Department of Medicine, Center for Infectious Diseases, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
J Acquir Immune Defic Syndr. 2013 Apr 15;62(5):505-8. doi: 10.1097/QAI.0b013e318285cd33.
Initiation of antiretroviral therapy during acute HIV-1 infection may prevent persistent immune activation. We analyzed longitudinal CD38+HLA-DR+ CD8+ T-cell percentages in 31 acutely infected individuals who started early (median 43 days since infection) and successful antiretroviral therapy, and maintained viral suppression through 96 weeks. Pretherapy a median of 72.6% CD8+ T cells were CD38+HLA-DR+, and although this decreased to 15.6% by 96 weeks, it remained substantially higher than seronegative controls (median 8.9%, P = 0.008). Shorter time to suppression predicted lower activation at 96 weeks. These results support the hypothesis that very early events in HIV-1 pathogenesis may result in prolonged immune dysfunction.
在急性 HIV-1 感染时启动抗逆转录病毒治疗可能会阻止持续的免疫激活。我们分析了 31 名早期（感染后中位数 43 天）开始成功抗逆转录病毒治疗并通过 96 周维持病毒抑制的急性感染者的纵向 CD38+HLA-DR+ CD8+ T 细胞比例。治疗前，中位数 72.6%的 CD8+ T 细胞为 CD38+HLA-DR+，尽管到 96 周时降至 15.6%，但仍明显高于血清阴性对照者（中位数 8.9%，P=0.008）。抑制时间越短，96 周时的激活越低。这些结果支持这样一种假设，即 HIV-1 发病机制中的早期事件可能导致持续的免疫功能障碍。
