TRIM2 negatively regulates antiviral immunity by degradation of MDA5 and STAT2 during influenza A virus infection - Nature
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AbstractThis study identifies TRIM2 as an interferon-stimulated gene (ISG) regulated by both type I and type II interferons. Contrary to the typical antiviral role of most ISGs, TRIM2 significantly enhances influenza A virus (IAV) replication both in vitro and in vivo. Mechanistically, TRIM2 functions as a negative regulator of the MDA5-mediated antiviral signaling pathway, contributing to the suppression of IFN-β production in part through promoting K48-linked polyubiquitination of MDA5. It directly interacts with MDA5 via its CC and Fn domains, promoting K48-linked polyubiquitination of MDA5 at Lysine 538, which leads to its proteasomal degradation and subsequent suppression of IFN-β production. Furthermore, TRIM2 interacts with and degrades STAT2 via K48-linked ubiquitination, further suppressing interferon signaling.
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