Antiviral activities directed against wild-type and interferon-sensitive mengovirus.
Two distinct antiviral activities can be detected in L cells treated with low levels of interferon and infected with a one-step interferon-sensitive mutant of mengovirus (is-1). The first antiviral activity (AVA-1) primarily delayed virus RNA and protein synthesis and thereby lengthened the virus replication cycle. It did not prevent cell death. The second antiviral activity (AVA-2) allowed the virus-induced inhibition of host macromolecular synthesis but inhibited all other virus functions. By 9 to 12 h post-infection host synthesis resumed and most cells survived. The data suggest that some step in the virus replication cycle activates AVA-2 leading to the destruction of the virus genome 6 to 12 h after infection. In unprotected cells the yields of parental virus (is+) and is-1 were similar. No qualitative or quantitative differences in virus products were observed by several techniques. The is-1 virus seems to have lost a wild-type function which normally blocks the action of AVA-2.
D000814:Aniline Compounds / Q000494:pharmacology; D000818:Animals; D002472:Cell Transformation, Viral; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004004:Dichlororibofuranosylbenzimidazole / Q000494:pharmacology; D006845:Hydrocarbons, Fluorinated / Q000494:pharmacology; D007372:Interferons / Q000633:toxicity*; D007700:Kinetics; D007739:L Cells / Q000187:drug effects; D008574:Mengovirus / Q000187:drug effects*; D051379:Mice; D008970:Molecular Weight; D014176:Protein Biosynthesis / Q000187:drug effects; D014158:Transcription, Genetic / Q000187:drug effects*; D014764:Viral Proteins / Q000235:genetics / Q000302:isolation & purification; D014779:Virus Replication / Q000187:drug effects
D000814:Aniline Compounds; D006845:Hydrocarbons, Fluorinated; D014764:Viral Proteins; D003609:Dactinomycin; D004004:Dichlororibofuranosylbenzimidazole; D007372:Interferons; D003513:Cycloheximide