Dataset for: Human microRNA-30 Inhibits Influenza Virus Infection by Suppressing the Expression of SOCS1, SOCS3, and NEDD4
datasetposted on 26.12.2019 by Xian Lin, Shiman Yu, Peilei Ren, Xiaomei Sun, Meilin Jin
Datasets usually provide raw data for analysis. This raw data often comes in spreadsheet form, but can be any collection of data, on which analysis can be performed.
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.