当前位置: X-MOL 学术J. Immunol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Porcine Reproductive and Respiratory Syndrome Virus Enhances Self-Replication via AP-1–Dependent Induction of SOCS1
The Journal of Immunology ( IF 3.6 ) Pub Date : 2019-12-11 , DOI: 10.4049/jimmunol.1900731
Xuegang Luo 1, 2 , Xin-Xin Chen 2 , Songlin Qiao 2 , Rui Li 2 , Sha Xie 2 , Xinyu Zhou 2 , Ruiguang Deng 2 , En-Min Zhou 1 , Gaiping Zhang 2, 3, 4
Affiliation  

Key Points PRRSV infection induces SOCS1 upregulation. PRRSV N protein upregulates SOCS1, and NLS-2 is essential for this function. AP-1 signaling pathways are indispensable for PRRSV-induced SOCS1 expression. 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-β 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.

中文翻译:

猪繁殖与呼吸综合征病毒通过 AP-1 依赖型 SOCS1 诱导增强自我复制

关键点 PRRSV 感染诱导 SOCS1 上调。PRRSV N 蛋白上调 SOCS1,而 NLS-2 对此功能至关重要。AP-1 信号通路对于 PRRSV 诱导的 SOCS1 表达是必不可少的。自 1980 年代后期出现以来,猪繁殖与呼吸综合征病毒 (PRRSV) 已给养猪业造成了巨大的经济损失。PRRSV 利用各种策略来逃避免疫反应并建立慢性持续感染。细胞因子信号抑制因子 (SOCS) 1 是 SOCS 家族的成员,是先天免疫的关键细胞内负调节因子。在这项研究中,表明 SOCS1 可以被 PRRSV 选择以逃避宿主免疫反应,促进病毒复制。据观察,PRRSV 在猪肺泡巨噬细胞、猴源性 Marc-145 细胞、和猪来源的 CRL2843-CD163 细胞。SOCS1 抑制 IFN-β 和 IFN 刺激基因的表达,从而显着增强 PRRSV 复制。据观察,PRRSV N 蛋白具有上调 SOCS1 产生的能力,并且核定位信号-2 (NLS-2) 对 SOCS1 的诱导至关重要。此外,SOCS1 上调依赖于 p38/AP-1 和 JNK/AP-1 信号通路,而不是经典的 I 型 IFN 信号通路。总之,据我们所知,这项研究的发现揭示了 PRRSV 感染期间 SOCS1 诱导的分子机制,为病毒免疫逃避和持续感染提供了新的见解。据观察,PRRSV N 蛋白具有上调 SOCS1 产生的能力,并且核定位信号-2 (NLS-2) 对 SOCS1 的诱导至关重要。此外,SOCS1 上调依赖于 p38/AP-1 和 JNK/AP-1 信号通路,而不是经典的 I 型 IFN 信号通路。总之,据我们所知,这项研究的发现揭示了 PRRSV 感染期间 SOCS1 诱导的分子机制,为病毒免疫逃避和持续感染提供了新的见解。据观察,PRRSV N 蛋白具有上调 SOCS1 产生的能力,并且核定位信号-2 (NLS-2) 对 SOCS1 的诱导至关重要。此外,SOCS1 上调依赖于 p38/AP-1 和 JNK/AP-1 信号通路,而不是经典的 I 型 IFN 信号通路。总之,据我们所知,这项研究的发现揭示了 PRRSV 感染期间 SOCS1 诱导的分子机制,为病毒免疫逃避和持续感染提供了新的见解。
更新日期:2019-12-11
down
wechat
bug