Purpose of review: This article describes the potential contribution of immune activation in the pathogenesis of HIV-associated cardiovascular disease (CVD) - a leading cause of morbidity and mortality among HIV-positive persons with access to antiretroviral therapy (ART).
Recent findings: We review recent literature that suggests abnormalities in both adaptive and innate immunity contributes to CVD risk among persons with HIV infection. In particular, potentially atherogenic T-cell mechanisms include persistent high-level T-cell activation (and associated proinflammatory mechanisms), as well as the presence of copathogens (e.g., cytomegalovirus) providing an ongoing stimulus for cytotoxic T-cell responses. More recent data have then emphasized the potential impact of monocyte-/macrophage-mediated inflammation and injury within atherosclerotic lesions. The abnormality driving innate immune activation many not fully reverse with antiretroviral therapy, highlighting the need for interventions that target inflammation as a CVD prevention strategy.
Summary: Premature CVD among persons with HIV infection is due, in part, to persistent abnormalities in immune activation and systemic inflammation despite viral suppression. Prevention strategies for persons with HIV infection include those that target traditional CVD risk factors, as well as newer candidate treatments with potential immunomodulatory benefits.