Specificity of protein synthesis inhibitors in the inhibition of encephalomyocarditis virus replication.
Effect of protein synthesis inhibitors on encephalomyocarditis virus production in L-cells was studied. Inhibition of initiation by hypertonicity, harringtonine, or pactamycin decreased viral protein synthesis to a lesser extent than that of host. Virus yield was unaffected or actually enhanced by low concentrations of these inhibitors. On the contrary, the elongation inhibitors cycloheximide, anisomycin, and emetine, shown previously to inhibit viral protein synthesis preferentially, had a greater effect on virus yield than on overall protein synthesis. These results support our earlier proposal that the antiviral activity of cycloheximide derives from its specific effect on the rate of elongation of protein synthesis, and that elongation inhibitors in general may show varying degrees of specific antiviral activity.
D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D003513:Cycloheximide / Q000494:pharmacology; D004640:Emetine / Q000494:pharmacology; D004686:Encephalomyocarditis virus / Q000187:drug effects / Q000254:growth & development*; D006248:Harringtonines / Q000494:pharmacology; D006982:Hypertonic Solutions; D007739:L Cells; D051379:Mice; D010142:Pactamycin / Q000494:pharmacology; D010441:Peptide Chain Elongation, Translational / Q000187:drug effects*; D010442:Peptide Chain Initiation, Translational / Q000187:drug effects*; D014764:Viral Proteins / Q000096:biosynthesis*; D014779:Virus Replication / Q000187:drug effects
D006248:Harringtonines; D006982:Hypertonic Solutions; D014764:Viral Proteins; D010142:Pactamycin; D000841:Anisomycin; D003513:Cycloheximide; D004640:Emetine