Vita Serena, Lichtner Miriam, Marchetti Giulia, Mascia Claudia, Merlini Esther, Cicconi Paola, Vullo Vincenzo, Viale Pierluigi, Costantini Andrea, DʼArminio Monforte Antonella
*Sapienza University of Rome, Rome, Italy; †Sapienza University of Rome, Polo Pontino, Latina, Italy; ‡University of Milan, Milan, Italy; §University of Bologna, Bologna, Italy; and ‖Polytechnic University of Marche, Ancona, Italy.
J Acquir Immune Defic Syndr. 2017 Mar 1;74(3):347-352. doi: 10.1097/QAI.0000000000001232.
To contribute to the understanding of the role played by cytomegalovirus (CMV) in sustaining monocyte/macrophage-mediated immune activation in antiretroviral therapy treated HIV-infected subjects.
We selected 23 CMV-uninfected and 46 CMV-infected HIV+ subjects, matched for age, CD4 nadir, HIV infection duration, and viral hepatitis serostatus. All subjects were on successful antiretroviral therapy since at least 1 year. A group of 16 healthy donors with similar age and sex was also included. Plasma levels of tumor necrosis factor-alpha, interleukin-6, sCD163, sCD14, and CMV immunoglobulin G levels were measured in duplicate with human enzyme-linked immunosorbent assay kits.
We found significantly higher sCD163 plasma levels in HIV+CMV+ compared with HIV+CMV- subjects and healthy donors. This augmentation was confirmed also when subjects positive for hepatitis C virus-Ab were excluded from analysis. Interestingly, a correlation between anti-CMV immunoglobulin G levels and sCD163, tumor necrosis factor-alpha, interleukin-6, and sCD14 in HIV+CMV+ subjects was found.
CMV coinfection could be a major driver of monocyte/macrophage activation in virally suppressed HIV+ individuals and might explain the increased risk of non-AIDS morbidity/mortality in HIV/CMV-coinfected subjects.
有助于理解巨细胞病毒(CMV)在接受抗逆转录病毒治疗的HIV感染受试者中维持单核细胞/巨噬细胞介导的免疫激活所起的作用。
我们选取了23名未感染CMV和46名感染CMV的HIV阳性受试者,根据年龄、CD4最低点、HIV感染持续时间和病毒性肝炎血清学状态进行匹配。所有受试者至少已成功接受抗逆转录病毒治疗1年。还纳入了一组16名年龄和性别相似的健康供者。使用人酶联免疫吸附测定试剂盒对血浆中肿瘤坏死因子-α、白细胞介素-6、可溶性CD163、可溶性CD14和CMV免疫球蛋白G水平进行了重复测量。
我们发现,与HIV+CMV-受试者和健康供者相比,HIV+CMV+受试者的血浆可溶性CD163水平显著更高。当丙型肝炎病毒抗体阳性的受试者被排除在分析之外时,这种升高也得到了证实。有趣的是,在HIV+CMV+受试者中发现抗CMV免疫球蛋白G水平与可溶性CD163、肿瘤坏死因子-α、白细胞介素-6和可溶性CD14之间存在相关性。
CMV合并感染可能是病毒抑制的HIV阳性个体中单核细胞/巨噬细胞激活的主要驱动因素,并且可能解释了HIV/CMV合并感染受试者中非艾滋病发病率/死亡率增加的风险。