Critical role for voltage-dependent anion channel 2 in infectious bursal disease virus-induced apoptosis in host cells via interaction with VP5.

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 Virol

journal_title

Journal of virology

authors

Li Z,Wang Y,Xue Y,Li X,Cao H,Zheng SJ

doi

10.1128/JVI.06104-11

subject

Has Abstract

pub_date

2012-02-01 00:00:00

pages

1328-38

issue

3

eissn

0022-538X

issn

1098-5514

pii

JVI.06104-11

journal_volume

86

pub_type

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