The viral proteins of influenza A virus competitively bind to TRIM31 with MAVS to fine-tune the antiviral innate immunity.

ABSTRACT: The influenza A virus (IAV) continues to pose a serious threat to animals and humans, making it urgent to reveal more about IAV-host interactions. Tripartite motif protein 31 (TRIM31), an E3 ubiquitin ligase, has been identified as an agonist of the type-I interferon (IFN-I) response against RNA viruses by targeting mitochondrial antiviral signaling protein (MAVS). Here, we demonstrated that TRIM31 plays critical and novel roles in the life cycle of IAV. TRIM31 promoted the IFN-I signaling induced by IAV; however, it was surprisingly found that TRIM31 does not affect IAV replication. Instead, IAV replication was significantly promoted by TRIM31 in MAVS- or interferon receptor-deficient cells, suggesting TRIM31 may facilitate IAV replication in an interferon-independent manner. Mechanistica

SUBMITTER: Huang J 

PROVIDER: S-EPMC12724384 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature