增加的ROS水平激活AMPK-ULK1介导的线粒,以促进伪狂犬病病毒的复制
Yuan Zhao1, Xiaoyi Qi1, Zhenbang Zhu1
1Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou, China.
Veterinary research
|July 21, 2025
概括
伪狂热病毒 (PRV) 感染通过破坏线粒体和阻碍ROS清除,导致氧化应激. 这使得PRV能够逃避免疫反应,促进病毒复制.
科学领域:
- 病毒学 病毒学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 氧化应激与病毒病原发生有关.
- 反应性氧物种 (ROS) 在细胞过程中起着至关重要的作用.
研究的目的:
- 研究ROS在伪狂犬病病毒 (PRV) 复制中的作用.
- 阐明PRV利用ROS逃避宿主免疫的机制.
主要方法:
- 研究了PRV诱导的线粒体功能和ROS生产的变化.
- 分析了Nrf2.2的细胞定位和活性.
- 检查了AMPK-ULK1轴和线粒细胞的激活.
- 评估了对MAVS介导的I型干扰素反应的影响.
主要成果:
- PRV感染增加了ER-线粒体接触,导致线粒体Ca2+ (mtCa2+) 的升高,线粒体膜潜能 (MMP) 的丧失,以及过度的ROS产生.
- PRV感染在细胞质中隔离了Nrf2,抑制了ROS的清理.
- 升高的ROS激活了AMPK-ULK1轴,启动了PINK1-帕金因依赖的线粒.
- 线粒细胞衰变降低了MAVS,抑制了I型干扰素反应,促进了病毒复制.
结论:
- PRV利用氧化应激来抑制宿主的抗病毒免疫力.
- 通过抑制干扰素反应,ROS积累有助于病毒复制.
- 这些发现为针对ROS的抗病毒策略提供了基础,以对抗PRV.
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