Kuniholm Mark H, OʼBrien Thomas R, Prokunina-Olsson Ludmila, Augenbraun Michael, Plankey Michael, Karim Roksana, Sarkar Monika, French Audrey L, Pierce Chris, Strickler Howard D, Anastos Kathryn
*Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY;†Infections and Immunoepidemiology Branch, National Cancer Institute, Bethesda, MD;‡Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD;§Department of Medicine, State University of New York Downstate Medical Center, Brooklyn, NY;‖Department of Medicine, Georgetown University Medical Center, Washington, DC;¶Department of Pediatrics, University of Southern California, Los Angeles, CA;#Department of Medicine, University of California, San Francisco, CA;**Department of Medicine, CORE Center/Stroger Hospital of Cook County, Chicago, IL;††Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; and‡‡Department of Medicine, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY.
J Acquir Immune Defic Syndr. 2016 Jun 1;72(2):162-70. doi: 10.1097/QAI.0000000000000928.
Recent studies reported that the CD4/CD8 T-cell ratio is inversely associated with biomarkers traditionally used to measure immune activation and systemic inflammation in highly active antiretroviral therapy-treated HIV-infected (HIV+) patients. The relation of hepatitis C virus (HCV) coinfection with the CD4/CD8 ratio in HIV+ patients is unknown.
We examined 50,201 CD4/CD8 ratios measured over 20 years in 3 groups of HIV+ women enrolled in the Women's Interagency HIV Study: HCV antibody negative (n = 1734), cleared HCV (n = 231), and chronic HCV (n = 751) in multivariate models. IFNL4-ΔG genotype and HCV viral load were also considered.
Compared with HCV antibody negative status, chronic HCV infection was associated with lower CD4/CD8 ratios when HIV viral load was suppressed to the lower limit of quantification (β = -0.08; P = 0.002). Cleared HCV (β = -0.10; P = 0.0009), but not IFNL4-ΔG genotype or HCV viral load, was also associated with lower CD4/CD8 ratios when HIV viral load was suppressed to the lower limit of quantification.
The association of HCV coinfection with CD4/CD8 ratio is consistent with previously observed associations of HCV coinfection with biomarkers traditionally used to measure immune activation and systemic inflammation in HIV+ patients. These data provide additional support for the use of CD4/CD8 ratio for routine monitoring of immune activation and inflammation in HIV+ patients, including those with HIV/HCV coinfection; however, the unexpected association between cleared HCV and lower CD4/CD8 ratio requires additional study.
近期研究报告称，在接受高效抗逆转录病毒治疗的HIV感染（HIV+）患者中，CD4/CD8 T细胞比值与传统上用于衡量免疫激活和全身炎症的生物标志物呈负相关。HIV+患者中丙型肝炎病毒（HCV）合并感染与CD4/CD8比值的关系尚不清楚。
我们在女性机构间HIV研究中纳入的3组HIV+女性中，对20年来测量的50201个CD4/CD8比值进行了多变量模型分析：HCV抗体阴性（n = 1734）、HCV已清除（n = 231）和慢性HCV感染（n = 751）。还考虑了IFNL4-ΔG基因型和HCV病毒载量。
与HCV抗体阴性状态相比，当HIV病毒载量被抑制到定量下限（β = -0.08；P = 0.002）时，慢性HCV感染与较低的CD4/CD8比值相关。当HIV病毒载量被抑制到定量下限（β = -0.10；P = 0.0009）时，HCV已清除（而非IFNL4-ΔG基因型或HCV病毒载量）也与较低的CD4/CD8比值相关。
HCV合并感染与CD4/CD8比值的关联与先前观察到的HCV合并感染与传统上用于衡量HIV+患者免疫激活和全身炎症的生物标志物的关联一致。这些数据为使用CD4/CD8比值对HIV+患者（包括HIV/HCV合并感染患者）的免疫激活和炎症进行常规监测提供了额外支持；然而，HCV已清除与较低的CD4/CD8比值之间的意外关联需要进一步研究。
