alexa Hyper-inflammation and Endothelial Activation in HIV Infected Patients with Detectable and Undetectable Viral Load | OMICS International | Abstract
ISSN 2155-6113

Journal of AIDS & Clinical Research
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Research Article

Hyper-inflammation and Endothelial Activation in HIV Infected Patients with Detectable and Undetectable Viral Load

Enrique Bernal1*, Jose Saban2, Angeles Munoz1, Irene Marin3, Ana Garcia-Medina1, Tomas Vicente3 and Alfredo Cano1

1Seccion de Enfermedades Infecciosas, Hospital General Universitario Reina Sofia de Murcia, Spain

2Unidad de Patologia Endotelial, Hospital Ramon y Cajal, Madrid, Spain

3Sección de Cardiologia, Hospital General Universitario Reina Sofia de Murcia, Spain

*Corresponding Author:
Enrique Bernal
Sección de Enfermedades Infecciosas
Hospital General Universitario Reina Sofia de Murcia
Avda Intendente Jorge Palacios 1, CP 30003, Spain
Tel: +34968369000
Fax: +34968359002
E-mail: [email protected]

Received Date: May 13, 2012; Accepted Date: July 30, 2012; Published Date: August 02, 2012

Citation: Bernal E, Saban J, Munoz A, Marin I, Garcia-Medina A, et al. (2012) Hyper-inflammation and Endothelial Activation in HIV Infected Patients with Detectable and Undetectable Viral Load. J AIDS Clinic Res 3:164. doi:10.4172/2155-6113.1000164

Copyright: © 2012 Bernal E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Although HIV and antiretroviral therapy (ART) have been linked with an increased cardiovascular risk, the pathological pathways remain unknown. We assessed whether secretory phospholipase A2 (sPLA2), high-sensitivity C-reactive protein (hs-CRP), vascular cell adhesion molecule (VCAM), thiobarbituric acid reactive species (TBARS), Superoxide dismutases (SOD), adiponectin and resistin were elevated in HIV infected patients with detectable and undetectable viral load compared to a control group matched for age, sex and cardiovascular risk factors. We evaluated its correlation with traditional and no traditional cardiovascular risk factors and carotid intima-media thickness. Levels of sPLA2 (median [IQR]) were 8.35 (5.36, 9.6) pg/ml, hsCRP were 3.3 (IQR, 1.27, 5.28) mg/L, VCAM 945.6 (IQR, 655.9, 1404.05) ng/ml and TBARS 1.69 (IQR, 1.39, 1.97) uM/L in HIV infected group compared to levels of sPLA2 1.22 (IQR, 0.69, 2.62) pg/ml (p<0.001), hsCRP 3.05 (IQR, 2.68, 3.27) mg/L (p=0.05), VCAM 678.35 (IQR, 530.39, 831.04) ng/ml (p<0.001) and TBARS 7.47 (IQR, 5.03, 10.4) uM/L (p<0.001) in control group. Levels of VCAM (median [IQR]) were 1047.19 (IQR, 609.06, 1084.1) ng/ml (p=0.015) and sPLA2 were 7.6 (IQR, 5.25, 9.6) pg/ml (p<0.001) in HIV infected patients with undetectable viral load compared to control group. There was a good correlation between all analyzed biomarkers and cardiovascular risk factors. In conclusion, HIV infection induces chronic inflammation and endothelial activation that is not completely suppressed by the treatment.

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