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MicroRNA‐92a inhibits macrophage antiviral response by targeting retinoic acid inducible gene‐I
Author(s) -
Sheng Yuanjian,
Wang Yong,
Lu Wei,
Zhou Yunlian,
Dong Guijuan,
Ge Xiaoxing,
Song Yinjing,
Zhang Yuanyuan
Publication year - 2018
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12640
Subject(s) - biology , vesicular stomatitis virus , innate immune system , irf3 , microrna , transcription (linguistics) , microbiology and biotechnology , retinoic acid , viral replication , interferon , immune system , gene , virology , virus , immunology , genetics , linguistics , philosophy
MicroRNAs are short, non‐coding RNAs that have been shown to regulate a wide range of biological processes, including host antiviral immune responses. In the present study, microRNA‐92a (miR‐92a) was identified as a negative regulator in macrophage‐mediated antiviral responses. Overexpression of miR‐92a decreases vesicular stomatitis virus (VSV)‐induced production of type‐I IFNs and facilitates viral replication in macrophages. The mechanism is that miR‐92a directly targets RIG‐I and reduces its expression, thereby attenuating VSV‐triggered activation of TBK‐binding kinase 1 and IRF3, both of which are crucial for initiating transcription of type‐I IFN genes. Our results demonstrate for the first time the novel role of miR‐92a in suppressing antiviral innate immunity.