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持续性肠道病毒感染:微小缺失,长期感染。

Persistent Enterovirus Infection: Little Deletions, Long Infections.

作者信息

Chapman Nora M

机构信息

Department of Pathology & Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

出版信息

Vaccines (Basel). 2022 May 12;10(5):770. doi: 10.3390/vaccines10050770.

Abstract

Enteroviruses have now been shown to persist in cell cultures and in vivo by a novel mechanism involving the deletion of varying amounts of the 5' terminal genomic region termed domain I (also known as the cloverleaf). Molecular clones of coxsackievirus B3 (CVB3) genomes with 5' terminal deletions (TD) of varying length allow the study of these mutant populations, which are able to replicate in the complete absence of wildtype virus genomes. The study of TD enteroviruses has revealed numerous significant differences from canonical enteroviral biology. The deletions appear and become the dominant population when an enterovirus replicates in quiescent cell populations, but can also occur if one of the cis-acting replication elements of the genome (CRE-2C) is artificially mutated in the element's stem and loop structures. This review discusses how the TD genomes arise, how they interact with the host, and their effects on host biology.

摘要

现已证明,肠道病毒可通过一种新机制在细胞培养物和体内持续存在,该机制涉及删除5'端基因组区域中不同数量的部分,称为结构域I(也称为苜蓿叶结构)。具有不同长度5'端缺失(TD)的柯萨奇病毒B3(CVB3)基因组分子克隆,使得对这些突变群体的研究成为可能,这些突变群体能够在完全没有野生型病毒基因组的情况下进行复制。对TD肠道病毒的研究揭示了其与典型肠道病毒生物学的诸多显著差异。当肠道病毒在静止细胞群体中复制时,缺失现象出现并成为主要群体,但如果基因组的一个顺式作用复制元件(CRE-2C)在其茎环结构中被人为突变,也可能发生缺失。本综述讨论了TD基因组如何产生、它们如何与宿主相互作用以及它们对宿主生物学的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1020/9143164/2125e5b38a93/vaccines-10-00770-g001.jpg

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