The Association of Receptor of Activated Protein Kinase C 1(RACK1) with Infectious Bursal Disease Virus Viral Protein VP5 and Voltage-dependent Anion Channel 2 (VDAC2) Inhibits Apoptosis and Enhances Viral Replication |
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| Authors: | Wencheng Lin Zhiqiang Zhang Zhichao Xu Bin Wang Xiaoqi Li Hong Cao Yongqiang Wang Shijun J Zheng |
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| Institution: | From the ‡State Key Laboratory of Agrobiotechnology.;§Key Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, and ;¶College of Veterinary Medicine, China Agricultural University, Beijing 100193, China |
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| Abstract: | Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by IBD virus (IBDV). Our previous report indicates that IBDV VP5 induces apoptosis via interaction with voltage-dependent anion channel 2 (VDAC2). However, the underlying molecular mechanism is still unclear. We report here that receptor of activated protein kinase C 1 (RACK1) interacts with both VDAC2 and VP5 and that they could form a complex. We found that overexpression of RACK1 inhibited IBDV-induced apoptosis in DF-1 cells and that knockdown of RACK1 by small interfering RNA induced apoptosis associated with activation of caspases 9 and 3 and suppressed IBDV growth. These results indicate that RACK1 plays an antiapoptotic role during IBDV infection via interaction with VDAC2 and VP5, suggesting that VP5 sequesters RACK1 and VDAC2 in the apoptosis-inducing process. |
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| Keywords: | Apoptosis Caspase Host-Pathogen Interaction Protein Complex Viral Replication Voltage-dependent Anion Channel (VDAC) Yeast Two-hybrid Infectious Bursal Disease Virus (IBDV) Receptor of Activated Protein Kinase C 1 (RACK1) |
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