Immunologic basis of cardiovascular disease in HIV-infected adults

Abstract

Cardiovascular complications are more common in human immunodeficiency virus-infected individuals than in age-matched uninfected individuals. Antiretroviral therapy reduces the risk of cardiovascular complications, suggesting that viral replication directly or indirectly causes vascular disease. Long-term effective antiretroviral therapy does not fully restore vascular health, and treated adults continue to have higher-than-expected rates of disease progression. Although this excess risk during therapy is likely due to multiple factors, a growing body of evidence suggests that chronic inflammation, which persists during effective antiretroviral therapy, is directly and causally associated with vascular dysfunction and the accelerated development of atherosclerosis.

Figure 1.

Human immunodeficiency virus (HIV) disease is associated with persistent inflammation. As shown in the figure, this effect is mediated via multiple pathways, including direct effect of viral replication, expanded burden of other copathogens as a consequence of immunodeficiency, loss of mucosal integrity, and chronic translocation of gut microbial products. These data, plus an emerging consensus regarding the central role of inflammation as a cause of cardiovascular disease in the general population, suggest that HIV-associated inflammation may be an important cause of the excess cardiovascular disease that has been consistently observed in HIV-infected adults. Abbreviation: HIV-1, HIV type 1.