Document Detail


The herpes simplex virus 1 vhs protein enhances translation of viral true late mRNAs and virus production in a cell type-dependent manner.
MedLine Citation:
PMID:  21430045     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The herpes simplex virus 1 (HSV-1) virion host shutoff protein (vhs) degrades viral and cellular mRNAs. Here, we demonstrate for the first time that vhs also boosts translation of viral true late mRNAs in a cell type-dependent manner and that this effect determines the viral growth phenotype in the respective cell type. Our study was prompted by the detection of stress granules, indicators of stalled translation initiation, in cells infected with vhs mutants but not in wild-type-virus-infected cells. Accumulation of true late-gene products gC and US11 was strongly reduced in the absence of vhs in HeLa cells and several other restrictive cell lines but not in Vero and other permissive cells and was independent of phosphorylation of the α subunit of eukaryotic initiation factor 2 (eIF2α). Polysome analysis showed that gC and US11 transcripts were poorly translated in vhs-null-virus-infected HeLa cells, while translation of a cellular mRNA was not affected. Interestingly, hippuristanol, an eIF4A inhibitor, produced a similar phenotype in HeLa cells infected with wild-type HSV-1, while Vero cells were much more resistant to the inhibitor. These results suggest that translation of true late-gene transcripts is particularly sensitive to conditions of limited access to translation factors and that vhs is able either to prevent the limiting conditions or to facilitate translation initiation under these conditions. The varied permissivity of cell lines to vhs-null infection may stem from differences in the resilience of the translation machinery or the ability to control the accumulation of mRNAs.
Authors:
Bianca Dauber; Jerry Pelletier; James R Smiley
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-03-23
Journal Detail:
Title:  Journal of virology     Volume:  85     ISSN:  1098-5514     ISO Abbreviation:  J. Virol.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-09     Completed Date:  2011-07-13     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  0113724     Medline TA:  J Virol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5363-73     Citation Subset:  IM    
Affiliation:
Li Ka Shing Institute of Virology, Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line
Eukaryotic Initiation Factor-2 / metabolism
Gene Deletion
Herpesvirus 1, Human / genetics,  growth & development,  physiology*
Humans
Mutant Proteins / genetics,  metabolism
Polyribosomes / metabolism
Protein Biosynthesis*
RNA, Messenger / metabolism
RNA, Viral / metabolism
Ribonucleases / genetics,  metabolism*
Viral Proteins / biosynthesis*,  genetics,  metabolism
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Eukaryotic Initiation Factor-2; 0/Mutant Proteins; 0/RNA, Messenger; 0/RNA, Viral; 0/Viral Proteins; 118367-50-3/virion host shutoff protein, Simplexvirus; EC 3.1.-/Ribonucleases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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