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TRIM29通过针对nsp11进行降解来抑制PRRSV的复制

Wei Wen¹, Zhenghong Xue¹, Yi Lu¹

¹Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou, People's Republic of China.

Journal of virology

|November 18, 2025

概括

猪生殖和呼吸系统综合征病毒nsp11通过K48链接的ubiquitination被ubiquitin-proteasome系统降解. 主体TRIM29链酶向NSP11,抑制病毒复制和免疫逃避.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

在病毒感染中,乌比基提尼作用至关重要.
猪生殖和呼吸系统综合征病毒 (PRRSV) nsp11是一种内啡核糖酶,对病毒复制至关重要.
PRRSV nsp11 抑制宿主干扰素的产生.

研究的目的:

为了研究PRRSV nsp11的无处不在性.
为了确定调节nsp11稳定性和功能的宿主因素.
阐明PRRSV规避宿主免疫力的机制.

主要方法:

局部定向的突变发生,以产生无处不在缺陷的nsp11突变.
西方斑点分析以检测无处不在和蛋白质水平.
同免疫沉用于识别相互作用的主体蛋白质.
干扰素报告员测试以评估抗病毒活性.
病毒复制试验. 病毒复制试验.

主要成果:

在PRRSV nsp11中,在lysine 173 (K173) 处经历K48结合的多比基化.
乌比基因化向NSP11通过乌比基因-蛋白酶体系统 (UPS) 进行降解.
主体E3泛基因酶TRIM29与nsp11结合,并调解其与K48结合的泛基因化和降解.
通过TRIM29介导的nsp11降解通过恢复干扰素的产生来抑制病毒复制.
这种无处不在的机制在大多数动脉病毒中保持着.

结论:

PRRSV nsp11是由UPS介导的降解通过K48连接的K173.3处的全域化调节的.
TRIM29通过降解nsp11作为宿主限制因子,从而抑制PRRSV.
这种保存的机制突出显示了动脉病毒感染中关键的宿主-病原体相互作用.

关键词:

PRRSVV 在这个问题上.在 TRIM29 中,内核酶活动部位.在NSP11中使用.蛋白质酶体降解的降解

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