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纽卡斯尔病病毒V蛋白与EFTUD2的相互作用调节MDA5通路以抑制病毒复制

Yin Han¹, Fan Zhang¹, Ziqing Zhou¹

¹College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, PR China; Zhaoqing Branch Centre of Guangdong Laboratory for Lingnan Modern Agricultural Science and Technology, Zhaoqing 526238, PR China.

Poultry science

|June 28, 2025

概括

延长因子Tu GTP结合域含蛋白2 (EFTUD2) 与纽卡斯尔病病毒 (NDV) 蛋白V相互作用. 这种相互作用增强宿主免疫力,通过增强肉MDA5剪接来抑制NDV复制.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
分子生物学分子生物学

背景情况:

延长因子Tu GTP结合域含蛋白2 (EFTUD2) 是U5的snRNP组成部分和一种新的先天免疫调节剂.
纽卡斯尔病病毒 (NDV) 利用其V蛋白进行免疫逃避,但其与结合体组件的相互作用尚不清楚.

研究的目的:

研究EFTUD2与NDV V蛋白之间的相互作用.
阐明EFTUD2在宿主防御NDV感染中的作用.

主要方法:

免疫沉质谱 (IP-MS) 用于识别相互作用的蛋白质.
同免疫沉 (Co-IP) 和共聚焦显微镜以确认和绘制相互作用.
过度表达和siRNA介导的EFTUD2的淘汰,以评估其功能.
对的MDA5拼接,干扰素刺激基因 (ISG) 和干扰素β (IFN-β) 生产的分析.

主要成果:

EFTUD2被确定为NDV V蛋白的相互作用伙伴.
相互作用被证实并映射到特定的EFTUD2残留物.
EFTUD2过度表达增强了的MDA5拼接,上调了ISG和IFN-β,并抑制了NDV复制.
EFTUD2的淘汰促进了病毒复制,表明其作为宿主限制因子的作用.

结论:

EFTUD2充当了对NDV的关键宿主限制因素.
在感染期间,NDV V蛋白可能会激活EFTUD2的拼接功能,突出显示病毒免疫逃避和宿主防御的新机制.

关键词:

肉 MDA5 5 年份延长因子Tu GTP结合域含有蛋白2的延长因子Tu 纽卡斯尔病病毒的病毒.拼接组合因子是什么?

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