The target reaction in the antiviral action of mouse interferon against vesicular stomatitis virus multiplication.
Treatment of mouse L929 cells with mouse interferon (IFN) lowered the yield of vesicular stomatitis virus (VSV) in a dose-dependent manner. Accumulation of viral proteins was severely inhibited in IFN-treated cells, whereas cellular protein synthesis was not, indicating that the virus-induced shutoff of cellular protein synthesis was prevented by IFN. In order to identify the major target of IFN action precisely, the effect of IFN treatment on the synthesis of viral RNAs and proteins at various stages during the course of viral replication was examined. Accumulation of viral RNAs late in infection was inhibited, as was the case with viral proteins, but the synthesis of leader RNA and mRNAs early in infection was not significantly inhibited by treatment with a moderate dose of IFN. On the other hand, viral protein synthesis at an early stage of infection was strongly inhibited by IFN. The results indicate that the major target reaction of antiviral action of IFN against VSV multiplication is the translation of viral mRNA.
D000818:Animals; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D004591:Electrophoresis, Polyacrylamide Gel; D007372:Interferons / Q000494:pharmacology*; D051379:Mice; D011494:Protein Kinases / Q000378:metabolism; D012330:RNA, Double-Stranded / Q000378:metabolism; D012367:RNA, Viral / Q000096:biosynthesis; D014721:Vesicular stomatitis Indiana virus / Q000187:drug effects / Q000502:physiology*; D014764:Viral Proteins / Q000096:biosynthesis; D014779:Virus Replication / Q000187:drug effects*
D012330:RNA, Double-Stranded; D012367:RNA, Viral; D014764:Viral Proteins; D007372:Interferons; D011494:Protein Kinases