传染病病毒VP5以转录依赖的方式触发宿主关闭
Xinxin Niu1,2, Jinze Han1,2, Mengmeng Huang1,2
1Avian Immunosuppressive Diseases Division, State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, the Chinese Academy of Agricultural Sciences, Harbin, China.
mBio
|January 30, 2024
概括
传染病病毒 (IBDV) 通过抑制基因转录来抑制宿主蛋白质合成. 病毒蛋白VP5破坏核细胞质运输,逃避宿主免疫力.
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:
- 病毒操纵宿主基因表达以逃避免疫.
- 宿主关闭,全球抑制宿主基因表达,是一个关键的病毒免疫逃避策略.
- 众所周知,传染性病病毒 (IBDV) 感染家禽,造成重大经济损失.
研究的目的:
- 研究IBDV抑制宿主蛋白质合成的机制.
- 为了识别IBDV感染期间主体关闭的病毒蛋白.
- 阐明涉及IBDV介导宿主基因表达操纵的分子途径.
主要方法:
- 在体外和体外病毒感染模型被用于研究IBDV感染.
- 研究了病毒蛋白VP5在宿主关闭中的作用.
- 分析了核细胞质运输中断的机制,包括RanBP1结合及其对蛋白质进口的影响.
主要成果:
- 证实IBDV感染抑制了宿主蛋白质合成.
- 病毒蛋白VP5被确定为抑制宿主基因转录的关键因素.
- VP5竞争性地与RanBP1结合,破坏了RanGDP/GTP梯度,并损害了核细胞质运输.
- 抑制了像p65和IRF7这样的转录因子的核进口,导致细胞因子和干扰素的表达减少.
结论:
- IBDV利用病毒蛋白VP5通过破坏核细胞质运输和抑制宿主基因转录来执行宿主关闭策略.
- 这种机制使IBDV能够逃避宿主天生的免疫力,并有效地建立感染.
- 这些发现为病毒免疫逃避策略和病毒感染期间宿主基因表达的调节提供了新的见解.
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