Critical role for voltage-dependent anion channel 2 in infectious bursal disease virus-induced apoptosis in host cells via interaction with VP5 |
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Authors: | Li Zhonghua Wang Yongqiang Xue Yanfei Li Xiaoqi Cao Hong Zheng Shijun J |
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Institution: | State Key Laboratory of Agrobiotechnology, Key Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, and College of Veterinary Medicine, China Agricultural University, Beijing, China. |
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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. |
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