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HIV-1 Vif versus APOBEC3G: newly appreciated warriors in the ancient battle between virus and host

机译:HIV-1 Vif与APOBEC3G:在病毒与宿主之间的古老战斗中新受到赞赏的战士

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摘要

Recent studies demonstrate that apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G (APOBEC3G), the newly identified target of HIV-1 Vif, represents an endogenous inhibitor of HIV-1 replication and is a viral-encapsidated cellular protein that deaminates minus-strand reverse transcript cytosine residues to uracils. HIV-1 Vif counteracts the inhibitory activity of APOBEC3G by forming a complex with the enzyme, inducing its degradation and preventing its viral encapsidation. This finding provides valuable insights into virus–host interactions and suggests a potential, novel anti-HIV-1 therapeutic approach.
机译:最近的研究表明,载脂蛋白B mRNA编辑酶,催化多肽样3G(APOBEC3G)是HIV-1 Vif的新发现靶标,代表HIV-1复制的内源性抑制剂,是一种病毒衣壳化的细胞蛋白,其脱氨性为负。链反转录胞嘧啶残基至尿嘧啶。 HIV-1 Vif通过与酶形成复合物来抵消APOBEC3G的抑制活性,诱导其降解并阻止其病毒衣壳化。这一发现提供了对病毒-宿主相互作用的宝贵见解,并提出了一种潜在的,新颖的抗HIV-1治疗方法。

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