The Influence of the Host Cell on the Inhibition of Virus Protein Synthesis in Cells Doubly Infected with Vesicular Stomatitis Virus and Mengovirus

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Abstract
The ability of mengovirus to inhibit the synthesis of vesicular stomatitis virus (VSV) proteins and of VSV to inhibit the synthesis of mengovirus proteins during double infection in 3 different cell lines was investigated. Although cellular protein synthesis was inhibited after infection of cells by each virus, the ability of one virus to decrease translation of the mRNA species of the co-infecting virus varied with the cell type. Superinfection of mengovirus-infected [murine fibroblast] L-929 cells by VSV resulted in essentially no inhibition in the synthesis of mengovirus or VSV proteins. In HeLa cells and CHO cells [human cervical carcinoma, Chinese hamster ovary] the synthesis of VSV and mengovirus proteins was inhibited under conditions of simultaneous or sequential infection. The inhibition of VSV protein synthesis after infection of HeLa cells by mengovirus was not a result of a modification or inactivation of virus mRNAs. When extracted from doubly infected cells, the VSV mRNAs manifested normal biological activity, as determined by their ability to stimulate the synthesis of VSV proteins in a micrococcal nuclease-treated cell-free system from L cells. The interference or non-interference of one virus by another in different cell lines was also measured by quantifying the number of infectious particles produced in each cell line. The results were similar to those reported above for protein synthesis inhibition. These experiments suggest that the interference of mengovirus with VSV mRNA translation in HeLa cells is not necessarily reflective of the mechanism by which mengovirus inhibits cellular protein synthesis. The host cell appears to influence the extent or nature of the interference of one virus by the other.