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在脑肌性心炎病毒感染的HeLa细胞中调节Ire1-Xbp1防御通路

Anna Shishova^1,2, Yury Ivin¹, Ekaterina Gladneva¹

¹Chumakov Federal Scientific Center for Research and Development of Immune-and-Biological Products of Russian Academy of Sciences (Institute of Poliomyelitis), 108819 Moscow, Russia.

|March 27, 2025

概括

脑肌心炎病毒抑制了一个关键的细胞防御途径,称为未折叠蛋白质反应 (UPR). 这种病毒干扰 IRE1-XBP1 信号传递,阻碍了细胞管理内质网膜压力的能力.

科学领域:

病毒学病毒学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

病毒病原性通常涉及破坏宿主细胞防御机制.
展开的蛋白质响应 (UPR) 是一个关键的细胞通路,可以减轻内分泌网膜 (ER) 的压力.
IRE1介导的XBP1mRNA剪接是UPR的一个主要分支,导致转录因子活性增加.

研究的目的:

为了研究脑肌心炎病毒 (EMCV) 与IRE1-依赖的UPR通路之间的相互作用.
为了确定EMCV是否可以调节XBP1mRNA拼接的激活.
阐明EMCV感染在细胞防御中对ER压力的作用.

主要方法:

用EMCV感染HeLa细胞.
在病毒感染期间监测化IRE1水平.
在感染细胞和模拟感染细胞中合的XBP1mRNA积累的量化.
用迪二甲醇 (DTT) 治疗,以诱导感染细胞和假感染细胞的ER压力.

主要成果:

在HeLa细胞中,EMCV感染调节了化IRE1水平.
病毒感染并没有导致拼接的XBP1mRNA的积累.
与模拟感染细胞相比,用DTT治疗的受感染细胞的拼接XBP1mRNA水平明显较低.

结论:

脑肌心炎病毒有效地抑制了IRE1依赖的UPR通路.
皮科纳病毒具有调节宿主细胞防御机制的能力,特别是展开的蛋白质反应.
这种病毒免疫规避策略可能有助于病毒病原性.

关键词:

压力ERER压力ERER压力爱尔兰的第一名.通过UPR进行全日制检查.在XBP1中使用.脑筋硬化炎病毒的病毒不传统的拼接方式.

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Regulation of the Unfolded Protein Response

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