Argall, KG; Armati, PJ; King, NJ; Douglas, MW. The effects of West Nile virus on major histocompatibility complex class I and II molecule expression by Lewis rat Schwann cells in vitro. Journal of Neuroimmunology. 1991 Dec; 35(1-3): 273-84. ISSN: 0165-5728.
Descriptors: tissue culture study, Schwann cells, infection with WNV, virally triggered autoimmune diseases of neural tissue.
Abstract: The expression of major histocompatibility complex (MHC) class I and II molecules by Lewis rat Schwann cells after infection with West Nile virus (WNV) in vitro was examined by fluorescence microscopy and flow cytometry. WNV enhanced the expression of MHC class I molecules and induced the expression of MHC class II molecules by Schwann cells. Irradiated medium from WNV-infected Schwann cell cultures upregulated class I molecule expression on dissociated Schwann cell cultures but did not induce the expression of class II molecules. This finding has implications for virally triggered autoimmune diseases of nervous tissue.
Debnath, NC; Tiernery, R; Sil, BK; Wills, MR; Barrett, AD. In vitro homotypic and heterotypic interference by defective interfering particles of West Nile virus. Journal of General Virology. 1991 Nov; 72 ( Pt 11): 2705-11. ISSN: 0022-1317.
NAL Call No.: QR360.A1J6
Descriptors: type testing, homology, 6 cell lines--Vero, LLC-MK2, L929, HeLa, BHK-21 and SW13, virus propagation, defective interfering WNV particles, yield reduction assay, compared to hemagglutionation inhibition testing, monoclonal antibodies.
Abstract: Defective interfering (DI) particles of the flavivirus West Nile (WN) were generated after as few as two high multiplicity serial passages in Vero and LLC-MK2 cells. Six cell lines (Vero, LLC-MK2, L929, HeLa, BHK-21 and SW13) were used to assay interference by DI particles in a yield reduction assay. Interference was found to vary depending on the cell type used. The highest levels of interference were obtained in LLC-MK2 cells, whereas no detectable effect was observed in BHK-21 and SW13 cells. The ability of DI virus to be propagated varied depending on the cell line used; no detectable propagation of DI virus was observed in SW13 cells. Optimum interference was obtained following co-infection of cells with DI virus and standard virus at a multiplicity of 5. Interference between DI and standard viruses occurred only when they were co-infected or when cells were infected with DI virus 1 h before standard virus. Investigation of heterotypic interference by DI particles of WN virus strains from Sarawak, India and Egypt revealed that interference was dependent on the strain of WN virus or flavivirus used as standard virus. A measure of the similarity between five strains of WN virus and other flaviviruses was made on the basis of interference by DI viruses, and was found to be similar to that based on haemagglutination inhibition tests using a panel of monoclonal antibodies.
Kulkarni, AB; Mullbacher, A; Blanden, RV. Effect of high ligand concentration on West Nile virus-specific T cell proliferation. Immunology and Cell Biology. 1991 Feb; 69 ( Pt 1): 27-38. ISSN: 0818-9641.
NAL Call No.: QR180 I43
Descriptors: T-cell proliferation suppression, cell cultures, evaluation study, contribution of major histocompatibility complex (MHC) Class II and nominal WNV antigens.
Abstract: In this paper the phenomenon of suppression of proliferation in vitro of 14 day primed, West Nile virus (WNV)-specific, murine CD4+ T cells by large numbers of antigen-presenting macrophages and B cells has been investigated. Suppression was apparently not mediated by prostaglandins, as the use of indomethacin in cultures at four times the usual concentration did not reverse suppression. Experiments were designed to evaluate the contribution of major histocompatibility complex (MHC) Class II and nominal WNV antigens in causing suppression of T cell proliferation. Listeria- or thioglycollate-induced macrophages from CBA/H (H-2k) mice, when treated with heat-killed Listeria in vitro for 1 h to maintain or increase, respectively, MHC Class II levels before the addition of alloreactive Iak-specific T cells caused inverse dose-responses; the highest T cell proliferation occurred at a stimulator to responder (S : R) ratio of 0.25 and profound suppression at a S : R ratio of 1 or 2. In contrast, untreated thioglycollate-induced macrophages, which express low MHC Class II levels, gave a direct dose-response with increasing T cell proliferation as antigen-presenting cell (APC) numbers increased. Addition of anti-Ia antibodies (or their Fab fragments) to cultures caused a significant reversal of suppression of anti-WNV T cells imposed by high numbers of Listeria-induced macrophages or 14 day WNV-primed B cell APC. Suppression was also reversed by reducing the concentration of WNV antigen. These observations support the notion that the suppression of T cell proliferation observed at high S : R ratios was due to high concentrations of ligand (WNV-derived peptide complexed with Class II MHC) on APC.
Kulkarni, AB; Mullbacher, A; Blanden, RV. Functional analysis of macrophages, B cells and splenic dendritic cells as antigen-presenting cells in West Nile virus-specific murine T lymphocyte proliferation. Immunology and Cell Biology. 1991 Apr; 69 ( Pt 2): 71-80. ISSN: 0818-9641.
