HIV infection results in excessive T cell activation and dysfunction which may persist even during effective antiretroviral therapy (ART). The dynamics of immune 'deactivation' and extent to which T cell memory subsets normalize after ART are unclear. We longitudinally assessed the influence of 1 year of ART on the phenotype of T cells in HIV-infected African women, relative to matched HIV-uninfected women, using activation (CD38, HLA-DR) and differentiation markers (CD27, CD45RO). ART induced a substantial reduction in T cell activation, but remained higher than HIV-uninfected controls. ART largely normalized the distribution of CD4+ T cell memory subsets, while the distribution of CD8+ T cell memory subsets remained significantly skewed compared to HIV-uninfected individuals. Thus, there was a considerable but only partial reversal of T cell defects upon ART. Understanding T cell impairment may provide important insights into mechanisms of HIV pathogenesis in the era of ART.

中文翻译：

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尽管存在抗逆转录病毒疗法引起的HIV抑制，但残余T细胞活化和CD8 + T细胞记忆分化偏向。

HIV感染导致过度的T细胞活化和功能障碍，甚至在有效的抗逆转录病毒疗法（ART）期间也可能持续存在。免疫“失活”的动态以及ART后T细胞记忆亚群正常化的程度尚不清楚。我们使用激活（CD38，HLA-DR）和分化标记（CD27，CD45RO），纵向评估了一年的ART对HIV感染的非洲女性相对于未感染HIV的女性T细胞表型的影响。ART诱导T细胞活化显着降低，但仍高于未感染HIV的对照。ART很大程度上使CD4 + T细胞记忆亚群的分布正常化，而与未感染HIV的个体相比，CD8 + T细胞记忆亚群的分布仍然明显偏斜。因此，ART时T细胞缺陷发生了相当大但仅部分的逆转。了解T细胞损伤可能为ART时代的HIV发病机理提供重要的见解。