RGD Reference Report - Reduced sTWEAK and increased sCD163 levels in HIV-infected patients: modulation by antiretroviral treatment, HIV replication and HCV co-infection. - Rat Genome Database

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Reduced sTWEAK and increased sCD163 levels in HIV-infected patients: modulation by antiretroviral treatment, HIV replication and HCV co-infection.

Authors: Beltrán, Luis M  Muñoz Hernández, Rocío  de Pablo Bernal, Rebeca S  García Morillo, José S  Egido, Jesús  Noval, Manuel Leal  Ferrando-Martinez, Sara  Blanco-Colio, Luis M  Genebat, Miguel  Villar, José R  Moreno-Luna, Rafael  Moreno, Juan Antonio 
Citation: Beltrán LM, etal., PLoS One. 2014 Mar 4;9(3):e90541. doi: 10.1371/journal.pone.0090541. eCollection 2014.
RGD ID: 149735575
Pubmed: PMID:24594990   (View Abstract at PubMed)
PMCID: PMC3942443   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0090541   (Journal Full-text)


BACKGROUND: Patients infected with the human immunodeficiency virus (HIV) have an increased risk of cardiovascular disease due to increased inflammation and persistent immune activation. CD163 is a macrophage scavenger receptor that is involved in monocyte-macrophage activation in HIV-infected patients. CD163 interacts with TWEAK, a member of the TNF superfamily. Circulating levels of sTWEAK and sCD163 have been previously associated with cardiovascular disease, but no previous studies have fully analyzed their association with HIV.
OBJECTIVE: The aim of this study was to analyze circulating levels of sTWEAK and sCD163 as well as other known markers of inflammation (hsCRP, IL-6 and sTNFRII) and endothelial dysfunction (sVCAM-1 and ADMA) in 26 patients with HIV before and after 48 weeks of antiretroviral treatment (ART) and 23 healthy subjects.
RESULTS: Patients with HIV had reduced sTWEAK levels and increased sCD163, sVCAM-1, ADMA, hsCRP, IL-6 and sTNFRII plasma concentrations, as well as increased sCD163/sTWEAK ratio, compared with healthy subjects. Antiretroviral treatment significantly reduced the concentrations of sCD163, sVCAM-1, hsCRP and sTNFRII, although they remained elevated when compared with healthy subjects. Antiretroviral treatment had no effect on the concentrations of ADMA and sTWEAK, biomarkers associated with endothelial function. The use of protease inhibitors as part of antiretroviral therapy and the presence of HCV-HIV co-infection and/or active HIV replication attenuated the ART-mediated decrease in sCD163 plasma concentrations.
CONCLUSION: HIV-infected patients showed a proatherogenic profile characterized by increased inflammatory, immune-activation and endothelial-dysfunction biomarkers that partially improved after ART. HCV-HIV co-infection and/or active HIV replication enhanced immune activation despite ART.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
human immunodeficiency virus infectious disease treatmentIEP 149735575 RGD 
human immunodeficiency virus infectious disease treatmentISOCD163 (Homo sapiens)149735575; 149735575 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cd163  (CD163 molecule)

Genes (Mus musculus)
Cd163  (CD163 antigen)

Genes (Homo sapiens)
CD163  (CD163 molecule)


Additional Information