HIV-1, reactive oxygen species, and vascular complications

Over 1 million people in the United States and 33 million individuals worldwide suffer from HIV/AIDS. Since its discovery, HIV/AIDS has been associated with an increased susceptibility to opportunistic infection due to immune dysfunction. Highly active antiretroviral therapies restore immune function and, as a result, people infected with HIV-1 are living longer. This improved survival of HIV-1 patients has revealed a previously unrecognized risk of developing vascular complications, such as atherosclerosis and pulmonary hypertension. The mechanisms underlying these HIV-associated vascular disorders are poorly understood. However, HIV-induced elevations in reactive oxygen species (ROS), including superoxide and hydrogen peroxide, may contribute to vascular disease development and progression by altering cell function and redox-sensitive signaling pathways. In this review, we summarize the clinical and experimental evidence demonstrating HIV- and HIV antiretroviral therapy-induced alterations in reactive oxygen species and how these effects are likely to contribute to vascular dysfunction and disease.

Graphical AbstractFigure optionsDownload high-quality image (70 K)Download as PowerPoint slideHighlights
► Vascular diseases are one of the most recognized non-AIDS events in HIV-1 patients.
► HIV-1 proteins and antiretrovirals have an impact on antioxidants and superoxide production.
► Increased reactive oxygen species (ROS) probably promote vascular disease.
► ROS also potentiate HIV-1 effects by altering viral replication and immune function.
► Targeting ROS sources or restoring antioxidants may reduce HIV vascular disease.