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无义介导的 mRNA 降解与病毒的分子相互作用。

Molecular Interaction of Nonsense-Mediated mRNA Decay with Viruses.

机构信息

College of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou 310018, China.

出版信息

Viruses. 2023 Mar 23;15(4):816. doi: 10.3390/v15040816.

DOI:10.3390/v15040816
PMID:37112798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10141005/
Abstract

The virus-host interaction is dynamic and evolutionary. Viruses have to fight with hosts to establish successful infection. Eukaryotic hosts are equipped with multiple defenses against incoming viruses. One of the host antiviral defenses is the nonsense-mediated mRNA decay (NMD), an evolutionarily conserved mechanism for RNA quality control in eukaryotic cells. NMD ensures the accuracy of mRNA translation by removing the abnormal mRNAs harboring pre-matured stop codons. Many RNA viruses have a genome that contains internal stop codon(s) (iTC). Akin to the premature termination codon in aberrant RNA transcripts, the presence of iTC would activate NMD to degrade iTC-containing viral genomes. A couple of viruses have been reported to be sensitive to the NMD-mediated antiviral defense, while some viruses have evolved with specific -acting RNA features or -acting viral proteins to overcome or escape from NMD. Recently, increasing light has been shed on the NMD-virus interaction. This review summarizes the current scenario of NMD-mediated viral RNA degradation and classifies various molecular means by which viruses compromise the NMD-mediated antiviral defense for better infection in their hosts.

摘要

病毒-宿主相互作用是动态和进化的。病毒必须与宿主进行斗争才能成功感染。真核宿主有多种防御机制来抵御入侵的病毒。宿主抗病毒防御之一是无意义介导的 mRNA 降解 (NMD),这是真核细胞中一种保守的 RNA 质量控制机制。NMD 通过去除含有过早终止密码子的异常 mRNA 来确保 mRNA 翻译的准确性。许多 RNA 病毒的基因组包含内部终止密码子 (iTC)。类似于异常 RNA 转录本中的过早终止密码子,iTC 的存在会激活 NMD 来降解含有 iTC 的病毒基因组。已经有报道称有几种病毒对 NMD 介导的抗病毒防御敏感,而有些病毒则进化出特定的作用 RNA 特征或作用病毒蛋白来克服或逃避 NMD。最近,人们越来越关注 NMD-病毒相互作用。本综述总结了 NMD 介导的病毒 RNA 降解的现状,并对病毒破坏 NMD 介导的抗病毒防御以在宿主中更好感染的各种分子手段进行了分类。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e92/10141005/3e42e144276c/viruses-15-00816-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e92/10141005/52c1764a3fa2/viruses-15-00816-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e92/10141005/7cbb9cf7e4af/viruses-15-00816-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e92/10141005/3e42e144276c/viruses-15-00816-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e92/10141005/52c1764a3fa2/viruses-15-00816-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e92/10141005/7cbb9cf7e4af/viruses-15-00816-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e92/10141005/3e42e144276c/viruses-15-00816-g003.jpg

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Rotaviral nonstructural protein 5 (NSP5) promotes proteasomal degradation of up-frameshift protein 1 (UPF1), a principal mediator of nonsense-mediated mRNA decay (NMD) pathway, to facilitate infection.轮状病毒非结构蛋白5(NSP5)促进无义介导的mRNA衰变(NMD)途径的主要介导因子移码上调蛋白1(UPF1)的蛋白酶体降解,以促进感染。
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