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了解HIV非进展者的新线索:低胆固醇可阻断HIV转染。

New clues to understanding HIV nonprogressors: low cholesterol blocks HIV trans infection.

作者信息

Prasad Vinayaka R, Bukrinsky Michael I

机构信息

Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, USA

Department of Microbiology, Immunology, and Tropical Medicine, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA

出版信息

mBio. 2014 Jun 10;5(3):e01396-14. doi: 10.1128/mBio.01396-14.

DOI:10.1128/mBio.01396-14
PMID:24917601
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4056555/
Abstract

A small percentage of HIV-infected subjects (2 to 15%) are able to control disease progression for many years without antiretroviral therapy. Years of intense studies of virologic and immunologic mechanisms of disease control in such individuals yielded a number of possible host genes that could be responsible for the preservation of immune functions, from immune surveillance genes, chemokines, or their receptors to anti-HIV restriction factors. A recent mBio paper by Rappocciolo et al. (G. Rappocciolo, M. Jais, P. Piazza, T. A. Reinhart, S. J. Berendam, L. Garcia-Exposito, P. Gupta, and C. R. Rinaldo, mBio 5:e01031-13, 2014) describes another potential factor controlling disease progression: cholesterol levels in antigen-presenting cells. In this commentary, we provide a brief background of the role of cholesterol in HIV infection, discuss the results of the study by Rappocciolo et al., and present the implications of their findings.

摘要

一小部分感染HIV的受试者(2%至15%)能够在不接受抗逆转录病毒治疗的情况下控制疾病进展多年。多年来,对这类个体疾病控制的病毒学和免疫学机制进行了深入研究,发现了许多可能负责维持免疫功能的宿主基因,从免疫监视基因、趋化因子或其受体到抗HIV限制因子。Rappocciolo等人最近发表在《mBio》杂志上的一篇论文(G. Rappocciolo、M. Jais、P. Piazza、T. A. Reinhart、S. J. Berendam、L. Garcia-Exposito、P. Gupta和C. R. Rinaldo,《mBio》5:e01031-13,2014)描述了另一个控制疾病进展的潜在因素:抗原呈递细胞中的胆固醇水平。在这篇评论中,我们简要介绍了胆固醇在HIV感染中的作用背景,讨论了Rappocciolo等人的研究结果,并阐述了他们研究结果的意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbf/4056555/f76d7f3587c7/mbo0031418780001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbf/4056555/f76d7f3587c7/mbo0031418780001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbf/4056555/f76d7f3587c7/mbo0031418780001.jpg

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2
HIV-1 latency in monocytes/macrophages.HIV-1在单核细胞/巨噬细胞中的潜伏状态。
Viruses. 2014 Apr 22;6(4):1837-60. doi: 10.3390/v6041837.
3
The major cellular sterol regulatory pathway is required for Andes virus infection.主要的细胞固醇调节途径是 Andes 病毒感染所必需的。
Proc Natl Acad Sci U S A. 2020 Sep 8;117(36):21896-21905. doi: 10.1073/pnas.2004807117. Epub 2020 Aug 25.
4
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HIV-1 viral protein R (Vpr) induces fatty liver in mice via LXRα and PPARα dysregulation: implications for HIV-specific pathogenesis of NAFLD.HIV-1 病毒蛋白 R(Vpr)通过 LXRα 和 PPARα 失调诱导小鼠脂肪肝:对 HIV 特异性非酒精性脂肪性肝病发病机制的影响。
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