Abstract

Superinfection of vesicular stomatitis virus (VSV)-infected cells with poliovirus causes a complete inhibition of VSV-directed protein synthesis, followed by normal replication of poliovirus. The “shut-off” of VSV protein synthesis appears similar in all respects to the inhibition of host cell protein synthesis normally induced by poliovirus infection. VSV messenger RNA (mRNA) synthesis continues at normal rates after superinfection. This RNA appears to accumulate and to remain intact, although it does not associate with ribosomes. The untranslated RNA is polyadenylated, capped, and methylated normally. Furthermore, when extracted from superinfected cells, it manifests normal biological function, measured by its ability to stimulate the synthesis of VSV proteins by a cell-free wheat germ protein-synthesizing extract. Thus, the inhibition of protein synthesis by poliovirus does not seem to be the result of a modification or inactivation of messenger RNA.

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