蛋白组分析揭示了猫类疹病毒1型突变体细胞间传播的差异
Weiwei Lin1,2, Xianglin Zhang1, Qian Jiang1
1State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150069, China.
Veterinary sciences
|December 31, 2025
概括
猫类疹病毒-1 (FHV-1) 血清/三联蛋白激酶 (pK) 删除显著损害病毒复制并改变宿主细胞酸化. 胺基酶 (TK) 缺乏也会影响宿主细胞的蛋白质组,影响染色体重塑通路.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 蛋白质组学是指蛋白质组学.
背景情况:
- 猫类疹病毒-1 (FHV-1) 是猫的重要病原体.
- 氨酸/氨酸蛋白激酶 (pK) 和胆氨酸激酶 (TK) 是潜在的FHV-1毒性因子,尽管它们在宿主细胞酸化和病毒复制中的确切作用尚未完全理解.
研究的目的:
- 研究FHV-1 pK和TK对病毒复制和宿主细胞蛋白质组的影响.
- 阐明pK和TK在FHV-1病原和复制机制中的作用.
主要方法:
- 使用CRISPR/Cas9介导的同源重组生成pK和TK缺乏的FHV-1突变体.
- 使用数据独立获取 (DIA) 定量蛋白质组学分析受感染细胞中的全球蛋白质表达和酸化变化.
- 基因本体学 (GO) 和基因和基因组的京都百科全书 (KEGG) 路径分析进行了功能性表征.
主要成果:
- 与TK缺乏病毒相比,pK缺乏的FHV-1表现出明显较小的斑块和减弱的复制动力学.
- FHV-1感染导致宿主细胞蛋白质组的广泛变化,pK缺陷病毒影响3632种蛋白质,TK缺陷病毒影响4529种蛋白质.
- 功能分析显示,pK缺乏影响结合体通路,而TK缺乏影响依赖ATP的染色体重塑通路,并对结合调节剂和染色体重塑因子产生特定的改变.
结论:
- 删除FHV-1 pK基因显著降低病毒复制能力.
- FHV-1感染严重改变宿主细胞酸化,影响关键细胞通路,如拼接和染色质重塑.
- 这项研究为FHV-1-诱导的调节网络和信号提供了新的见解,进步了我们对病毒复制的理解.
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