Boulassel Mohamed-Rachid, Samson Johanne, Khammy Ampha, Lapointe Normand, Soudeyns Hugo, Routy Jean-Pierre
Division of Hematology, Immunodeficiency Service, McGill University Health Centre, Quebec, Canada.
Viral Immunol. 2007 Dec;20(4):649-56. doi: 10.1089/vim.2007.0047.
We recently reported that interleukin-7 (IL-7), a potent stimulator of lymphopoiesis, is an independent predictor of virological response to antiretroviral therapy (ART) in HIV-1 infected adults. To determine if this cytokine also predicts treatment response in HIV-1-infected children, a longitudinal study was performed over 48 weeks in 36 treatment-naïve children vertically infected with HIV-1. Subjects who received treatment (n = 29) were stratified as complete virological responders (n = 12), partial virological responders (n = 11), or non-responders (n = 6), based on decline in viral load from baseline to week 48. Median plasma IL-7 levels at baseline were higher in complete responders (4.85 pg/mL, interquartile range [IQR] = 3.35-6.5) than in untreated controls (2.10 pg/mL, IQR = 1.50-3.50; p = 0.05). Linear regression analysis showed that baseline IL-7 levels were positively correlated with changes in HIV-1 viral load between baseline and week 24 (r = 0.40; p = 0.03) and between baseline and week 48 (r = 0.34; p = 0.07), but not with corresponding changes in CD4+ T-cell percentages and absolute counts. Collectively, these results indicate that IL-7 levels at baseline are predictive of virological but not immunological response to ART in children infected with HIV-1.
我们最近报告称,白细胞介素-7(IL-7)作为淋巴细胞生成的强效刺激因子,是HIV-1感染成人对抗逆转录病毒疗法(ART)病毒学应答的独立预测指标。为了确定这种细胞因子是否也能预测HIV-1感染儿童的治疗反应,我们对36名未经治疗的垂直感染HIV-1的儿童进行了为期48周的纵向研究。接受治疗的受试者(n = 29)根据从基线到第48周病毒载量的下降情况,被分层为完全病毒学应答者(n = 12)、部分病毒学应答者(n = 11)或无应答者(n = 6)。完全应答者基线时的血浆IL-7水平中位数(4.85 pg/mL,四分位间距[IQR]=3.35 - 6.5)高于未治疗的对照组(2.10 pg/mL,IQR = 1.50 - 3.50;p = 0.05)。线性回归分析显示,基线IL-7水平与基线至第24周(r = 0.40;p = 0.03)以及基线至第48周(r = 0.34;p = 0.07)期间HIV-1病毒载量的变化呈正相关,但与CD4 + T细胞百分比和绝对计数的相应变化无关。总体而言,这些结果表明,基线IL-7水平可预测HIV-1感染儿童对ART的病毒学应答,但不能预测免疫学应答。