gga-miR-9*inhibits IFN production in antiviral innate immunity by targeting interferon regulatory factor 2 to promote IBDV replication

文献类型： 外文期刊

第一作者： Ouyang, Wei

作者： Ouyang, Wei;Liu, Hua-jie;Zhang, Hai-bin;Ouyang, Wei;Wang, Yong-shan;Du, Xi-ning;Liu, Hua-jie;Ouyang, Wei;Wang, Yong-shan

作者机构：

关键词： Infectious bursal disease virus (IBDV);miRNA;gga-miR-9*;siRNA

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）

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收录情况： SCI

摘要： MicroRNAs (miRNAs) are small non-coding RNAs that contribute to the repertoire of host-pathogen interactions during viral infections. In the current study, miRNA analysis showed that a panel of microRNAs, including gga-miR-9*, were markedly upregulated in specific-pathogen-free (SPF) chickens upon infection with infectious bursal disease virus (IBDV); however, the biological function of gga-miR-9* during viral infection remains unknown. Using a TCID50 assay, it was found that ectopic expression of gga-miR-9* significantly promoted IBDV replication. In turn, gga-miR-9* negatively regulated IBDV-triggered type I IFN production, thus promoting IBDV replication in DF-1 cells. Bioinformatics analysis indicates that the 3' untranslated region (UTR) of interferon regulatory factor 2 (IRF2) has two putative binding sites for gga-miR-9*. Targeting of IRF2 3'UTR by gga-miR-9* was determined by luciferase assay. Functional overexpression of gga-miR-9*, using gga-miR-9* mimics, inhibited IRF2 mRNA and protein expression. Transfection of the gga-miR-9* inhibitor abolished the suppression of IRF2 protein expression. Furthermore, IRF2 knockdown mediated the enhancing effect of gga-miR-9* on the type I IFN-mediated antiviral response. These findings indicate that inducible gga-miR-9* feedback negatively regulates the host antiviral innate immune response by suppressing type I IFN production via targeting IRF2. (C) 2015 Elsevier B.V. All rights reserved.

分类号： S8

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