翻译(生物学)
冠状病毒
2019年冠状病毒病(COVID-19)
信使核糖核酸
寄主(生物学)
降级(电信)
细胞生物学
严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)
病毒学
2019-20冠状病毒爆发
化学
生物
医学
计算机科学
生物化学
遗传学
基因
内科学
电信
爆发
传染病(医学专业)
疾病
作者
Emilie Bäumlin,Dominic Andenmatten,Jonas Luginbühl,Aurélien Lalou,Nino Schwaller,Evangelos D. Karousis
出处
期刊:Cell Reports
[Cell Press]
日期:2025-03-29
卷期号:44 (4): 115488-115488
被引量:9
标识
DOI:10.1016/j.celrep.2025.115488
摘要
When host cells are infected with coronaviruses, the first viral protein produced is non-structural protein 1 (Nsp1). This protein inhibits host protein synthesis and induces host mRNA degradation to enhance viral proliferation. Despite its critical role, the mechanism by which Nsp1 mediates cellular mRNA degradation remains unclear. In this study, we use cell-free translation to address how host mRNA stability is regulated by Nsp1. We reveal that SARS-CoV-2 Nsp1 binding to the ribosome is enough to trigger mRNA degradation independently of ribosome collisions or active translation. MERS-CoV Nsp1 inhibits translation without triggering degradation, highlighting mechanistic differences between the two Nsp1 counterparts. Nsp1 and viral mRNAs appear to co-evolve, rendering viral mRNAs immune to Nsp1-mediated degradation in SARS-CoV-2, MERS-CoV, and Bat-Hp viruses. By providing insights into the mode of action of Nsp1, our study helps to understand the biology of Nsp1 better and find strategies for therapeutic targeting against coronaviral infections.
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