Year: 2016
Type: article
Study design: Observational Study
Abstract: HIV-infected individuals are at increased risk of cardiovascular disease (CVD), but the arterial vascular functions affected by persistent innate and cellular immune activation are not well described. We assessed the relationship between immunologic and vascular parameters in 70 HIV-infected adults on efavirenz, tenofovir, and emtricitabine with more than 2 years of virologic suppression and no history of CVD. We measured brachial artery flow-mediated dilation (FMD) using ultrasound and circulating intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) by multiple immunoassay. We also measured circulating naive (CD45RO−CCR7+CD27+), activated (CD38+ and CD38+DR+), exhausted (PD1+), senescent (CD57+), and memory (CD45RO+) CD4+ and CD8+ T cell subsets by flow cytometry, and macrophage activation markers by ELISA and multiple immunoassay. Regression models were adjusted for age, sex, smoking, duration of antiretroviral therapy (ART), and body mass index. Median age was 45 years (IQR 39, 50), median CD4+ count 701 cells/μl (IQR 540, 954), and 43% were female. Lower brachial FMD was associated with a higher percentage of activated CD8+ T cells (p < .01), but not associated with macrophage activation. In contrast, higher ICAM-1 and VCAM-1 were associated with sCD163 (p < = .01 for both), macrophage inflammatory protein-1α (p < = .02 for both), and sCD14 (p = .01 for ICAM-1 only). These findings are consistent with the hypothesis that circulating CD8+ T cell activation may impair arterial smooth muscle relaxation, while macrophage activation has a role in the expression of endothelial cell proteins involved in immune cell translocation. Both innate and cellular immune activation appear to promote arterial vascular disease in HIV-infected persons on ART using differing mechanisms.
Institution: Vanderbilt University Medical Center
Language: English
Subfield: Emergency Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Funders: Vanderbilt University, National Institutes of Health, Center for AIDS Research, University of Washington, Vanderbilt Digestive Diseases Research Center, Vanderbilt University Medical Center, National Heart, Lung, and Blood Institute, National Cancer Institute, National Institute of Allergy and Infectious Diseases, National Center for Research Resources
Awards: Immunity, Inflammation and Hypertension, G2268269956, G259079163, G3418543108, G3433274139, G4038955393, G4107354744, G453267231, G454225982, The Role of Obesity and Adipocytes in Immune Activation on Antiretroviral Therapy, G560889077, G563474107, G5853943267, G6219794387, Mentoring in HIV and Tuberculosis Research, G6488665543, The Vanderbilt Institute for Clinical and Translational Research (VICTR) UL1, G7520984233, G7653134492, The Role of The T Cell In The Genesis of Hypertension , G8658404038, G9000076948, Tennessee Center for AIDS Research (TN-CFAR), G9000081609, G9000300101, G9000313355, G9000337956, Cancer Center Support Grant
OpenAlex ID: W2519595224