白斑综合征病毒IE1蛋白质劫持了宿主酸通路,以推动病毒复制
Jia Zhang1, Kaiyu Lu1, Jinghua Zhu1
1Institute of Marine Sciences and Guangdong Provincial Key Laboratory of Marine Biology, Shantou University, Shantou, China.
PLoS pathogens
|January 27, 2026
概括
白斑综合征病毒 (WSSV) 通过宿主病毒蛋白相互作用激活酸通路 (PPP) 直接重新编程的新陈代谢. 这种病毒策略增强了WSSV的复制,并为水产养殖中的抗病毒疗法提供了新的点.
科学领域:
- 病毒学 病毒学
- 代谢途径 代谢途径
- 宿主-病原体相互作用
背景情况:
- 病毒重新编程宿主代谢以复制,通常针对酸途径 (PPP).
- PPP激活是脊椎动物中已知的前病毒机制,但其在无脊椎动物中的作用尚不清楚.
- 白斑综合征病毒 (WSSV) 感染,造成大量的水产养殖损失.
研究的目的:
- 为了研究WSSV如何重编程的主体代谢.
- 确定在WSSV感染期间参与PPP激活的病毒机制.
- 探索将PPP用于水产养殖中的抗病毒干预的潜力.
主要方法:
- 在感染WSSV的中分析PPP酶 (G6PD,TKTL2) 的基因表达.
- 测量TKTL2的酶活性和PPP代谢物 (NADPH,R5P) 的水平.
- 使用基因淘汰和药理抑制剂来评估PPP酶在WSSV复制中的作用.
- 使用蛋白质结合试验识别与宿主PPP酶相互作用的病毒蛋白.
- 研究病毒蛋白IE1对TKTL2活性和PPP流量的影响.
主要成果:
- WSSV感染上调了关键PPP酶 (G6PD,TKTL2) 和增强了TKTL2活性,增加了NADPH和R5P的产生.
- 抑制G6PD或TKTL2显著降低了WSSV负载,改善了的生存率.
- 病毒蛋白IE1直接与TKTL2结合,增强其酶活性并促进PPP流动.
- 通过IE1介导的PPP激活抑制了反应性氧物种 (ROS) 的积累.
- 结合IE1的TKTL2片段竞争性地抑制了相互作用,减少了PPP流量和病毒复制.
结论:
- 该病毒采用一种新的策略,通过病毒IE1和宿主TKTL2之间的相互作用直接激活宿主PPP.
- 这种对酸代谢的病毒重编程对于高效的WSSV复制至关重要.
- PPP及其与WSSV IE1的相互作用代表了在养殖中开发抗病毒策略的有希望的目标.
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