The macrophage: the intersection between HIV infection and atherosclerosis

Review of the increased risk of coronary artery disease with HIV‐1 infection, association with traditional risk factors, monocyte activation, and impaired cholesterol metabolism. 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.