APOBEC3G Antagonism by Vif, or When Structure Meets Biological and Evolutionary Studies.

IF 8.1 1区 医学 Q1 VIROLOGY
Yen-Li Li, Caroline Langley, Michael Emerman, John D Gross
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引用次数: 0

Abstract

Restriction factors serve as innate host defenses against viruses and act as critical barriers to cross-species transmission. In response, viruses have evolved accessory proteins to counteract restriction factors, enabling evasion of innate immune responses. The interplay between primate APOBEC3G (A3G) and lentiviral virion infectivity factor (Vif) exemplifies a molecular arms race between a restriction factor and its viral antagonist. This review integrates evolutionary and functional analyses of this system, showing how genetic signatures of molecular arms races map onto high-resolution cryo-electron microscopy structures. However, A3G's interaction with Vif is not limited to the evolutionary dynamic interface, characterized by rapidly evolving residues under selective pressure, but also involves a conserved interface mediated by RNA binding that positions A3G for antagonism by Vif. These findings propose a model wherein Vif and potentially other viral antagonists target functional complexes using a dual strategy: leveraging both adaptive interfaces subject to evolutionary pressures and conserved interfaces that constrain host escape mechanisms.

APOBEC3G拮抗Vif,或当结构满足生物学和进化研究。
限制因子是宿主对病毒的先天防御,也是跨物种传播的关键屏障。作为回应,病毒进化出附属蛋白来抵消限制因子,从而逃避先天性免疫反应。灵长类 APOBEC3G(A3G)和慢病毒病毒感染因子(Vif)之间的相互作用是限制因子与其病毒拮抗剂之间分子军备竞赛的典范。这篇综述综合了这一系统的进化和功能分析,展示了分子军备竞赛的遗传特征如何映射到高分辨率冷冻电镜结构上。然而,A3G 与 Vif 的相互作用并不局限于以在选择压力下快速进化的残基为特征的进化动态界面,还涉及一个由 RNA 结合介导的保守界面,该界面将 A3G 定位为 Vif 的拮抗剂。这些发现提出了一个模型,在这个模型中,Vif 和潜在的其他病毒拮抗剂使用双重策略来攻击功能复合物:既利用承受进化压力的适应性界面,也利用限制宿主逃脱机制的保守界面。
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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