Inhibition of host translation in encephalomyocarditis virus-infected L cells: a novel mechanism.
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 HeLa cells. However, the mechanisms of host shutoff are different in these two cases, for no reduction in the ability of lysates from encephalomyocarditis virus-infected L cells to translate capped mRNAs was observed. Instead, a change in the subcellular distribution of one or more initiation factors was seen. In particular, cap recognition activity in the high-speed supernatant fraction (S200) prepared from cell lysates increased threefold as a result of virus infection. The significance of this observation in terms of possible shutoff mechanisms is discussed. Inasmuch as the rapid host shutoff is not induced in at least four 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.
D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D004686:Encephalomyocarditis virus / Q000502:physiology*; D007700:Kinetics; D007739:L Cells; D051379:Mice; D010442:Peptide Chain Initiation, Translational; D010448:Peptide Initiation Factors / Q000378:metabolism; D014176:Protein Biosynthesis; D039381:RNA Cap-Binding Proteins; D012315:RNA Caps / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D013347:Subcellular Fractions / Q000032:analysis
D002352:Carrier Proteins; D010448:Peptide Initiation Factors; D039381:RNA Cap-Binding Proteins; D012315:RNA Caps; D012333:RNA, Messenger