Mir-302c mediates influenza A virus-induced IFNß expression by targeting NF-κB inducing kinase.

Little is known about the role of microRNA during influenza A virus (IAV) infection. We observed that NIK 3'UTR luciferase activity was elevated during IAV infection. Further studies demonstrated that miR-302c reduced NIK expression, resulting in the reduction of IFNß mRNA expression. We found that miR-302c prevented the translocation of NF-κB from the cytosol to the nucleus. Furthermore, IAV infection downregulated miR-302c expression, leading to the activation of IFNß expression and the inhibition of viral replication. Compared to miR-302c, miR-520e cannot promote viral replication and production, although the two microRNAs target the same site of the NIK 3'UTR. Collectively, our work defines a novel signaling pathway implicated in the control of IFNß mRNA expression during IAV infection.