通过激活PI3K/Akt路径,肠道病毒A71诱导的糖解对于病毒复制至关重要
1College of Basic Medicine, Chengde Medical University, Chengde, 067000, China.
Microbial pathogenesis
|March 24, 2025
概括
肠道病毒A71 (EV-A71) 劫持宿主细胞糖解,一种葡萄糖代谢途径,以复制. 抑制糖解或PI3K/Akt路径可降低病毒载量,揭示了关键的宿主-病原体相互作用.
科学领域:
- 病毒学 病毒学
- 细胞的新陈代谢
- 生物化学 生物化学
背景情况:
- 肠道病毒A71 (EV-A71) 需要宿主细胞代谢才能复制.
- 糖解在EV-A71复制中的特定作用尚不清楚.
研究的目的:
- 在EV-A71感染期间研究人类桃体上皮细胞 (HTEC) 中糖解的作用和调节.
- 阐明连接EV-A71复制和宿主糖解的基础分子机制.
主要方法:
- 在HTECs的EV-A71感染.
- 测量葡萄糖,乳酸盐和葡萄糖-6-酸盐 (G6P) 的水平.
- 对葡萄糖载体1 (Glut1) 表达的分析.
- 使用2-脱氧-D-葡萄糖 (2DG) 和酸盐抑制糖解.
- 对PI3K/Akt路径激活的评估.
- 添加时间测定和糖/乳酸盐度的操纵.
主要成果:
- EV-A71感染增加了葡萄糖的摄取和乳酸盐的产生,上调了Glut1的表达.
- 糖解,酸通路 (PPP),三碳酸 (TCA) 循环和细胞呼吸被激活.
- 抑制糖解或PI3K/Akt路径显著抑制了EV-A71复制.
- 最佳的葡萄糖和乳酸水平至关重要;极端情况会损害复制.
- 葡萄糖分解影响病毒生命周期的早期 (附着/进入) 和晚期 (释放) 阶段.
结论:
- EV-A71通过PI3K/Akt路径利用宿主糖解来促进病毒复制.
- 向糖解是一种潜在的治疗策略,可以对抗EV-A71感染.
- 这项研究为EV-A71宿主细胞代谢相互作用提供了新的见解.
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