The C-Terminal Effector Domain of Non-Structural Protein 1 of Influenza A Virus Blocks IFN-ß Production by Targeting TNF Receptor-Associated Factor 3

Qian, Wei; Wei, Xiaoqin; Guo, Kelei; Li, Yongtao; Lin, Xian; Zou, Zhong; Zhou, Hongbo; Jin, Meilin

PRRs of host cells recognize a PAMP and subsequently initiate a series of signaling cascades. The final step is activation of IRF3 and NF-κB, thus inducing the transcription of IFN-β (33) . Given the cascade of responses triggered by the host in response to infection, influenza viruses adapted different strategies to escape the IFN response. This survival tactic has proven successful in order for virus proliferation and infection. Both PB2 and PB1-F2 limit IFN production by associating with MAVS (10, 34, 35) . Other structural proteins, such as PB1, PA, NP, and even the genomic RNA itself, also contribute to impairing RIG-I-mediated antiviral responses (36) . Moreover, HA (HA1) was recently shown to drive the degradation of the IFN receptor chain IFNAR1, thereby suppressing IFN-triggered JAK/STAT signaling (37) . The most effective weapon influenza A viruses have at their disposal is NS1 protein.