人类贝塔冠状病毒OC43干扰受感染细胞中综合应激反应途径
Stacia M Dolliver1, Caleb Galbraith1, Denys A Khaperskyy1
1Department of Microbiology and Immunology, Faculty of Medicine, Dalhousie University, Halifax, NS B3H 4R2, Canada.
Viruses
|February 24, 2024
概括
人类冠状病毒OC43抑制细胞应激反应以促进病毒蛋白质的产生. 这项研究揭示了OC43破坏了GADD34反循环,独立于综合应激反应激活,确保病毒复制.
科学领域:
- 病毒学 病毒学
- 分子生物学分子生物学
- 细胞应激反应的应激反应
背景情况:
- 病毒在感染期间采用了优化蛋白质合成的策略.
- 综合应激反应 (ISR) 通过eIF2α酸化阻止细胞翻译.
- 人类冠状病毒OC43 (HCoV-OC43) 之前已经被证明可以抑制eIF2α酸化.
研究的目的:
- 为了研究HCoV-OC43对ISR的调制.
- 为了确定GADD34在HCoV-OC43介导的ISR抑制中的作用.
主要方法:
- 细胞感染HCoV-OC43.3.
- 对eIF2α酸化水平的分析.
- 测量GADD34的表达和诱导.
- 使用压力诱导剂评估ISR激活.
主要成果:
- 在感染细胞中,HCoV-OC43强烈诱导了GADD34表达.
- 通过HCoV-OC43对GADD34的上调独立于ISR激活.
- 对于HCoV-OC43对eIF2α酸化的抑制,GADD34并不重要.
- HCoV-OC43积极抑制eIF2α酸化.
结论:
- HCoV-OC43破坏了控制eIF2α酸化的GADD34负反循环.
- 这种干扰与ISR激活脱,促进病毒蛋白合成.
- 在HCoV-OC43和宿主ISR之间存在复杂的相互作用,有利于病毒复制.
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