剖析传染性支气管炎病毒诱导的宿主关闭在翻译水平
Jing Zhao1,2, Yahui Huang1, Chengyin Liukang1,2
1National Key Laboratory of Veterinary Public Health Security, College of Veterinary Medicine, China Agricultural University, Beijing, China.
Journal of virology
|June 28, 2024
概括
传染性支气管炎病毒 (IBV) 通过操纵翻译导致宿主细胞关闭,像NSP15这样的病毒蛋白质是关键. 这一策略允许IBV主导细胞mRNA并抑制免疫反应,帮助病毒复制.
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:
- 传染性支气管炎病毒 (IBV),一种马冠状病毒,对家禽部门造成重大经济损害.
- 了解IBV对宿主细胞机械的操纵对于开发控制策略至关重要.
- 病毒劫持宿主翻译的策略各不相同,但IBV的具体机制在很大程度上是未知的.
研究的目的:
- 阐明IBV操纵宿主细胞翻译的机制.
- 为了确定负责IBV诱导宿主基因关闭的病毒蛋白质.
- 描述IBV感染细胞的转化场景及其对宿主抗病毒反应的影响.
主要方法:
- 对23种病毒蛋白进行查,以确定那些参与宿主关闭的病毒蛋白.
- 核糖体分析 (Ribo-seq) 和RNA测序 (RNA-seq) 用于分析病毒和细胞mRNA的表达和翻译.
- 对转化停止事件和受影响宿主基因通路的丰富的分析.
主要成果:
- 感染IBV诱导宿主细胞关闭,同时保持病毒蛋白质合成.
- 多种病毒蛋白质有助于宿主关闭,Nsp15显示出明显的抑制作用.
- 越来越多的IBVmRNA在细胞池中占据主导地位,其翻译效率低于宿主mRNA.
- 主体基因的转化停止事件显著增加,特别是那些参与免疫反应和展开的蛋白质反应的基因.
- 免疫和炎症相关的mRNA的不有效翻译,延迟宿主抗病毒细胞因子的产生 (IFN-β和IFN-λ).
结论:
- IBV采用复杂的策略来关闭宿主基因表达和翻译.
- 病毒蛋白,包括NSP15,在诱导宿主关闭中起着至关重要的作用.
- IBV重塑宿主转化格局,以抑制抗病毒免疫力并促进病毒复制.
- 这些发现为IBV病原和宿主病毒相互作用提供了新的见解.
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