title: HIV-1, reactive oxygen species, and vascular complications.
abstract: 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.
authors.affiliation: Pulmonary, Allergy and Critical Care Division, Emory University School of Medicine/Atlanta VA Medical Center, 1670 Clairmont Road, Mailstop 151P, Decatur, GA 30033, USA. Kristi.porter@emory.edu
authors.forename: Kristi M
authors.initials: KM
authors.lastname: Porter
authors.forename: Roy L
authors.initials: RL
authors.lastname: Sutliff
mesh_terms: D015658:HIV Infections / Q000150:complications* / Q000503:physiopathology*; D015497:HIV-1 / Q000472:pathogenicity*; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014652:Vascular Diseases / Q000209:etiology*
chemical_list: D017382:Reactive Oxygen Species