title: Increased cardiovascular disease risk in the HIV-positive population on ART: potential role of HIV-Nef and Tat.
abstract: With effective antiretroviral therapy (ART), many HIV-infected people die of diseases other than acquired immune deficiency syndrome (AIDS). In particular, coronary artery disease has emerged as one of most critical complications of HIV infection and a major cause of morbidity and mortality. Although reportedly antiretroviral combination therapy itself may accelerate atherosclerosis by enhancing dyslipidemia, most recent epidemiological studies support the notion that HIV infection itself contributes to cardiovascular disease. However, it is still a mystery how the virus can contribute to cardiovascular disease development even while suppressed by ARTs. This review discusses the current understanding of interactions between HIV infection and cardiovascular diseases in both clinical and experimental studies with special focus on those viral proteins that are still produced by HIV. This will help infectious disease/vascular biology experts to gain insights into the pathophysiological mechanisms of HIV-associated cardiovascular disease and new trends to treat and prevent cardiovascular disease in the HIV-infected population.
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46204, USA; Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: wangt2@stanford.edu.
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46204, USA.
authors.forename: Ru
authors.initials: R
authors.lastname: Yi
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46204, USA.
authors.forename: Linden Ann
authors.initials: LA
authors.lastname: Green
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46204, USA.
authors.forename: Sarvesh
authors.initials: S
authors.lastname: Chelvanambi
authors.affiliation: Medical Clinic II, Department of Internal Medicine, Universities of Giessen and Marburg Lung Center, 35392 Giessen, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Seimetz
authors.affiliation: Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46204, USA. Electronic address: mclauss@iupui.edu.
authors.forename: Matthias
authors.initials: M
authors.lastname: Clauss
mesh_terms: D019380:Anti-HIV Agents / Q000009:adverse effects*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000821:virology*; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy*; D006801:Humans; D012307:Risk Factors; D054311:nef Gene Products, Human Immunodeficiency Virus / Q000378:metabolism; D054322:tat Gene Products, Human Immunodeficiency Virus / Q000378:metabolism
chemical_list: D019380:Anti-HIV Agents; D054311:nef Gene Products, Human Immunodeficiency Virus; D054322:tat Gene Products, Human Immunodeficiency Virus
keywords: ART; Cardiovascular diseases; Endothelial dysfunction; HIV Nef; HIV Tat