Farrow Melissa A, Sheehy Ann M
College of the Holy Cross, Department of Biology, 1 College Street, Worcester, MA 01610, USA.
Future Microbiol. 2008 Apr;3(2):145-54. doi: 10.2217/17460913.3.2.145.
It is now 26 years after the first published report on HIV, and the global epidemic continues unabated, with estimates of over 33 million people currently infected, worldwide. Development of targeted therapies aimed at perturbing the HIV life cycle can be achieved only with a detailed comprehension of the dynamics of virus-host interactions within the cell. One such critical virus-host interaction is the recently elucidated interplay between the viral Vif protein and the innate immune defense molecule Apobec3G. Apobec3G potently suppresses HIV replication, but Vif can alleviate this inhibition, rescuing viral infectivity. Early work describing the characterization of Vif and the cloning and identification of Apobec3G as an antiviral are discussed. Recent advances detailing the mechanisms of the Vif-Apobec3G regulatory circuit and our nascent understanding of Apobec3G endogenous function are also presented. Collectively, these studies have shed light on potential novel therapeutic strategies aimed at exploiting Apobec3G antiviral function to abrogate HIV replication.
自首次发表关于艾滋病毒的报告至今已有26年，全球疫情仍未减弱，据估计目前全球有超过3300万人感染。只有详细了解细胞内病毒与宿主相互作用的动态过程，才能开发出旨在干扰艾滋病毒生命周期的靶向疗法。病毒Vif蛋白与天然免疫防御分子载脂蛋白B mRNA编辑酶催化多肽样3G（Apobec3G）之间最近阐明的相互作用就是这样一种关键的病毒与宿主相互作用。Apobec3G能有效抑制艾滋病毒复制，但Vif可以减轻这种抑制作用，从而挽救病毒的感染性。文中讨论了早期描述Vif特征以及将Apobec3G克隆和鉴定为抗病毒物质的研究工作。还介绍了详述Vif-Apobec3G调节回路机制的最新进展以及我们对Apobec3G内源性功能的初步认识。总的来说，这些研究为旨在利用Apobec3G抗病毒功能消除艾滋病毒复制的潜在新型治疗策略提供了线索。
