Inhibitors of protein synthesis inhibit both La Crosse virus S-mRNA and S genome syntheses in vivo.
The effect of drugs such as puromycin and cycloheximide, which inhibit protein synthesis, on the accumulation of La Crosse virus S genome RNAs in vivo has been examined. We have found that if these drugs are added to the cultures before infection, minuscule amounts of S-mRNA can be detected late in infection. Genome replication, on the other hand, cannot be detected at any time. When these drugs are added later in infection when RNA synthesis is well established, S-mRNA accumulation decreases in a dose-dependent manner proportional to the effect of these drugs on protein synthesis. This decrease cannot be accounted for by increased turnover of the mRNA in the presence of the drug. S genome replication, curiously, was found to be hypersensitive to the effects of these drugs. Our results confirm those of Abraham and Pattnaik (1983) that ongoing protein synthesis is required for the accumulation of complete bunyavirus S-mRNA.
D000841:Anisomycin / Q000494:pharmacology; D002043:Bunyaviridae / Q000235:genetics*; D003513:Cycloheximide / Q000494:pharmacology*; D002141:Encephalitis Virus, California / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D005814:Genes, Viral / Q000187:drug effects; D010142:Pactamycin / Q000494:pharmacology; D014176:Protein Biosynthesis; D011691:Puromycin / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis*; D012367:RNA, Viral / Q000096:biosynthesis*; D014243:Trichodermin / Q000494:pharmacology
D012333:RNA, Messenger; D012367:RNA, Viral; D010142:Pactamycin; D014243:Trichodermin; D011691:Puromycin; D000841:Anisomycin; D003513:Cycloheximide