Systemic and cell-specific mechanisms of vasculopathy induced by human immunodeficiency virus and highly active antiretroviral therapy.

OBJECTIVE: Patients infected with human immunodeficiency virus (HIV) have higher rates of dyslipidemia, atherosclerosis, and chronic inflammation that can damage the vascular system compared with the general population. This can be attributed both to HIV itself and to highly active antiretroviral therapy (HAART) they receive. This review outlines the mechanisms by which HIV and HIV medications can cause vascular complications and identifies strategic areas of research to treat these dysfunctions. REVIEW: HIV and HAART affect the vascular system through several mechanisms that target systemic or metabolic systems and specific cells. HIV causes dyslipidemia and chronic immune activation, which can contribute to atherosclerosis. In addition, HIV damages macrophages, endothelial cells, smooth muscle cells, and platelets, and this damage also plays a role in the development of atherosclerosis. HAART, particularly protease inhibitors, interferes with cholesterol metabolism and can affect macrophages, endothelial cells, and smooth muscle cells. The metabolic changes and cell damage induced by HIV and HAART put HIV patients at increased risk for atherosclerosis, dyslipidemia, and serious cardiovascular events such as myocardial infarction and stroke.
CONCLUSIONS: HIV patients have increased risk of developing potentially life-threatening cardiovascular pathology, which cannot be explained by traditional cardiovascular risk factors alone. More research is needed into therapies to target this HIV-specific vasculopathy.