NAL Call No.: QR180 I43
Descriptors: immune responses, efficacy of macrophages, B cells and splenic dendritic cells, presenting West Nile virus (WNV) antigens to WNV memory CD4+ T cells, histocompatibility complex, antigen presenting cells, mouse model.
Abstract: In this paper, the relative efficacy of macrophages, B cells and splenic dendritic cells (SDC) in presenting West Nile virus (WNV) antigens to WNV memory CD4+ T cells is examined. The results indicate that, under appropriate conditions, all these cell types can function as antigen-presenting cells (APC). Listeria-induced peritoneal macrophages induced higher proliferative responses than SDC or B cells derived from naive or 14 day WNV-primed mice. The ability of Listeria-induced macrophage populations to present antigen was specifically inhibited by anti-Class II major histocompatibility complex (MHC) antibodies. On a cell population basis, B cells obtained from mice primed with WNV 14 days previously evoked higher responses than resting B cells. B cells from mice receiving weekly injections of WNV over a period of 4 weeks elicited optimal responses with lower doses of antigen than naive or 14 day WNV-primed B cells. When macrophages were used as APC, addition of specific antibodies to WNV resulted in increased efficiency of presentation, probably due to increased uptake of antigen by opsonization. In contrast, addition of anti-WNV antibodies to hyperimmune B cells reduced their efficacy presumably by reducing uptake of antigen by B cell surface immunoglobulin. When SDC from C57BL/6 mice were used as APC, WNV-specific proliferative responses were directly related to the number of stimulator cells used, and the background proliferation with mock antigen was two- to five-fold lower than specific responses. Higher levels of background proliferation were stimulated by SDC from CBA/H mice so that the antigen-specific responses were always less than two-fold higher than background.
Mirtskhulava, MB; Barnabishvili, NO; Ivanidze, EA; Tsibadze, AD; Khutsishvili, GI. Impact of a variable magnetic field on the West Nile fever virus. Soobshcheniya Akademii Nauk Gruzii. 1991; 143 (3) 317-319. In Georgian with summaries in Russian and English.
Descriptors: WNV, comparison of effects of magnetic field strengths.
Porter, KR; Oprandy, JJ; Dubois, DR; Summers, P; Nelson, WM; Henschal, EA;
Hayes, CG.
Detection of West Nile virus by the polymerase chain reaction and analysis of
strain variation.
40th
Annual Meeting of the American Society of Tropical Medicine and Hygiene, Boston,
Massachusetts, USA, December 1-5, 1991.
American Journal of Tropical Medicine and Hygiene.
Descriptors: PCR detection assay, WNV strains, genetic analysis, strain variation.
Summers,
PL; Martinez, BC; Dubois, DR; Silor, DL; Barvir, DA; Timchak, RL; Eckels, KH.
Antigenic comparison of
African and Indian strains of West Nile virus by western blot analysis.
40th
Annual Meeting of the American Society of Tropical Medicine and Hygiene, Boston,
Massachusetts, USA, December 1-5, 1991.
American Journal of Tropical Medicine and Hygiene.
Descriptors: Japanese encephalitis, St. Louis encephalitis, Murray Valley encephalitis, Kunjin virus, Dengue arbovirus, comparison study, immunology, Western blot assay, various strains.
Wengler, G; Czaya, G; Farber, PM; Hegemann, JH. In vitro synthesis of West Nile virus proteins indicates that the amino-terminal segment of the NS3 protein contains the active centre of the protease which cleaves the viral polyprotein after multiple basic amino acids. Journal of General Virology. 1991 Apr; 72 ( Pt 4): 851-8. ISSN: 0022-1317.
NAL Call No.: QR360.A1J6
Descriptors: processing flavivirus polyprotein, viral protease, NS3 protein, serine protease.
Abstract: A virus-encoded protease that cleaves after multiple basic amino acid residues has been implicated in the processing of the flavivirus polyprotein. Recently, a computer search of amino acid residues which might form the active site of a protease led to the suggestion that the amino-terminal segment of the NS3 protein represents a serine protease. To examine this possibility we constructed an mRNA which encodes a polyprotein with an amino-terminal signal sequence derived from the influenza virus haemagglutinin, followed by a segment of the West Nile flavivirus polyprotein which includes the non-structural (NS) proteins NS2A, NS2B and the amino-terminal part of the NS3 protein. This polyprotein contains two sequences, located at the termini of the NS2B protein, which are cleaved by the viral protease that cleaves after multiple basic residues in the authentic polyprotein. The proteins that are generated by this mRNA during in vitro translation in the presence of rough endoplasmic reticulum membranes indicate that these two proteolytic cleavages occur in vitro. In vitro translation of polyproteins shortened at the carboxy terminus shows that a polyprotein which does not contain the complete set of proposed catalytic residues present in the NS3 protein segment accumulates as a membrane-associated molecule without proteolytic processing. Similarly, substitution of residue histidine 51 of the NS3 polyprotein segment, which is predicted to be part of the protease catalytic centre, with an alanine residue, blocks the processing of the polyprotein in vitro.
Return to Contents
February 27, 2003