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Functionally defective high-density lipoproteins are related to heightened T-cell activation in vertically HIV-infected adolescents. [artículo]

Por: Rojo Conejo, Pablo [Pediatría].
Colaborador(es): Servicio de Pediatría-Neonatología.
Tipo de material: materialTypeLabelArtículoEditor: Journal of acquired immune deficiency syndromes (1999), 2014Descripción: 66(3):265-9.Recursos en línea: Solicitar documento Resumen: We assessed high-density lipoprotein (HDL) anti-inflammatory properties in a cohort of vertically HIV-infected adolescents. We hypothesized that proatherogenic mechanisms related to inflammation and immune activation during HIV infection may impair HDL functionality and impact on the atherosclerotic burden. Compared with healthy controls, HDL from HIV-infected adolescents presented impaired functionality, as determined by its ability to inhibit monocyte chemotaxis in vitro, which correlated with detectable viral loads (P = 0.044), lower CD4 nadir (P = 0.043), increased levels of CD4 T-cell activation (P = 0.018), higher C-reactive protein (P = 0.009), and a tendency toward thicker carotid intima-media thickness (P = 0.071).
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Artículo Artículo PC16294 (Navegar estantería) Disponible

Formato Vancouver:
Sainz T, Ortega-Hernández A, Serrano-Villar S, Navarro ML, Rojo P, Ramos JT et al; Madrid Cohort of HIV-infected children and adolescents, integrating the Pediatric branch of the National AIDS Research Network of Spain (CoRISpE). Functionally defective high-density lipoproteins are related to heightened T-cell activation in vertically HIV-infected adolescents. J Acquir Immune Defic Syndr. 2014 Jul 1;66(3):265-9.

PMID: 24732875

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We assessed high-density lipoprotein (HDL) anti-inflammatory properties in a cohort of vertically HIV-infected adolescents. We hypothesized that proatherogenic mechanisms related to inflammation and immune activation during HIV infection may impair HDL functionality and impact on the atherosclerotic burden. Compared with healthy controls, HDL from HIV-infected adolescents presented impaired functionality, as determined by its ability to inhibit monocyte chemotaxis in vitro, which correlated with detectable viral loads (P = 0.044), lower CD4 nadir (P = 0.043), increased levels of CD4 T-cell activation (P = 0.018), higher C-reactive protein (P = 0.009), and a tendency toward thicker carotid intima-media thickness (P = 0.071).

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