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由病毒蛋白触发的中心基DNA放大激活核cGAS

Xavier Lahaye¹, Patrick Tran Van¹, Camellia Chakraborty²

¹Institut Curie, PSL University, INSERM U932, Immunity and Cancer, Paris, France.

|June 3, 2025

概括

疹病毒通过扰乱中间体激活核cGAS免疫力,导致DNA放大. 这种病毒诱导的中位体DNA放大和识别 (VICAR) 机制揭示了中位体在免疫激活中的新作用.

科学领域:

免疫学
病毒学
细胞生物学

背景情况:

cGAS-cGAMP-STING通路对于检测细胞核DNA和启动抗病毒反应至关重要.
DNA 病毒通常通过进入细胞核来逃避细胞核DNA 传感器,其中染色体可以限制cGAS 激活.
病毒激活核cGAS的机制尚未完全理解.

研究的目的:

研究疹病毒如何激活细胞核中的cGAS-cGAMP-STING通路.
阐明在病毒感染期间核cGAS激活中的中间体的作用.

主要方法:

使用基于细胞的测试来研究疹病毒蛋白与中间体的相互作用.
研究了病毒蛋白,如HSV-1 ICP0和CMV IE1对中心DNA和cGAS激活的影响.
采用分析DNA合成途径的技术,包括转化DNA合成 (TLS).

主要成果:

发现一些疹病毒蛋白质通过破坏中间体触发核cGAS激活.
简单性疹病毒1型 (HSV-1) ICP0通过TLS促进中心DNA放大,激活静止细胞中的核cGAS.
HSV-1 UL36USP抑制了TLS以逃避这种免疫检测,而CMV IE1也诱导了中心基DNA放大和cGAS激活.

结论:

定义了一种称为病毒诱导的中心DNA放大和识别 (VICAR) 的新机制.
通过作为病毒诱导的DNA放大和cGAS激活的平台,证明中间体具有非线性,免疫激活的作用.
发现了疹病毒使用的新策略来操纵宿主细胞通路以逃避免疫.

关键词:

在CMV 在HSV-1 在 ICP0 UL36USP 其他维卡尔 cGAS 公司中分子内在的感觉转化DNA合成

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