Plaeger Susan F, Collins Brenda S, Musib Runa, Deeks Steven G, Read Sarah, Embry Alan
Division of AIDS, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
AIDS Res Hum Retroviruses. 2012 May;28(5):469-77. doi: 10.1089/aid.2011.0213. Epub 2011 Sep 27.
With the advent of highly effective antiretroviral therapy (ART), infection with human immunodeficiency virus (HIV) has become a chronic disease rather than a death sentence. Nevertheless, effectively treated individuals have a higher than normal risk for developing noninfectious comorbidities, including cardiovascular and renal disease. Although traditional risk factors of aging as well as treatment toxicity contribute to this risk, many investigators consider chronic HIV-associated inflammation a significant factor in such end-organ disease. Despite effective viral suppression, chronic inflammation persists at levels higher than in uninfected people, yet the stimuli for the inflammation and the mechanism by which inflammation persists and promotes disease pathology remain incompletely understood. This critical gap in scientific understanding complicates and hampers effective decision making about appropriate medical intervention. To better understand the mechanism(s) of chronic immune activation in treated HIV disease, three questions need answers: (1) what is the cause of persistent immune activation during treated HIV infection, (2) what are the best surrogate markers of chronic immune activation in this setting, and (3) what therapeutic intervention(s) could prevent or reverse this process? The NIH sponsored and convened a meeting to discuss the state of knowledge concerning these questions and the best course for developing effective therapeutic strategies. This report summarizes the findings of that NIH meeting.
随着高效抗逆转录病毒疗法（ART）的出现，人类免疫缺陷病毒（HIV）感染已成为一种慢性病，而非死刑判决。然而，接受有效治疗的个体患非感染性合并症（包括心血管疾病和肾脏疾病）的风险高于正常水平。尽管衰老的传统风险因素以及治疗毒性导致了这种风险，但许多研究人员认为，慢性HIV相关炎症是此类终末器官疾病的一个重要因素。尽管病毒得到了有效抑制，但慢性炎症仍持续存在，且程度高于未感染人群，然而，炎症的刺激因素以及炎症持续存在并促进疾病病理的机制仍未完全明确。这一科学认知上的关键差距使关于适当医疗干预的有效决策变得复杂并受到阻碍。为了更好地理解接受治疗的HIV疾病中慢性免疫激活的机制，需要回答三个问题：（1）接受治疗的HIV感染期间持续免疫激活的原因是什么？（2）在这种情况下，慢性免疫激活的最佳替代标志物是什么？（3）哪些治疗干预措施可以预防或逆转这一过程？美国国立卫生研究院（NIH）主办并召开了一次会议，讨论关于这些问题的知识现状以及制定有效治疗策略的最佳途径。本报告总结了那次NIH会议的结果。
