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人类免疫缺陷病毒合并感染的发病机制。

Pathogenesis of Human Immunodeficiency Virus- Co-Infection.

作者信息

Wong Kevin, Nguyen James, Blair Lillie, Banjanin Marina, Grewal Bunraj, Bowman Shane, Boyd Hailey, Gerstner Grant, Cho Hyun Jun, Panfilov David, Tam Cho Ki, Aguilar Delaney, Venketaraman Vishwanath

机构信息

College of Osteopathic Medicine of the Pacific-NorthWest, Western University of Health Sciences, Lebanon, OR 97355, USA.

College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA 91766, USA.

出版信息

J Clin Med. 2020 Nov 6;9(11):3575. doi: 10.3390/jcm9113575.

DOI:10.3390/jcm9113575
PMID:33172001
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7694603/
Abstract

Given that infection with () is the leading cause of death amongst individuals living with HIV, understanding the complex mechanisms by which exacerbates HIV infection may lead to improved treatment options or adjuvant therapies. While it is well-understood how HIV compromises the immune system and leaves the host vulnerable to opportunistic infections such as , less is known about the interplay of disease once active is established. This review explores how glutathione (GSH) depletion, T cell exhaustion, granuloma formation, and TNF-α upregulation, as a result of infection, leads to an increase in HIV disease severity. This review also examines the difficulties of treating coinfected patients and suggests further research on the clinical use of GSH supplementation.

摘要

鉴于感染()是艾滋病毒感染者死亡的主要原因,了解其加剧艾滋病毒感染的复杂机制可能会带来更好的治疗选择或辅助治疗方法。虽然人们很清楚艾滋病毒如何损害免疫系统并使宿主易受诸如()等机会性感染,但对于一旦活动性()确立后疾病之间的相互作用了解较少。本综述探讨了由于感染()导致的谷胱甘肽(GSH)耗竭、T细胞耗竭、肉芽肿形成和肿瘤坏死因子-α上调如何导致艾滋病毒疾病严重程度增加。本综述还研究了治疗合并感染患者的困难,并建议进一步研究补充GSH的临床应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/4e7f04cedf9c/jcm-09-03575-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/18f47ab1a621/jcm-09-03575-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/02ed6b625454/jcm-09-03575-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/6015e063b5a2/jcm-09-03575-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/4e7f04cedf9c/jcm-09-03575-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/18f47ab1a621/jcm-09-03575-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/02ed6b625454/jcm-09-03575-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/6015e063b5a2/jcm-09-03575-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d726/7694603/4e7f04cedf9c/jcm-09-03575-g004.jpg

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