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Atherosclerosis. 2014 Jan;232(1):52-8. doi: 10.1016/j.atherosclerosis.2013.10.021. Epub 2013 Oct 31.

Reduced CD14 expression on classical monocytes and vascular endothelial adhesion markers independently associate with carotid artery intima media thickness in chronically HIV-1 infected adults on virologically suppressive anti-retroviral therapy.

Author information

1
Hawaii Center for AIDS, University of Hawaii, Honolulu, HI, USA; Department of Tropical Medicine, John A. Burns School of Medicine, Honolulu, HI, USA. Electronic address: jbarbour@hawaii.edu.
2
Hawaii Center for AIDS, University of Hawaii, Honolulu, HI, USA; Department of Tropical Medicine, John A. Burns School of Medicine, Honolulu, HI, USA.
3
Hawaii Center for AIDS, University of Hawaii, Honolulu, HI, USA; Department of Medicine, John A. Burns School of Medicine, Honolulu, HI, USA.
4
Blood Systems Research Institute, San Francisco, CA, USA; Department of Laboratory Medicine, University of California, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, CA, USA.
5
Blood Systems Research Institute, San Francisco, CA, USA; Department of Laboratory Medicine, University of California, San Francisco, CA, USA.
6
Blood Systems Research Institute, San Francisco, CA, USA.
7
Hawaii Center for AIDS, University of Hawaii, Honolulu, HI, USA.
8
Hawaii Center for AIDS, University of Hawaii, Honolulu, HI, USA; Atherosclerosis Research Unit, University of Southern California, Los Angeles, CA, USA.
9
Hawaii Center for AIDS, University of Hawaii, Honolulu, HI, USA; Department of Medicine, John A. Burns School of Medicine, Honolulu, HI, USA; Straub Clinics and Hospital, Honolulu, HI, USA.
10
Atherosclerosis Research Unit, University of Southern California, Los Angeles, CA, USA.
11
Hawaii Center for AIDS, University of Hawaii, Honolulu, HI, USA; Queen's Medical Center, Honolulu, HI, USA.

Abstract

HIV infection causes systemic immune inflammation, and increases the risk for cardiovascular (CVD) disease even among those on virologically suppressive anti-retroviral treatment (ART). We performed a biostatistical analysis and screen of candidate cellular and plasma biomarkers for association with carotid artery intima-media thickness (CIMT), independent of traditional CVD risk factors such as age, gender, systolic blood pressure (SBP), lipid levels, smoking and diabetes. We conducted a multi-stage analysis based on a cross-sectional study of CVD risk in HIV-infected subjects age >45 years on ART for >6 months. The goal of this analysis was to identify candidate cellular and plasma biomarkers of CIMT in HIV-1 infected adults. We further sought to determine if these candidate biomarkers were independent of traditional CVD risk factors previously identified in HIV negative adults. High-resolution B-mode ultrasound images of the right common carotid common artery (CCA) were obtained. Plasma soluble inflammatory mediators, cytokines and chemokines were detected. Monocytes were defined by CD14/CD16 expression, and CD8+ T-cell activation by CD38/HLA-DR expression. Subjects were a median of 49.5 years old, 87% male, had a CIMT of 0.73 mm, FRS of 6%, a median viral load of 48 copies/mL, and CD4+ T cell count of 479 cells/μL. Soluble VCAM-1, and expansion of CD14dimCD16- monocytes each associated with higher CIMT independently of age and SBP. These factors are distinct components of a shared atherogenic process; 1) vascular endothelial molecular expression and 2) vascular monocytes that enter into the vascular endothelium and promote atherosclerotic plaque.

KEYWORDS:

Biomarker; CD14; CIMT; Cardiovascular disease; Carotid intima-media; Cytokines; Framingham risk score; HIV; Monocytes; Regression; Screen; VCAM-1

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