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寨卡病毒和登革热病毒差异调节宿主mRNA处理因子,定义其毒性

Aaron Scholl¹, Binsheng Gong², Bingjie Li¹

¹Tumor Vaccine and Biotechnology Branch, Division of Cellular Therapy 2, Office of Cellular Therapy and Human Tissue, Center for Biologics Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, MD 20993, United States.

NAR molecular medicine

|September 8, 2025

概括

寨卡病毒 (ZIKV) 通过降解宿主RNA衰变因子,导致比登革热病毒 (DENV) 更大的细胞损伤. 这一发现有助于开发新的 flavivirus 检测方法用于生物制剂.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

全球气候变化正在增加载体种群,导致更多的载体传播的黄状病毒感染.
像寨卡病毒 (ZIKV) 和登革热病毒 (DENV) 这样的病毒对包括细胞和基因疗法在内的人类生物制品构成风险.
了解宿主-病原体相互作用对于减轻弗拉维病毒威胁至关重要.

研究的目的:

调查寨卡病毒 (ZIKV) 和登革热病毒 (DENV) 毒性背后的分子机制.
为了确定参与病毒复制和宿主防御的宿主细胞因素.
为了比较ZIKV和DENV感染之间的病原性差异.

主要方法:

在受感染宿主细胞上进行了时间过程转录组 (RNA-seq) 和蛋白质组分析.
分析了不同的基因表达和蛋白质降解途径.
评估了病毒复制的宿主核运输要求.

主要成果:

与DENV相比,ZIKV表现出更大的毒性和细胞病变效应.
与DENV.不同的是,ZIKV感染导致宿主无意义介导RNA衰变 (NMD) 因素的降解,而DENV.
在ZIKV感染的细胞中观察到宿主内基转录的积累和活跃核运输的要求.

结论:

齐克病毒通过针对性降解必需的宿主蛋白质,特别是NMD因子,诱导早期宿主细胞损伤.
齐克病毒独特的宿主因子操纵机制有助于其增强的毒性.
这些发现为开发基于转录组学和蛋白质组学的新策略在生物学中检测黄状病毒铺平了道路.

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