Open AccessHuman microRNA‐30 inhibits influenza virus infection by suppressing the expression of SOCS1, SOCS3, and NEDD4
Author(s) -
Lin Xian,
Yu Shiman,
Ren Peilei,
Sun Xiaomei,
Jin Meilin
Publication year - 2020
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.13150
Subject(s) - biology , microrna , influenza a virus , suppressor of cytokine signaling 1 , socs3 , interferon , suppressor of cytokine signalling , immune system , stat , virology , virus , immunology , signal transduction , microbiology and biotechnology , gene , stat3 , genetics , suppressor
Abstract Influenza A virus (IAV) has evolved multiple mechanisms to compromise type I interferon (IFN) responses. The antiviral function of IFN is mainly exerted by activating the JAK/STAT signalling and subsequently inducing IFN‐stimulated gene (ISG) production. However, the mechanism by which IAV combat the type I IFN signalling pathway is not fully elucidated. In this study, we explored the roles of human microRNAs modulated by IAV infection in type I 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 member 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 signalling pathway. In addition, miR‐30 family members inhibited the expression of NEDD4, a negative regulator of IFITM3, which is important for host defence against influenza viruses. Our findings suggest that IAV utilises 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.