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

During the long-term symbiosis with the host, IAVs have evolved a series of unique mechanisms to adapt to the host and support their own replication. The MAVS-mediated IFN-I signaling pathway is crucial for host cells to defend against RNA virus invasion, with TRIM31 functioning as a specific agonist for the activation of IFN-I antiviral response. In the present study, we demonstrated that IAV exploits TRIM31 to promote the stability and activity of viral proteins and reduces the positive effect of TRIM31 on the IFN-I response, thereby preventing TRIM31 from inhibiting IAV replication. Therefore, our results revealed a novel mechanism employed by IAV to adapt to host antiviral response and expanded our understanding of virus-host interactions.