Coronavirus takeover of host cell translation and intracellular antiviral response: a molecular perspective

被引:3
|
作者
Karousis, Evangelos D. [1 ,2 ]
Schubert, Katharina [3 ]
Ban, Nenad [3 ]
机构
[1] Univ Bern, Multidisciplinary Ctr Infect Dis, Bern, Switzerland
[2] Univ Bern, Dept Chem & Biochem, Bern, Switzerland
[3] Swiss Fed Inst Technol, Inst Mol Biol & Biophys, Dept Biol, Zurich, Switzerland
来源
EMBO JOURNAL | 2024年 / 43卷 / 02期
基金
瑞士国家科学基金会;
关键词
Coronaviruses; Viral protein synthesis; SARS-CoV-2; Translation; Translation regulation; MESSENGER-RNA TRANSLATION; SARS-CORONAVIRUS; NONSTRUCTURAL PROTEIN-1; GENE-EXPRESSION; I INTERFERON; FUNCTIONAL CONSERVATION; EFFICIENT PROPAGATION; RIBOSOMAL FRAMESHIFT; PATHOGENICITY FACTOR; RATIONAL DESIGN;
D O I
10.1038/s44318-023-00019-8
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Coronaviruses are a group of related RNA viruses that cause respiratory diseases in humans and animals. Understanding the mechanisms of translation regulation during coronaviral infections is critical for developing antiviral therapies and preventing viral spread. Translation of the viral single-stranded RNA genome in the host cell cytoplasm is an essential step in the life cycle of coronaviruses, which affects the cellular mRNA translation landscape in many ways. Here we discuss various viral strategies of translation control, including how members of the Betacoronavirus genus shut down host cell translation and suppress host innate immune functions, as well as the role of the viral non-structural protein 1 (Nsp1) in the process. We also outline the fate of viral RNA, considering stress response mechanisms triggered in infected cells, and describe how unique viral RNA features contribute to programmed ribosomal -1 frameshifting, RNA editing, and translation shutdown evasion. This review discusses the unique features of coronaviruses that enable them to commandeer host cell translation while avoiding host immune defense responses.
引用
收藏
页码:151 / 167
页数:17
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