寨卡病毒调节关节动物组织基因组甲基化以使其在蚊子细胞中存活
Telvin Harrell1, Swarnendu Basak2, Hameeda Sultana2
1Department of Biological Sciences, Old Dominion University, Norfolk, VA, United States of America.
PloS one
|February 13, 2025
概括
寨卡病毒 (ZIKV) 操纵蚊子的S-adenosyl metionin (SAMe) 生产和基因素甲基化,这是它在关节动物载体中生存的关键过程. 这项研究揭示了ZIKV如何利用这些宿主机制进行复制.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 昆虫学 昆虫学是一门学科.
背景情况:
- 寨卡病毒 (ZIKV) 是蚊子传播的病原体,引起发烧性疾病和严重的神经缺陷.
- 脊椎动物细胞中的ZIKV复制与RNA甲基化有关.
- ZIKV诱导的表观遗传修饰在其关节动物载体中的作用仍然不清楚.
研究的目的:
- 为了研究ZIKV感染对蚊子细胞表观遗传修饰的影响.
- 为了确定S-adenosyl metionin (SAMe) 和组织素甲基化在ZIKV在其载体内的存活率中的作用.
主要方法:
- 蚊子C6/36细胞感染ZIKV.
- 逆转录定量PCR和免疫血栓检测用于评估基因和蛋白质表达.
- 测量SAME度和组织素甲基化标记物 (H3K27me3).
- 用SAME和EZH2抑制剂进行治疗.
主要成果:
- 寨卡病毒感染增加了蚊子细胞中的SAME合成酶表达和SAME水平.
- 齐克病毒感染增加了EZH2基因组甲基转移酶类基因转录和H3K27me3水平.
- 外源性SAME增强了ZIKV负载和EZH2表达;EZH2抑制降低了病毒负载和组织素甲基化.
结论:
- 在蚊子细胞中,ZIKV调节SAME的产生和基因素甲基化.
- 通过SAME和EZH2介导的基因素甲基化对ZIKV在其关节动物载体中的生存至关重要.
- 这些发现为ZIKV载体相互作用和潜在的控制策略提供了洞察力.
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