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从对不同正链RNA病毒群体的研究中涌现出的常见复制策略。

Common replication strategies emerging from the study of diverse groups of positive-strand RNA viruses.

作者信息

Pogue G P, Huntley C C, Hall T C

机构信息

Institute of Developmental and Molecular Biology, Texas A&M University, College Station.

出版信息

Arch Virol Suppl. 1994;9:181-94. doi: 10.1007/978-3-7091-9326-6_18.

Abstract

Studies using brome mosaic virus (BMV), Sindbis virus and poliovirus have provided evidence that disparate groups of plant and animal positive strand RNA viruses have remarkably similar replication strategies. The conservation of several functional domains within virus-encoded nonstructural proteins implies that, although the precise character of these and interacting host components varies for each virus, they employ similar mechanisms for RNA replication. For (+) strand replication, similarities in cis-acting sequence motifs and RNA secondary structures within 5' termini of genomic (+) strands have been identified and have been shown to participate in binding of host factors. The model presented for replication of BMV RNA suggests that binding of these factors to internal control region (ICR) sequence motifs in the double-stranded replication intermediate releases a single-stranded 3' terminus on the (-) strand that may be essential for initiation of genomic (+) strand synthesis. ICR sequences internal to the BMV genome were also found to be required for efficient replication. Asymmetric production of excess genomic (+) over (-) strand RNA, characteristic of all (+) strand viruses, may be accomplished through transition of the replicase from competence for (-) to (+) strand synthesis by the recruitment of additional host factors.

摘要

使用雀麦花叶病毒(BMV)、辛德毕斯病毒和脊髓灰质炎病毒进行的研究表明,不同类群的植物和动物正链RNA病毒具有非常相似的复制策略。病毒编码的非结构蛋白中几个功能域的保守性表明,尽管每种病毒的这些功能域以及与之相互作用的宿主成分的确切特性各不相同,但它们采用相似的RNA复制机制。对于(+)链复制,已在基因组(+)链5'末端内鉴定出顺式作用序列基序和RNA二级结构的相似性,并已证明它们参与宿主因子的结合。提出的BMV RNA复制模型表明,这些因子与双链复制中间体中的内部控制区(ICR)序列基序结合,会释放出(-)链上的单链3'末端,这可能是基因组(+)链合成起始所必需的。还发现BMV基因组内部的ICR序列对于有效复制是必需的。所有(+)链病毒的特征是基因组(+)链RNA比(-)链RNA过量产生不对称,这可能是通过募集额外的宿主因子,使复制酶从(-)链合成能力转变为(+)链合成能力来实现的。

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