Role of immune activation in HIV pathogenesis.
Role of immune activation in HIV pathogenesis.
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DOI：
10.1007/s11904-007-0007-8
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发表时间：
2007-02-01
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
长期以来，T细胞活化一直被认为是HIV发病机制的中心介质。高T细胞活化水平预测未经治疗的患者疾病进展更快，抗逆转录病毒治疗期间治疗介导的CD4+ T细胞增加减少，与血浆HIV RNA水平无关，可能是区分HIV感染的致病性和非致病性灵长类动物模型的主要特征。对HIV感染动物模型和个体的研究继续增强我们对HIV感染期间T细胞活化如何导致免疫缺陷的理解。这些研究的目的是确定新的免疫疗法可以针对的特定机制，这些疗法适用于尽管多年抗逆转录病毒治疗但迄今仍无法恢复正常免疫功能的患者。尽管迄今为止，大多数靶向T细胞活化的免疫疗法都不成功，但最近的科学发展将注意力集中在未来几代免疫疗法可能利用的特定途径上。
T-cell activation has long been considered a central mediator of HIV pathogenesis. High T-cell activation levels predict more rapid disease progression in untreated patients and decreased treatment-mediated CD4+ T-cell gains during antiretroviral therapy, independent of plasma HIV RNA levels, and may be the primary feature distinguishing pathogenic from nonpathogenic primate models of HIV infection. Studies in animal models and individuals with HIV infection continue to enhance our understanding of how T-cell activation causes immunodeficiency during HIV infection. The goal of these studies is to identify specific mechanisms that can be targeted by novel immune-based therapies for patients who have thus far been unable to recover normal immune function despite years of antiretroviral therapy. Although most immune-based therapies targeting T-cell activation have been unsuccessful to date, recent scientific developments have focused attention on specific pathways that may be exploited by future generations of immune-based therapies.