Journal
AIDS
Volume 23, Issue 8, Pages 941-949Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QAD.0b013e328329c76b
Keywords
atherosclerosis; cytokines; inflammation; risk factors; viral load
Categories
Funding
- Robert Wood Johnson Foundation [051898]
- National Center for Research Resources [K12-RR1767203]
- National Institute on Drug Abuse [R01 DA14998, R01 DA13564]
- National Institute of Mental Health [MH075679, MH070297]
- General Clinical Research Center [M01-RR12248]
- Center For AIDS Research [CFAR-5 P30AI-051519]
- Albert Einstein College of Medicine
- Yeshiva University/Montefiore Medical Center
- National Heart, Lung, and Blood Institute [R01 HL071021]
- American Heart Association
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Background: HIV-infected individuals may be at increased risk for atherosclerosis. Although this is partially attributable to metabolic factors, HIV-associated inflammation may play a role. Objective: To investigate associations of HIV disease with serum monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2 (MCP-1/CCL2) levels and atherosclerosis burden. Design: A cross-sectional analysis. Methods: Serum MCP-1/CCL2, fasting lipids, and glucose tolerance were measured in 98 HIV-infected and 79 demographically similar uninfected adults. Eighty-four participants had MRI of the carotid arteries and thoracic aorta to measure atherosclerosis burden. Multivariate analyses were performed using linear regression. Results: Mean MCP-1/CCL2 levels did not differ between HIV-infected and uninfected participants (P = 0.65). Among HIV-infected participants, after adjusting for age, BMI, and cigarette smoking, HIV-1 viral load was positively associated with MCP-1/CCL2 (P = 0.02). Multivariate analyses adjusting for sex, low-density lipoprotein cholesterol, total cholesterol: high-density lipoprotein cholesterol ratio, cigarette smoking, MCP-1/CCL2, and protease inhibitor use found that HIV infection was associated with greater mean thoracic aorta vessel wall area (VWA, P < 0.01) and vessel wall thickness (VWT, P = 0.03), but not with carotid artery parameters. Compared with being uninfected, having detectable HIV-1 viremia was associated with greater mean thoracic aorta VWA (P < 0.01) and VWT (P = 0.03), whereas being HIV-infected With undetectable viral load was associated with greater thoracic aorta VWA (P = 0.02) but not VWT (P = 0.15). There was an independent positive association of MCP-1/CCL2 with thoracic aorta VWA (P = 0.01) and VWT (P = 0.01). Conclusion: HIV-1 viral burden is associated with higher serum levels of MCP-1/CCL2 and with atherosclerosis burden, as assessed by thoracic aorta VWA and VWT. (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williarns & Wilkins
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