| A critical role for voltage-dependent anion channel(VDAC) 2 in infectious bursal disease virus (IBDV)-induced apoptosis in host cells via interacting with VP5. | |
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MedLine Citation:
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PMID: 22114330 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Infectious Bursal Disease (IBD) is an acute, highly contagious and immunosuppressive avian disease caused by IBD virus (IBDV). Although IBDV-induced host cell apoptosis has been established, the underlying molecular mechanism is still unclear. We report here that IBDV VP5 is a major apoptosis-inducer in DF-1 cells by interacting with the voltage-dependent anion channel 2 (VDAC2) in the mitochondrion. We found that in DF-1 cells, VP5-induced apoptosis can be completely abolished by 4, 4' -diisothiocyanatostibene-2, 2' -disulphonic acid (DIDS), an inhibitor of VDAC. Furthermore, knockdown of VDAC2 by siRNA markedly inhibits IBDV-induced apoptosis associated with decreased caspase-9 and -3 activation and cytochrome C release, leading to increased IBDV growth in host cells. Thus, VP5-induced apoptosis during IBDV infection is mediated by interacting with VDAC2, a protein that appears to restrict viral replication via inducing cell death. |
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Authors:
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Zhonghua Li; Yongqiang Wang; Yanfei Xue; Xiaoqi Li; Hong Cao; Shijun J Zheng |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-11-23 |
Journal Detail:
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Title: Journal of virology Volume: - ISSN: 1098-5514 ISO Abbreviation: - Publication Date: 2011 Nov |
Date Detail:
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Created Date: 2011-11-24 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0113724 Medline TA: J Virol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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State Key Laboratory of Agrobiotechnology. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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