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日本脑炎病毒感染诱导线粒体介导的亡通过BAX的proapoptotic蛋白质

Ke Yang¹, Xinran Li¹, Shuqing Yang¹

¹Research Center of Swine Disease, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.

Frontiers in microbiology

|November 12, 2024

概括

日本脑炎病毒 (JEV) 通过亡引发细胞死亡. 淘汰BAX基因显著降低了JEV增殖和病毒蛋白水平,揭示了BAX基因.

科学领域:

病毒学病毒学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

日本脑炎病毒 (JEV) 是亚洲病毒性脑炎的主要原因.
人们尚未完全理解JEV诱导的亡的确切机制.
以前的研究表明,亲亡基因BAX在JEV的扩散中起作用.

研究的目的:

为了阐明JEV诱导的亡的分子机制.
研究BAX基因在JEV增殖和亡中的作用.
为了探索JEV感染的潜在治疗点.

主要方法:

使用CRISPR/Cas9.9构建了一个BAX基因淘汰PK-15细胞系 (BAX.KO).
在野生型和BAX.KO细胞中评估了JEV增殖和病毒蛋白水平.
使用了DAPI染色,Annexin V-FITC/PI染色和西式涂抹来分析亡和相关蛋白质表达.
检查了线粒体损伤,细胞染色体C释放,线粒体膜潜力和反应性氧物种 (ROS) 水平.
研究了酶-3抑制剂对JEV扩散的影响.

主要成果:

BAX基因淘汰显著抑制了JEV的扩散,使病毒蛋白水平降低了39.9%.
致病病毒感染上调调节了亲细胞亡因子 (BAX,NOXA,PUMA,分裂-caspase-3/9) 并诱导了线粒体损伤,细胞染色体C释放和线粒体膜潜能降低.
过度表达BAX增强了JEV的扩散.
卡斯帕酶-3抑制减弱了JEV诱导的病毒扩散和释放在两种细胞类型.

结论:

JEV感染通过线粒体路径诱导亡,涉及BAX,P53和酶激活.
BAX基因对JEV的扩散和诱导亡至关重要.
准BAX或caspase-3可能提供针对JEV感染的治疗策略.

关键词:

巴克斯巴克斯 (BAX) 是一个在JEV中,JEV是通过P53-BAX路径.在PK-15中,PK-15是PK-15.线粒体亡途径的线粒体亡途径

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