病毒诱导的希斯乳化促进了类动物的病毒感染
Yu Zhang1,2, Xiaobo Zhang1,3,4
1College of Life Sciences, Zhejiang University, Hangzhou, 310058, P. R. China.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|June 14, 2024
概括
在中感染白斑综合征病毒 (WSSV) 会促进糖解,增加乳酸. 这种乳酸促进了基因乳化,增强了病毒复制,但病毒微RNA (miR-N20) 抑制了这一过程.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 病毒作为非细胞生物,依赖宿主细胞生存,改变宿主新陈代谢.
- 病毒诱导的代谢变化对病毒与宿主相互作用的影响尚未完全理解.
- 了解这些相互作用对于开发抗病毒策略至关重要.
研究的目的:
- 研究宿主代谢物在病毒与宿主相互作用中的作用.
- 为了阐明病毒诱导的基因素乳酸化机制.
- 为了确定控制WSSV感染的潜在目标.
主要方法:
- 在体内,挑战带有白斑综合征病毒 (WSSV).
- 分析代谢变化,特别是糖解和乳酸积累.
- 评估基因组乳化 (H3K18la,H4K12la) 和基因表达.
- 研究病毒微RNA (miR-N20) 和HIF-1α的作用.
主要成果:
- 感染WSSV增强了的糖解,导致乳酸的积累.
- 乳酸盐通过p300/HDAC1/HDAC3促进了基因组乳化 (H3K18la,H4K12la),上调了S6K2的表达,促进了病毒感染.
- 病毒miR-N20向HIF-1α,抑制糖解和抑制组织蛋白乳酸化.
结论:
- 病毒诱导的组素乳化是病毒与宿主相互作用的关键机制.
- 代谢变化,特别是乳酸积累,在促进病毒感染方面发挥着重要作用.
- 向激素乳化或相关途径为抗病毒疗法提供了一种新的方法.
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