title: [Physiopathology of cardiovascular disease in HIV-infected patients].
abstract: Patients with HIV have an increased risk of cardiovascular events related to arteriosclerosis. The virus is able to replicate in the arterial wall, implying severe inflammatory dysfunction. When this inflammatory dysfunction is accompanied by the metabolic disorders associated with HIV infection and its treatment, progression of the atheroma plaque is accelerated. HIV shows high replication in CD4+ T lymphocytes, which accumulate in the subendothelial space. CD4+ T lymphocytes produce viral proteins such as Tat, which leads to synthesis of chemokines such as monocyte chemoattractant protein-1 (MCP-1) or vascular cell adhesion molecule-1. This combination will attract monocytes into the subendothelial space, which penetrate rapidly if infected. These monocytes will also infect the smooth muscle cells, producing the initiation of endothelial dysfunction. Dyslipidemia and insulin resistance will then provoke modification of lipoproteins, which will be phagocytized through CD36 receptors by macrophages of the subendothelial space. Reverse cholesterol transport will be damaged, since the Nef viral protein is able to block the ABCA1 receptor. These events will produce rapid cholesterol accumulation in the atheroma plaque nucleus. Subsequently, the plaque will become complicated, either by rupture or erosion. Then, a juxtalesional thrombus is formed, where the platelet is activated.
authors.affiliation: Unidad VIH, Servicio de Medicina Interna, Centre de Recerca Biomèdica, Hospital Universitario San Juan de Reus, Reus, Tarragona, España. cavillaverde@grupsagessa.com
authors.forename: Carlos
authors.initials: C
authors.lastname: Alonso-Villaverde Lozano
mesh_terms: D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology; D015496:CD4-Positive T-Lymphocytes / Q000473:pathology / Q000821:virology; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology* / Q000821:virology; D018925:Chemokines / Q000378:metabolism; D002634:Chemotaxis, Leukocyte; D002784:Cholesterol / Q000378:metabolism; D018450:Disease Progression; D050171:Dyslipidemias / Q000150:complications; D004730:Endothelium, Vascular / Q000503:physiopathology / Q000821:virology*; D006678:HIV / Q000502:physiology; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism; D054298:Human Immunodeficiency Virus Proteins / Q000502:physiology; D006801:Humans; D007249:Inflammation; D007333:Insulin Resistance; D008264:Macrophages / Q000502:physiology; D008954:Models, Biological; D010587:Phagocytosis; D012306:Risk; D013927:Thrombosis / Q000209:etiology; D014779:Virus Replication
chemical_list: D018925:Chemokines; D054298:Human Immunodeficiency Virus Proteins; D002784:Cholesterol