The association of ribosomal protein L18 (RPL18) with infectious bursal disease virus viral protein VP3 enhances viral replication.
[No authors listed]
摘要
Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by IBD virus (IBDV). IBDV VP3 is a multifunctional protein playing a key role in virus assembly and pathogenesis. To investigate the role of VP3 in pathogenesis, we transfected DF-1 cells with pRK5-FLAG-vp3 and found that VP3 enhanced type I interferon expression and suppressed IBDV replication. Furthermore we found that VP3 interacted with chicken Ribosomal Protein L18 (chRPL18) in host cells and knockdown of chRPL18 by significantly promoted Type I interferon expression and inhibited IBDV replication. Moreover, our data show that chicken double-stranded RNA-activated protein kinase (chPKR) interacted with both VP3 and chRPL18. Thus chRPL18 in association with VP3 and chPKR affects viral replication.
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基因功能
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原始数据
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文献解读
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