Translational elongation rate changes in encephalomyocarditis virus-infected and interferon-treated cells.

摘要: Infection of mouse L cells with encephalomyocarditis virus results in a rapid inhibition host protein synthesis before the viral proteins. Although no alterations initiation factor activities have been demonstrated virus-infected cells, defect polypeptide chain elongation has shown to occur infected cell extracts. We investigated significance this shutoff phenomenon vivo. Average rates were measured at various times after infection. Interferon was used as reagent separate temporarily virus-induced alterations. Encephalomyocarditis infection lead progressive reduction rate. Whereas interferon pretreatment delayed decrease rate dose-dependent manner, it failed alter kinetics shutoff, suggesting that slowing steps played significant role phenomenon. In addition, either mock-infected or led could be attributed action.