TRIM35 mediates protection against influenza infection by activating TRAF3 and degrading viral PB2

文献类型： 外文期刊

第一作者： Sun, Nan

作者： Sun, Nan;Jiang, Li;Ye, Miaomiao;Wang, Yihan;Wang, Guangwen;Wan, Xiaopeng;Zhao, Yuhui;Wen, Xia;Liang, Libin;Ma, Shujie;Liu, Liling;Bu, Zhigao;Chen, Hualan;Li, Chengjun

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关键词： influenza A virus; PB2; TRIM35; TRAF3; ubiquitination; antiviral immunity

期刊名称：PROTEIN & CELL （ 影响因子：14.87； 五年影响因子：11.279 ）

ISSN： 1674-800X

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收录情况： SCI

摘要： Tripartite motif (TRIM) family proteins are important effectors of innate immunity against viral infections. Here we identified TRIM35 as a regulator of TRAF3 activation. Deficiency in or inhibition of TRIM35 suppressed the production of type I interferon (IFN) in response to viral infection.Trim35-deficient mice were more susceptible to influenza A virus (IAV) infection than were wild-type mice. TRIM35 promoted the RIG-I-mediated signaling by catalyzing Lys63-linked polyubiquitination of TRAF3 and the subsequent formation of a signaling complex with VISA and TBK1. IAV PB2 polymerase countered the innate antiviral immune response by impeding the Lys63-linked polyubiquitination and activation of TRAF3. TRIM35 mediated Lys48-linked polyubiquitination and proteasomal degradation of IAV PB2, thereby antagonizing its suppression of TRAF3 activation. Ourin vitroandin vivofindings thus reveal novel roles of TRIM35, through catalyzing Lys63- or Lys48-linked polyubiquitination, in RIG-I antiviral immunity and mechanism of defense against IAV infection.

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