Mode of sensitivity and resistance of vaccinia virus replication to interferon.
In this study we show that vaccinia virus replication can be sensitive or resistant to interferon (IFN) in the same strain of mouse L cells. When IFN-treated L cells were maintained in suspension culture, infection led to a rapid inhibition of both viral and cellular protein synthesis together with breakdown of viral RNA and of rRNA. When IFN-treated L cells were maintained in monolayer culture, infection did not lead to significant inhibition of viral protein or RNA synthesis and breakdown of viral or of rRNA was not observed. The resistance of vaccinia virus replication to IFN was not dependent on the input multiplicity or state of growth of the cells (actively dividing or resting). Qualitative and quantitative differences in viral transcription and translation were observed between the two virus-cell systems. Our findings are consistent with the hypothesis that the sensitivity or resistance of vaccinia virus to IFN is mediated by specific viral products that act as activators or selective inhibitors of, at least, the dsRNA-dependent ppp(A2'p)nA synthetase/RNase system.
D015088:2',5'-Oligoadenylate Synthetase / Q000378:metabolism; D000818:Animals; D007370:Interferon Type I / Q000494:pharmacology*; D007739:L Cells; D051379:Mice; D014176:Protein Biosynthesis; D012330:RNA, Double-Stranded / Q000494:pharmacology; D012335:RNA, Ribosomal / Q000378:metabolism; D012367:RNA, Viral / Q000378:metabolism; D014616:Vaccinia virus / Q000378:metabolism / Q000502:physiology*; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication
D007370:Interferon Type I; D012330:RNA, Double-Stranded; D012335:RNA, Ribosomal; D012367:RNA, Viral; D014764:Viral Proteins; D015088:2',5'-Oligoadenylate Synthetase