Association of HIV viral load with monocyte chemoattractant protein-1 and atherosclerosis burden measured by magnetic resonance imaging
| Autor: | Yungtai Lo, Michelle Floris-Moore, Zahi A. Fayad, Venkatesh Mani, Valentin Fuster, Karen B Weinshelbaum, Joan W. Berman, Andrea A. Howard, Robyn S. Klein, Alison D. Schecter, Ellie E. Schoenbaum |
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| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Male
Pathology medicine.medical_specialty Chemokine Sexual Behavior Immunology New York Inflammation Aorta Thoracic HIV Infections CCL2 Article Pathogenesis Risk Factors medicine Immunology and Allergy Humans Prospective Studies Substance Abuse Intravenous Chemokine CCL2 biology business.industry Vascular disease Monocyte Middle Aged Viral Load medicine.disease Atherosclerosis Magnetic Resonance Imaging Infectious Diseases medicine.anatomical_structure Atheroma Carotid Arteries Cross-Sectional Studies Case-Control Studies cardiovascular system biology.protein HIV-1 Female medicine.symptom business Viral load Biomarkers |
| DOI: | 10.17615/8yv6-mf67 |
| Popis: | Highly active antiretroviral therapy (HAART) has markedly increased life expectancy among persons infected with HIV. As HIV-infected persons age, chronic diseases like atherosclerosis have become increasingly important in their healthcare. Use of HAART has been linked to dyslipidemia and insulin resistance, well-established risk factors for atherosclerosis.[1-3] Individuals infected with HIV may also be at risk for vascular disease secondary to direct viral effects which induce chronic immune activation leading to increased expression of pro-inflammatory mediators by activated T cells and macrophages within the vasculature.[4, 5] Several pro-inflammatory cytokines and chemokines associated with HIV infection are linked to atherosclerosis, and may participate in vascular dysfunction in infected individuals. Monocyte chemoattractant protein-1 (MCP-1/CCL2) plays a crucial role in the pathogenesis of atherosclerosis, attracting monocytes into the arterial intima where they differentiate into macrophages, accumulate lipoproteins and become lipid-laden foam cells.[6] We previously demonstrated that human arterial smooth muscle cells (SMC) express the chemokine receptors CXCR4 and CCR5, and that HIV-infected SMC are themselves a source of MCP-1/CCL2, and have shown that MCP-1/CCL2 induces tissue factor, a major contributor to thrombosis associated with plaque rupture, in vascular SMC.[7, 8] These findings suggest that HIV infection promotes an inflammatory response in the vessel wall and may thereby accelerate atherosclerosis. Studies examining relationships of HIV infection and HAART with carotid artery intima-media thickness (IMT) as a surrogate marker for atherosclerosis have had conflicting results. Some have found little association with HIV infection or specific classes of antiretrovirals, whereas others have reported greater IMT among HIV-infected subjects but no association with antiretrovirals, and yet others have shown greater IMT associated with protease inhibitors (PIs).[9-12] Carotid artery ultrasound enables imaging of exophytic plaque on the carotid artery wall and measures IMT. However ultrasound may be unable to detect early atheromatous changes, cannot image the adventitial layer to gauge outward remodeling, and is unable to assess atherosclerosis in the thoracic aorta. Magnetic resonance imaging (MRI) is a noninvasive imaging modality that detects early atheroma formation and allows more global assessment of vascular structure, including the aorta.[13, 14] To assess whether HIV infected individuals have increased serum markers of inflammation and increased atherosclerosis plaque burden, we measured MCP-1/CCL2 levels and performed MRI of the thoracic aorta and carotid arteries in a well-characterized sample of HIV-infected and demographically similar uninfected individuals. |
| Databáze: | OpenAIRE |
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