Inhibition of host translation in encephalomyocarditis virus-infected L cells: a novel mechanism

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Abstract
Encephalomyocarditis virus induced a rapid shutoff of host translation in mouse L cells shortly after infection and before viral proteins were made in detectable amounts. This kinetic pattern is similar to that seen in poliovirus-infected [human cervical carcinoma] HeLa cells. The mechanisms of host shutoff are different in these 2 cases, for no reduction in the ability of lysates from encephalomyocarditis virus-infected L cells to translate capped mRNA was observed. Instead, a change in the subcellular distribution of .gtoreq. 1 initiation factors was seen. In particular, cap recognition activity in the high-speed supernatant fraction (S200) prepared from cell lysates increased 3-fold as a result of virus infection. The significance of this observation in terms of possible shutoff mechanisms is discussed. Since the rapid host shutoff is not induced in at least 4 other cell types by encephalomyocarditis virus infection, it may be concluded that host shutoff mechanisms not only vary within the picornavirus group, but also depend upon the particular cell type employed.