Dataset for: Human microRNA-30 Inhibits Influenza Virus Infection by Suppressing the Expression of SOCS1, SOCS3, and NEDD4

Influenza A virus (IAV) has evolved multiple mechanisms to compromise type I interferon (IFN) responses. The antiviral function of interferon is mainly exerted by activating the JAK/STAT signaling and subsequently inducing interferon-stimulated genes (ISGs) production. However, the mechanism by which IAV combat the type I IFN signaling pathway is not fully elucidated. In the present study, we explored the roles of human microRNAs modulated by IAV infection in type I interferon (IFN) responses. We demonstrated that microRNA-30 (miR-30) family members were downregulated by IAV infection. Our data showed that the forced expression of miR-30 family members inhibited IAV proliferation, while miR-30 family members inhibitors promoted IAV proliferation. Mechanistically, we found that miR-30 family members targeted and reduced SOCS1 and SOCS3 expression, and thus relieved their inhibiting effects on IFN/JAK/STAT signaling pathway. In addition, miR-30 family members inhibited the expression of NEDD4, a negative regulator of IFITM3, which is important for host defense against influenza viruses. Our findings suggest that IAV utilizes a novel strategy to restrain host type I IFN-mediated antiviral immune responses by decreasing the expression of miR-30 family members, and add a new way to understand the mechanism of immune escape caused by influenza viruses.