Antiretroviral therapy (ART) prolongs life, but individuals infected with human immunodeficiency virus (HIV) have a shorter life span than their uninfected counterparts and a greater than expected risk of cardiovascular disease (CVD).1,2 Part of the increased CVD risk associated with HIV infection can be attributed to an increased burden of traditional risk factors such as cigarette smoking, as well as the effects of ART on lipids, insulin resistance, and body composition. However, increasing evidence suggests that chronic inflammation and immune activation may play key roles in HIV-associated CVD.
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