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衰老、炎症与HIV感染。

Aging, inflammation, and HIV infection.

作者信息

Aberg Judith A

机构信息

New York University School of Medicine, New York, NY, USA.

出版信息

Top Antivir Med. 2012 Aug-Sep;20(3):101-5.

PMID:22954610
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6148943/
Abstract

Prolonged survival in HIV infection is accompanied by an increased frequency of non-HIV-related comorbidities. A number of age-related comorbidities occur earlier in HIV-infected patients than in individuals without HIV infection. This "accelerated aging" appears to be largely related to chronic inflammation, chronic immune activation, and immunosenescence in HIV infection. Levels of markers of inflammation and coagulopathy are elevated in HIV-infected patients, and elevations in markers such as high-sensitivity C-reactive protein, D-dimer, and interleukin 6 (IL-6) have been associated with increased risk for cardiovascular disease, opportunistic conditions, or all-cause mortality. In both HIV infection and aging, immunosenescence is marked by an increased proportion of CD28-, CD57+ memory CD8+ T cells with reduced capacity to produce interleukin 2 (IL-2), increased production of IL-6, resistance to apoptosis, and shortened telomeres. A number of AIDS Clinical Trials Group studies are under way to examine treatment aimed at reducing chronic inflammation and immune activation in HIV infection. This article summarizes a presentation by Judith A. Aberg, MD, at the IAS-USA live continuing medical education course held in New York City in October 2011.

摘要

HIV感染患者的长期生存伴随着非HIV相关合并症发生频率的增加。一些与年龄相关的合并症在HIV感染患者中比在未感染HIV的个体中出现得更早。这种“加速衰老”似乎在很大程度上与HIV感染中的慢性炎症、慢性免疫激活和免疫衰老有关。HIV感染患者炎症和凝血障碍标志物水平升高,高敏C反应蛋白、D-二聚体和白细胞介素6(IL-6)等标志物的升高与心血管疾病、机会性疾病或全因死亡风险增加有关。在HIV感染和衰老过程中,免疫衰老的特征是CD28阴性、CD57阳性记忆CD8+T细胞比例增加,产生白细胞介素2(IL-2)的能力降低,IL-6产生增加,抗凋亡能力增强以及端粒缩短。多项艾滋病临床试验组研究正在进行,以检验旨在减少HIV感染中慢性炎症和免疫激活的治疗方法。本文总结了医学博士朱迪思·A·阿伯格在2011年10月于纽约市举行的IAS-USA现场继续医学教育课程上的一次演讲。

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