Document Detail


Coxsackievirus protein 2BC blocks host cell apoptosis by inhibiting caspase-3.
MedLine Citation:
PMID:  16608851     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Virus infection may induce host cell death by apoptosis, but some DNA viruses are capable of preventing this process. RNA viruses were thought not to display anti-apoptotic activities, as their spread appears to benefit from a rapid induction of cell death. Here, we report an antiapoptotic activity in the Picornavirus Coxsackievirus B4 (CVB4). CVB4 infection of HeLa cells induced negligible apoptosis over a period of 10 h. However, infected cells developed resistance to drug-induced apoptosis using staurosporine and actinomycin D and to death receptor-induced apoptosis using tumor necrosis factor-related apoptosis-inducing ligand. Despite this resistance, the apoptotic machinery was nonetheless fully activated in these drug-treated infected cells because the levels of pro-caspase-3 processing to its active form were similar to control cells. However, the DEVDase (Asp-Glu-Val-Asp protease) activity of the processed caspase was significantly inhibited in the virus-infected staurosporine-treated cells compared with drug treatment alone. Likewise, extracts of CVB4-infected cells suppressed recombinant caspase-3 activity in vitro. Immunoprecipitation of activated caspase-3 from radiolabeled virus-infected cells revealed the co-precipitation of a 48-kDa protein that was tentatively identified as viral protein 2BC. Recombinant caspase-3 was found to co-precipitate with virus protein 2BC. Finally, when protein 2BC was expressed in HeLa cells, both staurosporine-induced apoptosis and in vitro caspase-3 DEVDase activity were significantly reduced. Taken together these data imply that CVB4 infection suppresses apoptosis through virus protein 2BC associating with caspase-3 and inhibiting its function. Thus, 2BC is the first reported RNA virus inhibitor of apoptosis protein.
Authors:
Michael A Salako; Michael J Carter; George E N Kass
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-04-11
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  281     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2006 Jun 
Date Detail:
Created Date:  2006-06-12     Completed Date:  2006-08-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  16296-304     Citation Subset:  IM    
Affiliation:
School of Biomedical and Molecular Sciences, University of Surrey, Guildford, GU2 7XH, United Kingdom.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Apoptosis*
Apoptosis Regulatory Proteins / metabolism
Caspase 3
Caspases / antagonists & inhibitors*,  metabolism
Dactinomycin / pharmacology
Enterovirus*
Enzyme Inhibitors / pharmacology*
Flow Cytometry
Hela Cells
Humans
Membrane Glycoproteins / metabolism
Molecular Sequence Data
Recombinant Proteins / chemistry
Sequence Homology, Amino Acid
TNF-Related Apoptosis-Inducing Ligand
Tumor Necrosis Factor-alpha / metabolism
Viral Nonstructural Proteins / metabolism*
Chemical
Reg. No./Substance:
0/Apoptosis Regulatory Proteins; 0/Enzyme Inhibitors; 0/Membrane Glycoproteins; 0/Recombinant Proteins; 0/TNF-Related Apoptosis-Inducing Ligand; 0/TNFSF10 protein, human; 0/Tumor Necrosis Factor-alpha; 0/Viral Nonstructural Proteins; 50-76-0/Dactinomycin; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases

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