Host involvement in vaccinia virus replication.
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.
D000818:Animals; D002460:Cell Line; D003588:Cytopathogenic Effect, Viral; D004261:DNA Replication; D004279:DNA, Viral / Q000096:biosynthesis; D004259:DNA-Directed DNA Polymerase / Q000096:biosynthesis; D003851:Deoxyribonucleases / Q000378:metabolism; D004790:Enzyme Induction; D007700:Kinetics; D008574:Mengovirus / Q000502:physiology; D013937:Thymidine Kinase / Q000096:biosynthesis; D014616:Vaccinia virus / Q000201:enzymology / Q000502:physiology*; D014779:Virus Replication
D004279:DNA, Viral; D013937:Thymidine Kinase; D004259:DNA-Directed DNA Polymerase; D003851:Deoxyribonucleases