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简短报告:在ICONA队列中接受病毒学抑制抗逆转录病毒治疗的巨细胞病毒感染和未感染受试者中的可溶性CD163

Brief Report: Soluble CD163 in CMV-Infected and CMV-Uninfected Subjects on Virologically Suppressive Antiretroviral Therapy in the ICONA Cohort.

作者信息

Vita Serena, Lichtner Miriam, Marchetti Giulia, Mascia Claudia, Merlini Esther, Cicconi Paola, Vullo Vincenzo, Viale Pierluigi, Costantini Andrea, DʼArminio Monforte Antonella

机构信息

*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.

出版信息

J Acquir Immune Defic Syndr. 2017 Mar 1;74(3):347-352. doi: 10.1097/QAI.0000000000001232.

Abstract

AIMS

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.

DESIGN AND METHODS

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.

RESULTS

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.

CONCLUSIONS

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.

摘要

目的

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。

设计与方法

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。

结果

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。

结论

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。

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