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MicroRNA 373 Facilitates the Replication of Porcine Reproductive and Respiratory Syndrome Virus by Its Negative Regulation of Type I Interferon Induction

文献类型： 外文期刊

作者： Chen, Jing 1 ; Shi, Xibao 2 ; Zhang, Xiaozhuan 2 ; Wang, Aiping 5 ; Wang, Li 3 ; Yang, Yanyan 3 ; Deng, Ruiguang 3 ; Zhan 1 ;

作者机构： 1.Jilin Univ, Coll Anim Sci & Vet Med, Changchun, Peoples R China

2.Henan Normal Univ, Coll Life Sci, Xinxiang, Peoples R China

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

4.Henan Agr Univ, Coll Anim Sci & Vet Med, Zhengzhou, Peoples R China

5.Zhengzhou Univ, Dept Bioengn, Zhengzhou, Peoples R China

6.Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou, Jiangsu, Peoples R China

关键词： PRRSV;miR-373;Sp1;NFIA;NFIB;IFN-beta

期刊名称：JOURNAL OF VIROLOGY （ 影响因子：5.103； 五年影响因子：5.078 ）

ISSN：

年卷期：

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收录情况： SCI

摘要： MicroRNAs (miRNAs) play an important role in the regulation of immune responses. Previous studies have indicated that dysregulating the miRNAs leads to the immunosuppression of porcine reproductive and respiratory syndrome virus (PRRSV). However, it is not clear how PRRSV regulates the expression of host miRNA, which may lead to immune escape or promote the replication of the virus. The present work suggests that PRRSV upregulated the expression of miR-373 through elevating the expression of specificity protein 1 (Sp1) in MARC-145 cells. Furthermore, this work demonstrated that miR-373 promoted the replication of PRRSV, since miR-373 was a novel negative miRNA for the production of beta interferon (IFN-beta) by targeting nuclear factor IA (NFIA), NFIB, interleukin-1 receptor-associated kinase 1 (IRAK1), IRAK4, and interferon regulatory factor 1 (IRF1). We also found that both NFIA and NFIB were novel proteins for inducing the production of IFN-beta, and both of them could inhibit the replication of PRRSV. In conclusion, PRRSV upregulated the expression of miR-373 by elevating the expression of Sp1 and hijacked the host miR-373 to promote the replication of PRRSV by negatively regulating the production of IFN-beta.

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