Abstract:
: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 viral protein 5 (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'-disulfonic acid (DIDS), an inhibitor of VDAC. Furthermore, knockdown of VDAC2 by small interfering RNA 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 induction of cell death.
journal_name
J Viroljournal_title
Journal of virologyauthors
Li Z,Wang Y,Xue Y,Li X,Cao H,Zheng SJdoi
10.1128/JVI.06104-11subject
Has Abstractpub_date
2012-02-01 00:00:00pages
1328-38issue
3eissn
0022-538Xissn
1098-5514pii
JVI.06104-11journal_volume
86pub_type
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