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.
*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.
Correspondence to: Serena Vita, MD, PhD, Department of Public Health and Infectious Disease, Sapienza University of Rome, Viale del Policlinico 155, 00161 Rome, Italy (e-mail: email@example.com).
Supported in part by Gilead Fellowship Program 2011 and SIMIT grant 2014 and by the grant from Fondazione ICONA. Icona Foundation cohort is supported by unrestricted grants of Abbvie, ViV, Gilead, Jannsen, BMS Italy.
Presented orally in part at the 15th Conference on Retroviruses and Opportunistic Infections (CROI), February 23–26, 2015, Seattle, WA.
The authors have no conflicts of interest to disclose.
Received May 27, 2016
Accepted September 26, 2016