Moanna Abeer, Dunham Richard, Paiardini Mirko, Silvestri Guido
Emory Vaccine Center, Emory University School of Medicine, 954 Gatewood Road NE, Atlanta, GA 30329, USA.
Curr HIV/AIDS Rep. 2005 Feb;2(1):16-23. doi: 10.1007/s11904-996-0004-3.
Recent studies have emphasized the role of a chronic, generalized activation of the immune system as a prominent cause of CD4+ T-cell depletion in HIV-infected patients. The HIV-induced immune activation is a strong predictor of disease progression in humans, and lack of immune activation is a key feature of nonpathogenic simian immunodeficiency virus (SIV) infection of natural hosts. The mechanisms by which immune activation induces CD4+ T-cell depletion are still incompletely understood, but likely involve changes in the complex dynamics of the naive, memory, and effector subsets of T cells. A better understanding of how HIV-induced immune activation leads to CD4+ T-cell depletion may provide new targets for immune-based interventions that could be used, in addition to standard antiretroviral therapy, to slow disease progression in HIV-infected individuals.
最近的研究强调,免疫系统的慢性全身性激活是导致HIV感染患者CD4+ T细胞耗竭的一个主要原因。HIV诱导的免疫激活是人类疾病进展的一个强有力预测指标,而缺乏免疫激活是非致病性猿猴免疫缺陷病毒(SIV)感染天然宿主的一个关键特征。免疫激活诱导CD4+ T细胞耗竭的机制仍未完全明了,但可能涉及T细胞的初始、记忆和效应亚群复杂动态变化。更好地理解HIV诱导的免疫激活如何导致CD4+ T细胞耗竭,可能为基于免疫的干预措施提供新靶点,除标准抗逆转录病毒疗法外,这些靶点可用于减缓HIV感染个体的疾病进展。