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miR-382-5p promotes porcine reproductive and respiratory syndrome virus (PRRSV) replication by negatively regulating the induction of type I interferon

文献类型： 外文期刊

作者： Chang, Xiaobo 1 ; Shi, Xibao 1 ; Zhang, Xiaozhuan 3 ; Chen, Jing 4 ; Fan, Xiaomin 3 ; Yang, Yuanhao 3 ; Wang, Li 1 ; Wang 1 ;

作者机构： 1.Henan Acad Agr Sci, Henan Prov Key Lab Anim Immunol, 116 Huayuan Rd, Zhengzhou 450002, Henan, Peoples R China

2.Northwest A&F Univ, Coll Vet Med, Yangling, Shaanxi, Peoples R China

3.Henan Normal Univ, Coll Life Sci, Xinxiang, Henan, 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

关键词： antiviral protein; HSP60; MAVS

期刊名称：FASEB JOURNAL （ 影响因子：5.191； 五年影响因子：5.955 ）

ISSN： 0892-6638

年卷期： 2020 年 34 卷 3 期

页码：

收录情况： SCI

摘要： Previous studies have indicated that inhibition of type I interferon production may be an important reason for porcine reproductive and respiratory syndrome virus (PRRSV) to achieve immune escape, revealing the mechanism of inhibiting the production of type I interferon will help design novel strategies for controlling PRRS. Here, we found that PRRSV infection upregulated the expression of miR-382-5p, which in turn inhibited polyI:C-induced the production of type I interferon by targeting heat shock protein 60 (HSP60), thus facilitating PRRSV replication in MARC-145 cells. Furthermore, we found that HSP60 could interact with mitochondrial antiviral signaling protein (MAVS), an important signal transduction protein for inducing production of type I interferon, and promote polyI:C-mediated the production of type I interferon in a MAVS-dependent manner. Finally, we also found that HSP60 could inhibit PRRSV replication in a MAVS-dependent manner, which indicated that HSP60 was a novel antiviral protein against PRRSV replication. In conclusion, the study demonstrated that miR-382-5p was upregulated during PRRSV infection and may promote PRRSV replication by negatively regulating the production of type I interferon, which also indicated that miR-382-5p and HSP60 might be the potential therapeutic targets for anti-PRRSV.

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