학술논문

Immunologic predictors of coronary artery calcium progression in a contemporary HIV cohort
Document Type
article
Source
AIDS. 28(6)
Subject
Medical Microbiology
Biomedical and Clinical Sciences
Immunology
Infectious Diseases
Heart Disease - Coronary Heart Disease
HIV/AIDS
Prevention
Cardiovascular
Heart Disease
Clinical Research
Good Health and Well Being
Adult
Calcium
Cohort Studies
Coronary Artery Disease
Coronary Vessels
Female
Flow Cytometry
HIV Infections
Humans
Immunophenotyping
Leukocytes
Mononuclear
Male
Middle Aged
Prospective Studies
cardiovascular disease
coronary artery calcium
HIV
immune activation
inflammation
monocyte activation
CDC SUN Study Investigators
Biological Sciences
Medical and Health Sciences
Psychology and Cognitive Sciences
Virology
Biomedical and clinical sciences
Health sciences
Language
Abstract
BackgroundIdentifying immunologic mechanisms that contribute to premature cardiovascular disease (CVD) among HIV-positive patients will inform prevention strategies.MethodsCoronary artery calcium (CAC) progression was studied in an HIV cohort. Immunophenotypes were measured on baseline cryopreserved peripheral blood mononuclear cells using multicolor flow cytometry. Logistic regression identified predictors of CAC progression after adjusting for traditional and HIV-related risk factors.ResultsBaseline characteristics for the analysis cohort (n=436) were median age 42 years, median CD4 cell count 481 cells/μl, and 78% receiving antiretroviral therapy. Higher frequencies of CD16 monocytes were associated with greater likelihood of CAC progression, after adjusting for traditional and HIV risk factors [odds ratio per doubling was 1.66 for CD14/CD16 (P=0.02), 1.36 for CD14/CD16 (P=0.06), and 1.69 for CD14/CD16 (P=0.01)]. Associations for CD16 monocytes persisted when restricted to participants with viral suppression. We found no significant associations for CAC progression with other cellular phenotypes, including T-cell activation and senescence markers.ConclusionCirculating CD16 monocytes, potentially reflecting a more pro-atherogenic subpopulation, independently predicted greater CAC progression among HIV-infected persons at low risk for AIDS. In contrast to T-cell abnormalities classically associated with AIDS-related disease progression, these data highlight the potential role of monocyte activation in HIV-related CVD risk.