animal subtypes Hsw 1 and
Heq 2 whereby the latter was mainly demonstrated in elderly persons 60 to 100
years old. The findings of Hav 7 are due to H 3 antibodies and reflect the
relationship between both antigens. In the NI test we obtained positive results
in 21.8% of the human sera with the neuraminidase subtype N 3 (Nav 2/3) with a
peak in persons who were 60 to 70 years old. 11.0% of the sera contained
antibodies to the neuraminidase subtype N 8 (Neq 2) and were found exclusively
in people 60 to 100 years old, and 9.3% of sera showed positive reactions with
the subtype N5 (Nav 5). Until now an immunological relationship between the
neuraminidase subtypes N 1, N 2, and N 3 is not known, and could'nt be found in
our own studies. Contaminations of antigens can also be excluded. The possible
origin of these antibodies to avian neuraminidase subtypes is discussed.
Descriptors: antibodies, viral analysis, influenza A virus
avian immunology, neuraminidase immunology, adolescent, adult, aged, child,
preschool, Germany, East, hemagglutination inhibition tests, infant, porcine
immunology, middle aged, serologic tests methods.
Zitzow, L.A., T. Rowe, T. Morken, W.J. Shieh, S.
Zaki, and J.M. Katz (2002). Pathogenesis of avian influenza A (H5N1) viruses
in ferrets. Journal of Virology 76(9): 4420-9. ISSN: 0022-538X.
NAL
Call Number: QR360.J6
Abstract: Highly pathogenic avian influenza A H5N1
viruses caused outbreaks of disease in domestic poultry and humans in Hong Kong
in 1997. Direct transmission of the H5N1 viruses from birds to humans resulted
in 18 documented cases of respiratory illness, including six deaths. Here we
evaluated two of the avian H5N1 viruses isolated from humans for their ability
to replicate and cause disease in outbred ferrets. A/Hong Kong/483/97 virus was
isolated from a fatal case and was highly pathogenic in the BALB/c mouse model,
whereas A/Hong Kong/486/97 virus was isolated from a case with mild illness and
exhibited a low-pathogenicity phenotype in mice. Ferrets infected intranasally
with 10(7) 50% egg infectious doses (EID(50)) of either H5N1 virus exhibited
severe lethargy, fever, weight loss, transient lymphopenia, and replication in
the upper and lower respiratory tract, as well as multiple systemic organs,
including the brain. Gastrointestinal symptoms were seen in some animals. In
contrast, weight loss and severe lethargy were not noted in ferrets infected
with 10(7) EID(50) of two recent human H3N2 viruses, although these viruses
were also isolated from the brains, but not other extrapulmonary organs, of
infected animals. The results demonstrate that both H5N1 viruses were highly
virulent in the outbred ferret model, unlike the differential pathogenicity
documented in inbred BALB/c mice. We propose the ferret as an alternative model
system for the study of these highly pathogenic avian viruses.
Descriptors: disease models, animal, ferrets, influenza
physiopathology, influenza A virus avian pathogenicity, adolescent, child,
preschool, influenza pathology, influenza virology, lung pathology, lung virology, virulence,
virus replication.