Premium
Mir‐302c mediates influenza A virus‐induced IFNβ expression by targeting NF‐κB inducing kinase
Author(s) -
Gui Shulin,
Chen Xueyuan,
Zhang Mo,
Zhao Fanpeng,
Wan Yushun,
Wang Li,
Xu Gang,
Zhou Li,
Yue Xin,
Zhu Ying,
Liu Shi
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.11.011
Subject(s) - microrna , influenza a virus , messenger rna , microbiology and biotechnology , biology , viral replication , virus , virology , cytosol , untranslated region , signal transduction , rig i , gene , rna , enzyme , genetics , biochemistry
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 IFNβ 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 IFNβ 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 IFNβ mRNA expression during IAV infection.