Natural Selection, Intracellular Bottlenecks of Virus Populations, and Viral Superinfection Exclusion.

IF 8.1 1区 医学 Q1 VIROLOGY Annual Review of Virology Pub Date : 2022-05-13 DOI:10.1146/annurev-virology-100520-114758
Camila Perdoncini Carvalho, Ruifan Ren, Junping Han, F. Qu
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引用次数: 7

Abstract

Natural selection acts on cellular organisms by ensuring the genes responsible for an advantageous phenotype consistently reap the phenotypic advantage. This is possible because reproductive cells of these organisms are almost always haploid, separating the beneficial gene from its rival allele at every generation. How natural selection acts on plus-strand RNA viruses is unclear because these viruses frequently load host cells with numerous genome copies and replicate thousands of progeny genomes in each cell. Recent studies suggest that these viruses encode the Bottleneck, Isolate, Amplify, Select (BIAS) mechanism that blocks all but a few viral genome copies from replication, thus creating the environment in which the bottleneck-escaping viral genome copies are isolated from each other, allowing natural selection to reward beneficial mutations and purge lethal errors. This BIAS mechanism also blocks the genomes of highly homologous superinfecting viruses, thus explaining cellular-level superinfection exclusion. Expected final online publication date for the Annual Review of Virology, Volume 9 is September 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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自然选择、病毒群体的细胞内瓶颈和病毒重叠感染排除。
自然选择通过确保负责有利表型的基因持续获得表型优势来作用于细胞生物体。这是可能的,因为这些生物的生殖细胞几乎总是单倍体,在每一代都将有益基因与其竞争等位基因分离。自然选择如何作用于正链RNA病毒尚不清楚,因为这些病毒经常在宿主细胞中装载大量基因组拷贝,并在每个细胞中复制数千个后代基因组。最近的研究表明,这些病毒编码瓶颈、分离、扩增、选择(BIAS)机制,该机制阻断了除少数病毒基因组拷贝外的所有病毒基因组拷贝的复制,从而创造了一种环境,在这种环境中,逃离瓶颈的病毒基因组拷贝相互分离,使自然选择能够奖励有益的突变并清除致命的错误。这种BIAS机制还阻断了高度同源的重叠感染病毒的基因组,从而解释了细胞水平的重叠感染排除。《病毒学年度评论》第9卷预计最终在线出版日期为2022年9月。请参阅http://www.annualreviews.org/page/journal/pubdates用于修订估算。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
19.40
自引率
0.90%
发文量
28
期刊介绍: The Annual Review of Virology serves as a conduit for disseminating thrilling advancements in our comprehension of viruses spanning animals, plants, bacteria, archaea, fungi, and protozoa. Its reviews illuminate novel concepts and trajectories in basic virology, elucidating viral disease mechanisms, exploring virus-host interactions, and scrutinizing cellular and immune responses to virus infection. These reviews underscore the exceptional capacity of viruses as potent probes for investigating cellular function.
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