Influenza A virus use of BinCARD1 to facilitate the binding of viral NP to importin alpha 7 is counteracted by TBK1-p62 axis-mediated autophagy

文献类型： 外文期刊

第一作者： Wang, Xuyuan

作者： Wang, Xuyuan;Shi, Wenjun;Chen, Hualan;Wang, Xuyuan;Li, Chengjun;Chen, Hualan;Wang, Xuyuan;Jiang, Li;Wang, Guangwen;Shi, Wenjun;Hu, Yuzhen;Wang, Bo;Zeng, Xianying;Tian, Guobin;Deng, Guohua;Shi, Jianzhong;Liu, Liling;Li, Chengjun;Chen, Hualan

作者机构：

关键词： Influenza A virus; BinCARD1; TRAF3; TBK1; p62

期刊名称：CELLULAR & MOLECULAR IMMUNOLOGY （ 影响因子：22.096； 五年影响因子：17.7 ）

ISSN： 1672-7681

年卷期： 2022 年 19 卷 10 期

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收录情况： SCI

摘要： As a major component of the viral ribonucleoprotein (vRNP) complex in influenza A virus (IAV), nucleoprotein (NP) interacts with isoforms of importin alpha family members, leading to the import of itself and vRNP complex into the nucleus, a process pivotal in the replication cycle of IAV. In this study, we found that BinCARD1, an isoform of Bcl10-interacting protein with CARD (BinCARD), was leveraged by IAV for efficient viral replication. BinCARD1 promoted the nuclear import of the vRNP complex and newly synthesized NP and thus enhanced vRNP complex activity. Moreover, we found that BinCARD1 interacted with NP to promote NP binding to importin alpha 7, an adaptor in the host nuclear import pathway. However, we also found that BinCARD1 promoted RIG-I-mediated innate immune signaling by mediating Lys63-linked polyubiquitination of TRAF3, and that TBK1 appeared to degrade BinCARD1. We showed that BinCARD1 was polyubiquitinated at residue K103 through a Lys63 linkage, which was recognized by the TBK1-p62 axis for autophagic degradation. Overall, our data demonstrate that IAV leverages BinCARD1 as an important host factor that promotes viral replication, and two mechanisms in the host defense system are triggered-innate immune signaling and autophagic degradation-to mitigate the promoting effect of BinCARD1 on the life cycle of IAV.

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