SPECIFIC VIRAL INTERFERENCE IN HELA CELL CULTURES CHRONICALLY INFECTED WITH COXSACKIE B5 VIRUS

J Bacteriol. 1963 September; 86(3): 517–526.

PMCID: PMC278466

SPECIFIC VIRAL INTERFERENCE IN HELA CELL CULTURES CHRONICALLY INFECTED WITH COXSACKIE B5 VIRUS¹

Richard L. Crowell²

^aLangbord Virus Laboratory, Department of Microbiology, Hahnemann Medical College, Philadelphia, Pennsylvania

² Research Career Development Award grantee of the National Institute of Allergy and Infectious Diseases, U.S. Public Health Service.

¹ Presented in part as a preliminary report before the American Society for Microbiology, Kansas City, Mo., 7 May 1962.

This article has been cited by other articles in PMC.

Abstract

Crowell, Richard L. (Hahnemann Medical College, Philadelphia, Pa.). Specific viral interference in HeLa cell cultures chronically infected with Coxsackie B5 virus. J. Bacteriol. 86:517–526. 1963.—The presence of large amounts of Coxsackie B5 virus in culture fluids of a HeLa subline, serially propagated over a 3-year period, provided evidence for attainment of a viral carrier state. Human serum in the growth medium of carrier cultures appeared prerequisite for maintenance of a stable virus-cell equilibrium. Virus was eliminated from HeLa cells by addition of B5 antiserum to the growth medium, whereas subcultivation in calf serum medium resulted in cellular degeneration by virus. HeLa cells, chronically infected by B5 virus, retained normal morphology in monolayer cultures and were found preservable by freezing. Persistently infected HeLa cells formed colonies with high efficiency in a medium containing B5 antiserum, to provide evidence that the majority of cells in carrier populations were not fatally infected. The significance of occurrence of small and large plaque variants of B5 virus in the carrier system remains to be determined. Coxsackie B5-carrier cultures were found specifically resistant to superinfection by all members of Coxsackie group B. This resistance, due to viral interference, was not extended to three immunological types of Coxsackie group A, poliovirus types 1 to 3, adenovirus T1, or vaccinia virus. Viral interference was found to be a consequence of altered surfaces of carrier cells, as reflected by decreased adsorption kinetics and cell penetration by Coxsackie group B viruses. The data suggested that Coxsackie group B viruses share a unique requirement, distinct from that of polioviruses, for reception and eclipse by HeLa cells. Interference between polioviruses and members of Coxsackie group B is discussed.

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Selected References

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