Abstract
HIV-infected individuals are at increased risk of coronary artery disease (CAD) with underlying mechanisms including chronic immune activation and inflammation secondary to HIV-induced microbial translocation and low-grade endotoxemia; direct effects of HIV and viral proteins on macrophage cholesterol metabolism; and dyslipidemia related to HIV infection and specific antiretroviral therapies. Monocytes are the precursors of the lipid-laden foam cells within the atherosclerotic plaque and produce high levels of proinflammatory cytokines such as IL-6. The minor CD14+/CD16+ "proinflammatory" monocyte subpopulation is preferentially susceptible to HIV infection and may play a critical role in the pathogenesis of HIV-related CAD. In this review, the central role of monocytes/macrophages in HIV-related CAD and the importance of inflammation and cholesterol metabolism are discussed.
MeSH terms
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Animals
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Cholesterol / immunology*
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Cholesterol / metabolism
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Coronary Artery Disease / etiology
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Coronary Artery Disease / immunology*
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Coronary Artery Disease / metabolism
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Coronary Artery Disease / pathology
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Coronary Artery Disease / therapy
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Dyslipidemias / etiology
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Dyslipidemias / immunology
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Dyslipidemias / metabolism
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Dyslipidemias / pathology
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Dyslipidemias / therapy
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GPI-Linked Proteins
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HIV Infections / complications
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HIV Infections / immunology*
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HIV Infections / metabolism
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HIV Infections / pathology
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HIV Infections / therapy
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Humans
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Inflammation / etiology
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Inflammation / immunology
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Inflammation / metabolism
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Inflammation / therapy
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Interleukin-6 / immunology
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Interleukin-6 / metabolism
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Lipopolysaccharide Receptors / immunology
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Lipopolysaccharide Receptors / metabolism
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Macrophage Activation / immunology*
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Macrophages / immunology*
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Macrophages / metabolism
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Macrophages / pathology
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Receptors, IgG / immunology
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Receptors, IgG / metabolism
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Risk Factors
Substances
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FCGR3B protein, human
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GPI-Linked Proteins
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IL6 protein, human
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Interleukin-6
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Lipopolysaccharide Receptors
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Receptors, IgG
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Cholesterol