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Downregulation of miR-296-3p by highly pathogenic porcine reproductive and respiratory syndrome virus activates the IRF1/TNF-alpha signaling axis in porcine alveolar macrophages

文献类型： 外文期刊

作者： Zhang, Yanbing 1 ; Xiang, Xiao 1 ; Lu, Yan 1 ; Li, Hui 1 ; Wahaab, Abdul 1 ; Sharma, Mona 1 ; Liu, Ke 1 ; Wei, Jianchao 1 ;

作者机构： 1.Chinese Acad Agr Sci CAAS, Shanghai Vet Res Inst, 518 Ziyue Rd, Shanghai 200241, Peoples R China

期刊名称：ARCHIVES OF VIROLOGY （ 影响因子：2.574； 五年影响因子：2.466 ）

ISSN： 0304-8608

年卷期： 2021 年 166 卷 2 期

页码：

收录情况： SCI

摘要： Porcine reproductive and respiratory syndrome virus (PRRSV, species Betaarterivirus suid 1 or 2) is a major pathogen affecting pigs on farms throughout the world. miR-296-3p is a multifunctional microRNA involved in the regulation of the inflammatory response in mice and humans. However, little is known about the biological functions of miR-296-3p in pigs. In this study, we used a highly pathogenic PRRSV-2 (species Betaarterivirus suid 2) strain to show that PRRSV infection robustly downregulates the expression of miR-296-3p in porcine alveolar macrophages (PAMs). Furthermore, we demonstrated that overexpression of miR-296-3p increases the replication of highly pathogenic (HP)-PRRSV in PAMs. Notably, the overexpression of miR-296-3p inhibited the induction of TNF-alpha, even with increased viral replication, compared with that in the HP-PRRSV-infected control group. We also demonstrated that miR-296-3p targets IRF1-facilitated viral infection and modulates the expression of TNF-alpha in PAMs during HP-PRRSV infection and that IRF1 regulates the expression of TNF-alpha by activating the TNF promoter via IRF1 response elements. In summary, these findings show that HP-PRRSV infection activates the IRF1/TNF-alpha signaling axis in PAMs by downregulating host miR-296-3p. This extends our understanding of the inflammatory response induced by HP-PRRSV infection.

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