Signaling Lymphocytic Activation Molecule Family Member 1 Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication

文献类型： 外文期刊

第一作者： Song, Haofei

作者： Song, Haofei;Quan, Jima;Zhang, Lan;Li, Peng;Song, Haofei;Quan, Jima;Li, Chang;Liang, Wan;Zhang, Lan;Wang, Shuangshuang;Lu, Hongyu;Yang, Keli;Zhou, Danna;Tian, Yongxiang

作者机构：

关键词： PRRSV; SLAMF1; replication; innate immunity; inflammatory cytokines

期刊名称：ANIMALS （ 影响因子：3.231； 五年影响因子：3.312 ）

ISSN： 2076-2615

年卷期： 2022 年 12 卷 24 期

页码：

收录情况： SCI

摘要： Simple Summary PRRS is one of the most important diseases that has brought significant economic losses to the swine industry worldwide. SLAMF1 is a costimulatory factor that is involved in innate immunity, inflammation, and infection. In this study, we demonstrate that overexpression of the SLAMF1 gene inhibited PRRSV replication significantly and reduced the levels of key signaling pathways, including MyD88, RIG-I, TLR2, TRIF, and inflammatory factors IL-6, IL-1 beta, IL-8, TNF-beta, TNF-alpha, and IFN-alpha in vitro. However, the knockdown of the SLAMF1 gene could enhance the replication of the PRRSV and the levels of key signaling pathways and inflammatory factors. Overall, our results identify a new antagonist of the PRRSV, providing a new reference and direction for PRRSV disease resistance breeding. The porcine reproductive and respiratory syndrome virus (PRRSV) causes a highly contagious disease in domestic swine. Signaling lymphocytic activation molecule family member 1 (SLAMF1) is a costimulatory factor that is involved in innate immunity, inflammation, and infection. Here, we demonstrate that overexpression of the SLAMF1 gene inhibited PRRSV replication significantly and reduced the levels of key signaling pathways, including MyD88, RIG-I, TLR2, TRIF, and inflammatory factors IL-6, IL-1 beta, IL-8, TNF-beta, TNF-alpha, and IFN-alpha in vitro. However, the knockdown of the SLAMF1 gene could enhance replication of the PRRSV and the levels of key signaling pathways and inflammatory factors. Overall, our results identify a new, to our knowledge, antagonist of the PRRSV, as well as a novel antagonistic mechanism evolved by inhibiting innate immunity and inflammation, providing a new reference and direction for PRRSV disease resistance breeding.

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