Avian leukosis virus p15 interacts with interferon regulatory factor 7 to antagonize the cGAS-STING signaling pathway and promote viral replication

Among all subgroups, avian leukosis virus subgroup J is one of the most pathogenic, capable of inducing severe malignant tumors and immunosuppressive effects on the infected host. Although there have been some reports on the immunosuppressive mechanisms of ALV-J, the immune evasion mechanism mediated by ALV-J-encoded proteins remains largely unknown. In this study, we found that p15 interacted with IRF7 and inhibited the dimerization and nuclear translocation of IRF7, resulting in the suppression of the expression of IFN-β. Of note, the results demonstrated that the enzymatic active site of p15 (37D, 38S) plays a crucial role in this process. Our findings revealed that p15 enhanced ALV-J replication by inhibiting the cGAS-STING signaling pathway, which highlights the possibility of p15 as a potential drug target.