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Replication Kinetics and Cytopathic Effect of Hepatitis A Virus

Theresa Cromeans^1,2,

¹ University of North Carolina, School of Public Health, Chapel Hill, North Carolina 27514
and² Hepatitis Branch, Centers for Disease Control, 1600 Clifton Road, Atlanta, Georgia 30333, U.S.A.

The replication kinetics and c.p.e. of hepatitis A virus (HAV) strain HM-175 were shown to depend upon the passage level of the cell line, and the passage level and method of selection of the virus population. Maximum virus production under singlestep growth curve conditions occurred as early as 24 to 28 h or as late as 10 days post-infection. Although rapid replication of an isolate of HM-715 (pHM-175) occurred initially in BS-C-1 cells, its most pronounced c.p.e. was induced in FRhK-4 cells. The replication kinetics of pHM-175 in BS-C-1 cells were similar to those in FRhK-4 cells, although a higher yield of virus was obtained in the latter. The HAV that generated c.p.e. in FRhK-4 cells was obtained by two different selection processes: virus passage, or cloning of large focus-forming variants from the radioimmunofocus assay. The c.p.e. and yield of infectious pHM-175 in FRhK-4 cells could be reduced by 3 mM-guanidine. Another HAV isolate, strain MD-1, isolated directly from contaminated ground water in cell culture demonstrated c.p.e. in FRhK-4 cells after passage as persistently infected A-549 cells.

Keywords: hepatitis A virus, replication kinetics, cytopathic effect

Present address: Viral Exanthems and Herpesvirus Branch, Centers for Disease Control, Atlanta, Georgia 30333, U.S.A.

Received 28 July 1988; accepted 12 April 1989.

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