The role of autocrine motility factor receptor in antiviral immunity

The interplay between AMFR and the cGAS-STING pathway is crucial for shaping antiviral immune responses across various viral contexts. Recent studies have demonstrated that AMFR facilitates STING activation through K27-linked polyubiquitination, which is essential for TBK1 recruitment and enhances interferon production, thereby underscoring its pivotal role in antiviral mechanisms. However, viral evasion strategies, particularly those employed by the HIV-1 p6 protein, complicate this landscape by disrupting the AMFR-STING interaction and impairing host immunity. Additionally, AMFR downregulates MAVS, further complicating the RLR-MAVS signaling pathway. Our review highlights a working model to explain how AMFR exerts opposing effects on these two pathways during different viral infections, thus providing corresponding treatment strategies. Moreover, the intricate dynamics between AMFR and viral proteins, such as NS2A and prM in flavivirus pathogenesis, reveal additional layers of regulatory interactions that are critical for understanding viral replication mechanisms. Collectively, these findings position AMFR as an important regulator of innate antiviral immunity and open potential therapeutic avenues for patients with various viral infections.