Abstract
Treatment of monolayers of mouse L cells with 7.5 vesicular stomatitis virus plaque reduction units/ml of mouse interferon (specific activity 2 × 10 7 NIH mouse reference standard units/mg protein) results in a 95% decrease in the reovirus yield and, as shown earlier, an about 80% decrease in double-stranded and an about 60% decrease in single-stranded reo RNA accumulation in cells infected with 10 plaque-forming units of virus/cell. Interferon at this concentration does not affect the rate of accumulation of host proteins in uninfected or reovirus-infected cells. It inhibits reo virion protein accumulation in infected cells. In control cells the rate of reo virion protein accumulation increases about 2-fold between 10 and 14 hr after infection. In cells treated with interferon it remains at the same low inhibited level. Reo virion proteins were assayed in cell extracts by immunoprecipitation with antisera specific for various size classes or by gel electrophoresis. These results reveal the selective nature of the inhibition of protein accumulation in interferon-treated, virus-infected cells. The effect of treating L cells with interferon was also tested on the capacity of their extracts to translate various mRNAs. The translation of endogenous mRNA, of mRNA in L cell polysomes (added as such) and of polyuridylic acid is at most only slightly inhibited whereas that of added natural mRNAs (including reovirus and encephalomyocarditis virus mRNA, rabbit globin mRNA, and a mixture of L cell mRNAs) is strongly inhibited. The dominant nature of the inhibitor(s) is indicated by the fact that translation of added mRNA is impaired in a mixture of extracts from interferon-treated and from control cells. Thus an effect of interferon treatment of cells is manifested in subcellular systems. However, the selectivity of the effect in vivo, is not well reflected in vitro.
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