白斑综合征病毒劫持主机PP2A-FOXO轴以促进其传播
Cang Li1, Peng Zhang1, Pan-Pan Hong1
1Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, Shandong 266237, China.
International journal of biological macromolecules
|November 25, 2023
概括
白斑综合征病毒 (WSSV) 通过宿主LCMT1-PP2A或病毒VP26-PP2A通路劫持FOXO蛋白. 这种操纵促进病毒复制,为水产养殖中WSSV控制提供了潜在的目标.
科学领域:
- * 病毒学和分子生物学
- * 甲动物病理学
- * 无脊椎动物免疫学
背景情况:
- * 病毒使用复杂的机制来克服宿主免疫反应并促进感染.
- *分叉盒转录因子O (FOXO) 蛋白质在病毒感染中超出人类细胞巨乳病毒再激活的作用以前尚不清楚.
- *白斑综合征病毒 (WSSV) 是影响养殖的重要病原体.
研究的目的:
- * 调查WSSV利用宿主因子进行复制的机制.
- * 为了阐明FOXO蛋白在WSSV感染中的作用.
- * 为了确定WSSV控制的潜在治疗点.
主要方法:
- *分析WSSV感染期间的基因表达变化.
- *研究病毒和宿主因子之间的蛋白质-蛋白质相互作用.
- *功能性测试以确定FOXO,LCMT1,PP2A和VP26在病毒复制中的作用.
主要成果:
- * WSSV感染上调节白氨酸碳基甲基转移酶1 (LCMT1),通过甲基化激活蛋白酸酶2A (PP2A),导致FOXO脱和核转移.
- * 脱化FOXO促进了WSSV直接早期基因wsv079的转录,从而启动病毒基因表达.
- *在晚期感染阶段,WSSV包膜蛋白26 (VP26) 与FOXO和PP2A的B55亚单元结合,增强PP2A的活性并促进WSSV的复制.
结论:
- * WSSV利用宿主LCMT1-PP2A-FOXO和VP26-PP2A-FOXO轴,分别在早期和晚期感染阶段增强病毒传播.
- *这项研究揭示了新的病毒策略来劫持宿主因子.
- * 这些已识别的途径代表了在养殖中开发WSSV控制策略的潜在目标.
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