Gras Luuk, de Wolf Frank, Smit Colette, Prins Maria, van der Meer Jan T M, Vanhommerig Joost W, Zwinderman Aeilko H, Schinkel Janke, Geskus Ronald B
*Stichting HIV Monitoring, Amsterdam, the Netherlands; †Department of Infectious Disease Epidemiology, Imperial College School of Medicine, London, United Kingdom; ‡Department of Internal Medicine, Division of Infectious Diseases, Tropical Medicine and AIDS, and Centre for Infection and Immunity Amsterdam (CINIMA), Academic Medical Centre of the University of Amsterdam, Amsterdam, the Netherlands; §Cluster of Infectious Diseases, Department of Research, Public Health Service of Amsterdam, Amsterdam, the Netherlands; ‖Department of Medical Microbiology, Section of Clinical Virology, Academic Medical Center of the University of Amsterdam, Amsterdam, the Netherlands; and ¶Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Centre of the University of Amsterdam, Amsterdam, the Netherlands.
J Acquir Immune Defic Syndr. 2015 Apr 15;68(5):536-42. doi: 10.1097/QAI.0000000000000514.
Little is known about the impact of acute hepatitis C virus (HCV) co-infection on HIV-1 disease progression. We investigated CD4 cell count and HIV RNA concentration changes after HCV infection in individuals chronically infected with HIV-1.
We selected individuals that had the last negative and first positive HCV RNA test less than 1 year apart. Bivariate linear mixed-effects regression was used to model trends in HIV RNA level and CD4 cell count from 2 years before the last negative HCV RNA test until the first of the following dates: start of anti-HCV medication, change in combination antiretroviral therapy (cART) status, and end of follow-up.
At the estimated time of HCV co-infection, of 89 individuals, 63 (71%) were cART-treated and 26 (29%) were not on cART. In persons on cART, median CD4 cell count declined from 587 to 508 cells per cubic millimeter (P < 0.0001) during the first 5 months after HCV infection and returned to 587 cells per cubic millimeter after 2.2 years. Also, the probability of an HIV RNA >50 copies per milliliter peaked to 18.6% at HCV co-infection, with lower probabilities 6 months before (3.5%, P = 0.006 compared with peak probability) and after (2.9%, P = 0.009). In persons not on cART, no significant impact of HCV co-infection on trends in the HIV RNA level or CD4 cell count was observed.
Acute HCV infection in cART-treated, chronically HIV-infected patients was associated with a temporary decrease in CD4 cell counts and increased risk of HIV viremia >50 copies per milliliter. This may increase the risk of further HIV transmission.
关于急性丙型肝炎病毒(HCV)合并感染对HIV-1疾病进展的影响,人们了解甚少。我们调查了长期感染HIV-1的个体在感染HCV后CD4细胞计数和HIV RNA浓度的变化。
我们选择了最后一次HCV RNA检测为阴性和首次检测为阳性的时间间隔小于1年的个体。采用双变量线性混合效应回归模型,对从最后一次阴性HCV RNA检测前2年直至以下日期中的第一个日期(抗HCV药物开始使用、联合抗逆转录病毒治疗(cART)状态改变以及随访结束)的HIV RNA水平和CD4细胞计数趋势进行建模。
在估计的HCV合并感染时,89名个体中,63名(71%)接受了cART治疗,26名(29%)未接受cART治疗。在接受cART治疗的患者中,HCV感染后的前5个月,CD4细胞计数中位数从每立方毫米587个降至508个(P<0.0001),2.2年后恢复到每立方毫米587个。此外,HIV RNA>50拷贝/毫升的概率在HCV合并感染时达到峰值18.6%,在合并感染前6个月(3.5%,与峰值概率相比P = 0.006)和之后(2.9%,P = 0.009)概率较低。在未接受cART治疗的患者中,未观察到HCV合并感染对HIV RNA水平或CD4细胞计数趋势有显著影响。
在接受cART治疗的慢性HIV感染患者中,急性HCV感染与CD4细胞计数暂时下降以及HIV病毒血症>50拷贝/毫升的风险增加有关。这可能会增加进一步传播HIV的风险。