16th International AIDS Conference Toronto, Canada - August 13 - 18, 2006

NUMBER AND MIGRATORY ACTIVITY OF CIRCULATING ENDOTHELIAL PROGENITOR CELLS IN HIV-INFECTED PATIENTS RECEIVING HIGHLY ACTIVE ANTIRETROVIRAL THERAPY

Int Conf AIDS. 2006 Aug 13-18;16 Abstract No. ThAb0102

O. Korzh, S. Krasnokutskiy, G. Kotchuev
Kharkov Medical Academy of Postgraduate Education, Kharkov, Ukraine

BACKGROUND: Increased risk of cardiovascular disease in HIV-infected patients receiving highly active antiretroviral therapy (HAART) has been explained by accelerated atherosclerosis and impaired angiogenesis, in which endothelial progenitor cells (EPCs) may play key roles. We hypothesized that altered EPC biology may contribute to the pathophysiology of cardiovascular complications.

METHODS: EPCs were determined in HIV-infected patients receiving HAART (n=52) and in a normal control group (n=47) by fluorescence-activated cell-sorting (FACS) analysis. Cells that were positive by flow cytometry for CD34/KDR/AC133 within the lymphocyte population were characterized as EPCs.

RESULTS: HIV-infected patients receiving HAART showed markedly decreased numbers of EPC (43.7%) and colonies (74.5%) when compared with the controls (P<0.001). These findings were corroborated by 29.8% decrease in EPC migratory function in response to vascular endothelial growth factor (VEGF) (P=0.039) and 47.6% decrease in EPC incorporation into human umbilical vein endothelial cells (HUVEC) (P<0.001). In addition, Framingham's risk factor score of both HIV-infected patients (r=-0.472, P=0.01) and normal group (r=-0.376, P=0.012) significantly correlated with the numbers of EPC. Indeed, the number of circulating EPC was significantly lower in HIV-infected patients patients than in normal group under the same burden of risk factors (P<0.001).

CONCLUSIONS: EPC biology, which is critical for neovascularization and the maintenance of vascular function, is altered in HIVinfected patients receiving HAART. Our data strongly suggest that dysfunction of circulating EPC has a role in the progression of cardiovascular disease in these patients.

Download PDF of this abstract.

2006-08-13
ThAb0102

Copyright © 2006 - International AIDS Society (IAS). All information and content relating to the abstracts from the 16th International AIDS Conference, such as text, graphics, logos, button icons, images, audio clips, and software is protected by copyright. Permission is hereby granted for the non-commercial use or reproduction of the information on this web site, provided that the use of such information is accompanied by an acknowledgement that IAS is the source of the information and the name of the author of the article.

AEGiS is a 501c(3) not-for-profit organization made possible through unrestricted funding from Boehringer Ingelheim, Bridgestone/Firestone Charitable Trust, Bristol-Myers Squibb Company, Elton John AIDS Foundation, GlaxoSmithKline, the National Library of Medicine, Roche / Trimeris, and donations from users like you. Always watch for outdated information. This article first appeared in 2006. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 2006. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. Permission is hereby granted for the non-commercial use or reproduction of the information herein, provided that the use of such information is accompanied by an acknowledgement that IAS is the source of the information and the name of the author of the article.