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miR-541-3p Promoted Porcine Reproductive and Respiratory Syndrome Virus 2 (PRRSV-2) Replication by Targeting Interferon Regulatory Factor 7

文献类型： 外文期刊

作者： Shi, Xibao 1 ; Yang, Yuanhao 1 ; Zhang, Xiaozhuan 1 ; Chang, Xiaobo 2 ; Chen, Jing 3 ; Wang, Chao 2 ; Wang, Aiping 4 ; Wang, Jianhua 1 ; Qin, Jianru 1 ; Ye, Xianlong 1 ; Jin, Wei 1 ; Zhang, Gaiping 2 ;

作者机构： 1.Henan Normal Univ, Coll Life Sci, Ctr Pathogen Res, Engn Lab Bioconvers Technol Funct Microbes, Xinxiang 453007, Peoples R China

2.Henan Acad Agr Sci, Henan Prov Key Lab Anim Immunol, Zhengzhou 450002, Peoples R China

3.Henan Agr Univ, Coll Anim Sci & Vet Med, Int Joint Res Ctr Natl Anim Immunol, Henan Engn Lab Anim Biol Prod, Zhengzhou 450000, Peoples R China

4.Zhengzhou Univ, Dept Bioengn, Zhengzhou 450000, Peoples R China

关键词： PRRSV; type I interferon; miR-541-3p; IRF7

期刊名称：VIRUSES-BASEL （ 影响因子：5.818； 五年影响因子：5.811 ）

ISSN：

年卷期： 2022 年 14 卷 1 期

页码：

收录情况： SCI

摘要： Porcine reproductive and respiratory syndrome (PRRS) is a disease caused by PRRS virus (PRRSV), which seriously harms the pig industry. Revealing the mechanism by which PRRSV inhibits immune response will help prevent and control PRRS. Here, we found that PRRSV-2 may hijack host miR-541-3p to inhibit host innate immune response. Firstly, this work showed that miR-541-3p mimics could facilitate the replication of PRRSV-2 and the results of the quantitative real time polymerase chain reaction (qRT-PCR) showed that PRRSV-2 could up-regulate the expression of miR-541-3p in MARC-145 cells. Since previous studies have shown that type I interferon could effectively inhibit the replication of PRRSV-2, the present work explored whether miR-541-3p regulated the expression of type I interferon and found that miR-541-3p could negatively regulate the transcription of type I interferon by targeting interferon regulatory factor 7 (IRF7). More importantly, PRRSV-2 infection could down-regulate the expression of IRF7 and over-expression of IRF7 could down-regulate the replication of PRRSV-2 in MARC-145 cells. In conclusion, PRRSV-2 infection up-regulated the expression of miR-541-3p to promote its replication in MARC-145 cells, since miR-541-3p can negatively regulate the transcription of type I interferon by targeting IRF7.

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