日本脑炎病毒通过激活RIG-1信号通路来诱导亡
Mingxing Gao1, Zelin Liu1, Xiaoyan Guo1
1College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, People's Republic of China.
Archives of virology
|May 26, 2023
概括
日本脑炎病毒 (JEV) 通过亡导致神经元死亡. 干扰微质中的RIG-1抑制了JEV复制和亡,这表明JEV诱导的大脑损伤的治疗标.
科学领域:
- 病毒学 病毒学
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
背景情况:
- 日本脑炎病毒 (JEV) 感染导致脑损伤和神经元死亡.
- 细胞亡,或编程细胞死亡,在JEV诱导的神经病变中起作用.
研究的目的:
- 研究小鼠微质细胞 (BV2细胞) 中JEV诱导的亡机制.
- 探索RIG-1 (网红酸诱导基因I) 在JEV感染和亡中的作用.
主要方法:
- 感染BV2细胞与JEV.
- 使用 Hoechst 33342 和 TUNEL 染色检测亡.
- 对与亡相关的蛋白质 (Bcl-2,Bax,cytochrome c,caspases) 和信号分子 (RIG-1,MAVS,TBK1,NF-κB,IRF3) 的西部斑点分析.
- 细胞染色体c的免疫光染色.
- 使用siRNA的RIG-1表达的干扰.
主要成果:
- 疹病毒感染显著促进了BV2细胞亡,在感染后36小时达到峰值.
- JEV上调调节了亲细胞亡的蛋白质 (Bax,分裂的亡酶-3,分裂的亡酶-9) 和细胞染色体c,同时降低了抗细胞亡的Bcl-2.
- 与RIG-1表达的干扰减少了亡,降低了病毒蛋白水平,并调节了与亡相关的蛋白质表达.
结论:
- 通过线粒体依赖的途径,JEV会诱导微质中的亡.
- 在JEV诱导的亡和病毒复制中,RIG-1信号传递至关重要.
- 准RIG-1可能提供一种抑制JEV复制和减轻JEV诱导的神经元损伤的策略.
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