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CHID1 positively regulates RLR antiviral signaling by targeting the RIG‐I/VISA signalosome
Author(s) -
Li ShengNa,
Ling Ting,
Yang YaXian,
Huang JingPing,
Xu LiangGuo
Publication year - 2019
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.25508
Subject(s) - irf3 , rig i , biology , signal transducing adaptor protein , interferon regulatory factors , microbiology and biotechnology , signal transduction , sendai virus , interferon , gene knockdown , receptor , virology , innate immune system , virus , gene , genetics
Retinoic acid‐inducible gene‐I (RIG‐I) belongs to the RIGI‐like receptors (RLRs), a class of primary pattern recognition receptors. It senses viral double‐strand RNA in the cytoplasm and delivers the activated signal to its adaptor virus‐induced signaling adapter (VISA), which then recruits the downstream TNF receptor‐associated factors and kinases, triggering a downstream signal cascade that leads to the production of proinflammatory cytokines and antiviral interferons (IFNs). However, the mechanism of RIG‐I‐mediated antiviral signaling is not fully understood. Here, we demonstrate that chitinase domain‐containing 1 (CHID1), a member of the chitinase family, positively regulates the RLR antiviral signaling pathway by targeting the RIG‐I/VISA signalosome. CHID1 overexpression enhances the activation of nuclear factor κB (NF‐кB) and interferon regulatory factor 3 (IRF3) triggered by Sendai virus (SeV) by promoting the polyubiquitination of RIG‐I and VISA, thereby potentiating IFN‐β production. CHID1 knockdown in human 239T cells inhibits SeV‐induced activation of IRF3 and NF‐κB and the induction of IFN‐β. These results indicate that CHID1 positively regulates RLR antiviral signal, revealing the novel mechanism of the RIG‐I antiviral signaling pathway.