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PMID: 6287000 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

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

Journal of virology ·Vol. 43 ·No. 1 ·1982-07-00 ·Pages 250-61

Jen G, Thach RE

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 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.

MeSH Terms
Animals Carrier Proteins/metabolism Encephalomyocarditis virus/physiology Kinetics L Cells Mice Peptide Chain Initiation, Translational Peptide Initiation Factors/metabolism Protein Biosynthesis RNA Cap-Binding Proteins RNA Caps/metabolism RNA, Messenger/genetics Subcellular Fractions/analysis
Chemicals
Carrier Proteins Peptide Initiation Factors RNA Cap-Binding Proteins RNA Caps RNA, Messenger
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Jen G
Thach R E
References (34)
34 references, click to expand
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
Published
1982-07-00
Pages
250-61
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC256116
Subset
IM
Grants
NCI NIH HHS · CA 13008 · United States
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