HIV and Inflammation: Mechanisms and Consequences
HIV and Inflammation: Mechanisms and Consequences
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DOI：
10.1007/s11904-012-0118-8
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发表时间：
2012-06-01
影响因子：
4.6
通讯作者：
Hunt, Peter W.
中科院分区：
文献类型：
--
作者：
Hunt, Peter W.
尽管持续的抗逆转录病毒疗法（ART）介导的病毒抑制，但持续的免疫激活和炎症已成为现代HIV治疗时代的主要挑战。虽然免疫激活、炎症和凝血标志物通常在抑制性ART期间下降，但它们在许多艾滋病毒感染者中仍然异常升高，并预测随后的死亡率和非艾滋病发病率，包括心血管疾病。本综述的目的是总结我们目前对ART介导的病毒抑制过程中持续免疫激活的根本原因以及持续免疫激活与这种情况下的发病率和死亡率之间的联系的认识。最近的几项研究将这种持续性炎症状态的替代标志物与临床结果联系起来，验证了持续性免疫激活作为可行的治疗靶点。最近的其他研究有助于澄清持续的HIV表达和/或复制，微生物易位和合并感染在驱动这种持续的炎症状态中的作用，确定新干预措施的目标。
Persistent immune activation and inflammation despite sustained antiretroviral therapy (ART)-mediated viral suppression has emerged as a major challenge of the modern HIV treatment era. While immune activation, inflammatory, and coagulation markers typically decline during suppressive ART, they remain abnormally elevated in many HIV-infected individuals and predict subsequent mortality and non-AIDS morbidities including cardiovascular disease. The goal of this review is to summarize the current state of our knowledge regarding the underlying causes of persistent immune activation during ART-mediated viral suppression as well as the link between persistent immune activation and morbidity and mortality in this setting. Several recent studies have linked surrogate markers of this persistent inflammatory state to clinical outcomes, validating persistent immune activation as a viable therapeutic target. Other recent studies have helped clarify the roles of persistent HIV expression and/ or replication, microbial translocation, and co-infections in driving this persistent inflammatory state, identifying targets for novel interventions.