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APOBEC3 对 HIV-1 的宿主限制作用和 Vif 对病毒的逃逸作用。

Host restriction of HIV-1 by APOBEC3 and viral evasion through Vif.

机构信息

Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.

出版信息

Curr Top Microbiol Immunol. 2009;339:1-25. doi: 10.1007/978-3-642-02175-6_1.

Abstract

The arms race between virus and host is a constant battle. APOBEC3 proteins are known to be potent innate cellular defenses against both endogenous retroelements and diverse retroviruses. However, retroviruses have developed their own methods to launch counter-strikes. Most primate lentiviruses encode a protein called the viral infectivity factor (Vif). Vif induces targeted destruction of APOBEC3 proteins by hijacking the cellular ubiquitin-proteasome pathway. Here we review the research that led up to the identification of A3G, the mechanisms by which APOBEC3 proteins can inhibit retroelements, and the counter-mechanisms that HIV-1 Vif has developed to evade its antiviral activities.

摘要

病毒和宿主之间的军备竞赛是一场持续不断的战斗。APOBEC3 蛋白已被证实是针对内源性逆转录元件和各种逆转录病毒的强大先天细胞防御机制。然而,逆转录病毒已经发展出自己的方法来发起反击。大多数灵长类慢病毒编码一种称为病毒感染因子(Vif)的蛋白。Vif 通过劫持细胞泛素-蛋白酶体途径诱导 APOBEC3 蛋白的靶向破坏。在这里,我们回顾了导致 A3G 被鉴定的研究,APOBEC3 蛋白抑制逆转录元件的机制,以及 HIV-1 Vif 为逃避其抗病毒活性而发展的对策机制。

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