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PDCD4以依赖eIF4A的方式限制PRRSV复制,并受到病毒非结构蛋白9的对抗

Ruiping Wei¹, Xiaoxiao Zhang¹, Xiaoying Wang¹

¹State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China.

Journal of virology

|April 1, 2024

概括

猪生殖和呼吸系统综合征病毒 (PRRSV) 降解宿主蛋白编程细胞死亡4 (PDCD4),是一种病毒限制因子. PRRSV Nsp9蛋白针对PDCD4进行降解,削弱抗病毒防御并促进感染.

科学领域:

病毒学病毒学
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

病毒采用策略来逃避宿主免疫力,包括操纵宿主蛋白酶体系统.
猪生殖和呼吸系统综合征病毒 (PRRSV) 造成重大经济损失,并且很难控制.

研究的目的:

通过蛋白质体通路识别PRRSV降解的宿主蛋白质.
阐明PRRSV对抗宿主抗病毒因素的机制.
了解编程细胞死亡4 (PDCD4) 在PRRSV感染中的作用.

主要方法:

用蛋白酶体抑制剂MG132治疗的PRRSV感染细胞的定量蛋白质组学选.
同焦显微镜来追踪PDCD4的定位.
西方涂抹和免疫沉以分析蛋白质相互作用和降解途径.
RNA干扰 (RNAi) 和过度表达研究,以评估PDCD4在病毒复制中的作用.

主要成果:

PRRSV降低了编程细胞死亡4 (PDCD4) 表达的调节,这种表达通过蛋白酶体抑制得到挽救.
PRRSV感染诱导PDCD4转移到细胞质,病毒Nsp9通过Akt-mTOR-S6K1途径促进其降解.
PDCD4作为一种限制因子,通过破坏真核细胞翻译启动因子4A (eIF4A) 功能来抑制PRRSV复制.
在PDCD4的MA3域中,四个特定的位点对于其与eIF4A和抗病毒活性的相互作用至关重要.

结论:

PDCD4是一种针对PRRSV的新型宿主限制因子.
PRRSV通过Nsp9介导的蛋白质体降解来对抗PDCD4,从而促进病毒复制.
了解这种相互作用为PRRSV免疫逃避和潜在的抗病毒点提供了见解.

关键词:

在 Nsp9 中使用.在PDCD4中使用PDCD4.PRRSVV 在这个问题上.在 eIF4A 中,主体限制因素是主体限制因素.病毒与宿主之间的相互作用

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