Growing evidence suggests that the risk for atherosclerosis is higher among HIV-infected individuals than among HIV-negative persons; potential explanations include deleterious effects of antiretroviral therapy (ART), virus-induced endothelial injury, and chronic inflammation. To examine the role of these factors, investigators studied carotid intima-media thickness (IMT; a measure of atherosclerosis) and C-reactive protein (CRP; a marker for systemic inflammation) levels in HIV elite controllers (infected patients who maintain undetectable viral loads without taking ART), untreated HIV-infected patients, HIV-infected patients on ART, and HIV-negative controls (total, 494 participants). The median carotid IMT was significantly higher in HIV-infected patients than in HIV-negative individuals, even after adjustment for cardiovascular risk factors. The median carotid IMT in elite controllers was significantly higher than that in HIV-negative individuals and was similar to that in untreated HIV-infected patients. The median CRP level was significantly higher in HIV-infected patients, including controllers, than in HIV-negative patients. Published in Journal Watch. Hsue PY et al. Role of viral replication, antiretroviral therapy, and immunodeficiency in HIV-associated atherosclerosis. AIDS 2009 Apr 22. Comments: these data and others seems to suggest that HIV infection by itself , not medications, cause inflammation maybe due to viral replication (with and without treatment for HIV); this inflammation can lead to atherosclerosis and heart disease. People with HIV infection should be screened for heart disease early and aggressively _BA