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本文引用的文献

1
HIV-1 assembly, budding, and maturation.HIV-1 组装、出芽和成熟。
Cold Spring Harb Perspect Med. 2012 Jul;2(7):a006924. doi: 10.1101/cshperspect.a006924.
2
Origins of HIV and the AIDS pandemic.HIV 的起源与艾滋病大流行。
Cold Spring Harb Perspect Med. 2011 Sep;1(1):a006841. doi: 10.1101/cshperspect.a006841.
3
Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein.Vpx 缓解 SAMHD1 蛋白介导的巨噬细胞中 HIV-1 感染的抑制作用。
Nature. 2011 Jun 29;474(7353):658-61. doi: 10.1038/nature10195.
4
SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx.SAMHD1 是树突状细胞和髓样细胞特异性的 HIV-1 限制因子,可被 Vpx 拮抗。
Nature. 2011 May 25;474(7353):654-7. doi: 10.1038/nature10117.
5
Hexagonal assembly of a restricting TRIM5alpha protein.TRIM5alpha 限制蛋白的六方组装
Proc Natl Acad Sci U S A. 2011 Jan 11;108(2):534-9. doi: 10.1073/pnas.1013426108. Epub 2010 Dec 27.
6
Structural insight into the mechanisms of enveloped virus tethering by tetherin.解析包膜病毒被 tetherin 固定的结构机制
Proc Natl Acad Sci U S A. 2010 Oct 26;107(43):18428-32. doi: 10.1073/pnas.1011485107. Epub 2010 Oct 12.
7
Structural and functional studies on the extracellular domain of BST2/tetherin in reduced and oxidized conformations.关于 BST2/ tetherin 胞外结构域在还原和氧化构象下的结构和功能研究。
Proc Natl Acad Sci U S A. 2010 Oct 19;107(42):17951-6. doi: 10.1073/pnas.1008206107. Epub 2010 Sep 29.
8
The HIV-1 central polypurine tract functions as a second line of defense against APOBEC3G/F.HIV-1 中央多嘧啶tract 作为抵御 APOBEC3G/F 的第二道防线发挥作用。
J Virol. 2010 Nov;84(22):11981-93. doi: 10.1128/JVI.00723-10. Epub 2010 Sep 15.
9
Stably expressed APOBEC3F has negligible antiviral activity.稳定表达的 APOBEC3F 几乎没有抗病毒活性。
J Virol. 2010 Nov;84(21):11067-75. doi: 10.1128/JVI.01249-10. Epub 2010 Aug 11.
10
Human APOBEC3G-mediated editing can promote HIV-1 sequence diversification and accelerate adaptation to selective pressure.人类 APOBEC3G 介导的编辑可以促进 HIV-1 序列多样化,并加速对选择压力的适应。
J Virol. 2010 Oct;84(19):10402-5. doi: 10.1128/JVI.01223-10. Epub 2010 Jul 21.

HIV 限制因子和逃逸机制。

HIV Restriction Factors and Mechanisms of Evasion.

机构信息

Department of Infectious Diseases, King's College London School of Medicine, Guy's Hospital, London Bridge, London SE1 9RT, United Kingdom.

出版信息

Cold Spring Harb Perspect Med. 2012 May;2(5):a006940. doi: 10.1101/cshperspect.a006940.

DOI:10.1101/cshperspect.a006940
PMID:22553496
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3331687/
Abstract

Retroviruses have long been a fertile model for discovering host-pathogen interactions and their associated biological principles and processes. These advances have not only informed fundamental concepts of viral replication and pathogenesis but have also provided novel insights into host cell biology. This is illustrated by the recent descriptions of host-encoded restriction factors that can serve as effective inhibitors of retroviral replication. Here, we review our understanding of the three restriction factors that have been widely shown to be potent inhibitors of HIV-1: namely, APOBEC3G, TRIM5α, and tetherin. In each case, we discuss how these unrelated proteins were identified, the mechanisms by which they inhibit replication, the means used by HIV-1 to evade their action, and their potential contributions to viral pathogenesis as well as inter- and intraspecies transmission.

摘要

逆转录病毒长期以来一直是发现宿主-病原体相互作用及其相关生物学原理和过程的丰富模型。这些进展不仅为病毒复制和发病机制的基本概念提供了信息,而且还为宿主细胞生物学提供了新的见解。最近描述的宿主编码限制因子可以作为有效的逆转录病毒复制抑制剂,就说明了这一点。在这里,我们回顾了我们对已被广泛证明是 HIV-1 有效抑制剂的三种限制因子的理解:APOBEC3G、TRIM5α 和 tetherin。在每种情况下,我们讨论了这些不相关的蛋白质是如何被鉴定出来的,它们抑制复制的机制,HIV-1 用来逃避它们作用的手段,以及它们在病毒发病机制以及种间和种内传播中的潜在贡献。