Mechanism of interferon action Differential effect of interferon on the synthesis of simian virus 40 and reovirus polypeptides in monkey kidney cells

Abstract

The effect of interferon (IFN) treatment on the synthesis of viral proteins was examined in BSC-1 monkey kidney cells singly and doubly infected with simian virus 40 (SV40) and reovirus. The pattern and amount of SV40 T antigen and reovirus λ, μ, and σ polypeptide synthesis were comparable in the singly and doubly infected cells in the absence of IFN treatment. As determined by Yakobson et al. ( Cell 12: 73–81, 1977) and Kingsman and Samuel ( Virology 101: 458–465, 1980) SV40-specific RNA synthesis is inhibited by treatment of cells with IFN before infection, but is not inhibited by IFN treatment after infection. IFN treatment initiated before infection inhibited the synthesis of both SV40 T antigen and reovirus polypeptides. However, SV40 T antigen synthesis was not inhibited in SV40 wt or tsA mutant-infected cells when treated with monkey kidney or human leukocyte IFN after infection. By contrast, reovirus polypeptide synthesis was markedly inhibited in BSC-1 cells treated with IFN after SV40 infection and superinfected with reovirus. SV40 infection did not rescue reovirus polypeptide synthesis from the inhibitory action of IFN, and reovirus infection did not alter the resistance of SV40 T antigen synthesis to IFN in cells IFN-treated after SV40 infection. Total cellular protein synthesis was not significantly affected by IFN treatment. These results suggest that the interferon-induced inhibitor(s) of protein synthesis discriminate between SV40 and reovirus mRNAs; the translation of SV40 mRNA, like most cellular mRNAs, is not affected under conditions where the IFN-induced inhibitor(s) significantly affect the translation of reovirus mRNA.