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Porcine Reproductive and Respiratory Syndrome Virus Enhances Self-Replication via AP-1-Dependent Induction of SOCS1

文献类型： 外文期刊

作者： Luo, Xuegang 1 ; Chen, Xin-xin 2 ; Qiao, Songlin 2 ; Li, Rui 2 ; Xie, Sha 2 ; Zhou, Xinyu 2 ; Deng, Ruiguang 2 ; Zhou, En 1 ;

作者机构： 1.Northwest A&F Univ, Coll Vet Med, Yangling 712100, Shaanxi, Peoples R China

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

3.Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Jiangsu, Peoples R China

期刊名称：JOURNAL OF IMMUNOLOGY （ 影响因子：5.422； 五年影响因子：6.029 ）

ISSN： 0022-1767

年卷期： 2020 年 204 卷 2 期

页码：

收录情况： SCI

摘要： Porcine reproductive and respiratory syndrome virus (PRRSV) has caused tremendous economic losses in the swine industry since its emergence in the late 1980s. PRRSV exploits various strategies to evade immune responses and establish chronic persistent infections. Suppressor of cytokine signaling (SOCS) 1, a member of the SOCS family, is a crucial intracellular negative regulator of innate immunity. In this study, it was shown that SOCS1 can be co-opted by PRRSV to evade host immune responses, facilitating viral replication. It was observed that PRRSV induced SOCS1 production in porcine alveolar macrophages, monkey-derived Marc-145 cells, and porcine-derived CRL2843-CD163 cells. SOCS1 inhibited the expression of IFN-beta and IFN-stimulated genes, thereby markedly enhancing PRRSV replication. It was observed that the PRRSV N protein has the ability to upregulate SOCS1 production and that nuclear localization signal-2 (NLS-2) is essential for SOCS1 induction. Moreover, SOCS1 upregulation was dependent on p38/AP-1 and JNK/AP-1 signaling pathways rather than classical type I IFN signaling pathways. In summary, to our knowledge, the findings of this study uncovered the molecular mechanism that underlay SOCS1 induction during PRRSV infection, providing new insights into viral immune evasion and persistent infection.

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