Critical Role for Voltage-Dependent Anion Channel 2 in Infectious Bursal Disease Virus-Induced Apoptosis in Host Cells via Interaction with VP5
- 1 February 2012
- journal article
- research article
- Published by American Society for Microbiology in Journal of Virology
- Vol. 86 (3), 1328-1338
- https://doi.org/10.1128/jvi.06104-11
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.Keywords
This publication has 40 references indexed in Scilit:
- Infectious bursal disease virus activates the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway by interaction of VP5 protein with the p85α subunit of PI3KVirology, 2011
- Recombinant Infectious Bursal Disease Virus Carrying Hepatitis C Virus EpitopesJournal of Virology, 2011
- Nuclear Factor NF45 Interacts with Viral Proteins of Infectious Bursal Disease Virus and Inhibits Viral ReplicationJournal of Virology, 2010
- Voltage-dependent anion channel (VDAC) is involved in apoptosis of cell lines carrying the mitochondrial DNA mutationBMC Medical Genetics, 2009
- The VP5 protein of infectious bursal disease virus promotes virion release from infected cells and is not involved in cell deathArchiv für die gesamte Virusforschung, 2009
- VDAC2 is required for truncated BID‐induced mitochondrial apoptosis by recruiting BAK to the mitochondriaEMBO Reports, 2009
- Viral Control of Mitochondrial ApoptosisPLoS Pathogens, 2008
- VP1 of infectious bursal disease virus is an RNA-dependent RNA polymeraseJournal of General Virology, 2004
- Bid, but Not Bax, Regulates VDAC ChannelsOnline Journal of Public Health Informatics, 2004
- A non-canonical Lon proteinase lacking the ATPase domain employs the Ser-Lys catalytic dyad to exercise broad control over the life cycle of a double-stranded RNA virusThe EMBO Journal, 2000