Host involvement in vaccinia virus replication.

V Zaslavsky; P H Hofschneider

doi:10.1159/000149686

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Host involvement in vaccinia virus replication.

V Zaslavsky·P H Hofschneider

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Abstract

Nutrient-depleted conditions, which induced an inhibited state in uninfected cell monolayers, rendered the cells nonpermissive for vaccinia virus, while not affecting their ability to support propagation of an unrelated mengovirus. When the inhibited state was reversed, the ability to propagate vaccinia virus was restored. The inhibited cells retained the ability to support some early-induced events (thymidine kinase synthesis and its arrest, which are DNA synthesis-independent functions in a mouse cell host), but lost the ability to support some others (sensitization of input viral DNA to DNase, induction of DNA polymerase synthesis, and virus-induced CPE). The data are consistent with involvement of a host factor(s) in induction of early vaccinia virus-induced events in infected cells.

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Animals Cell Line Cytopathogenic Effect, Viral DNA Replication DNA, Viral DNA-Directed DNA Polymerase Deoxyribonucleases Enzyme Induction Kinetics Mengovirus Thymidine Kinase Vaccinia virus Virus Replication Journal Article

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V Zaslavsky, P H Hofschneider. 1986. Host involvement in vaccinia virus replication.. https://doi.org/10.1159/000149686

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