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http://purl.uniprot.org/citations/29122683http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29122683http://www.w3.org/2000/01/rdf-schema#comment"The aim of this study was to investigate the modulation of plasma CXCL10, CCL20, CCL22, CCL2, CCL17 and CCL24 levels in HIV-positive patients grouped according to extreme phenotypes of progression to AIDS, and at different stages of HIV infection. HIV-positive individuals with extreme phenotypes of AIDS progression (n=58) at different clinical stages (chronic individuals, both pre-HAART and under-HAART) and HIV-negative controls (n=20) were evaluated. Additionally, HIV-positive individuals that initiated HAART with >350CD4+T-cells/mm3 were compared with those who initiated treatment with <350CD4+T-cells/mm3. Plasma levels of six chemokines were quantified by a Luminex assay. Higher CXCL10 levels were observed in individuals immediately before their CD4+T-cell levels were indicative for HAART (pre-HAART), independently of their progressor status, i.e. slow (SPs) or rapid progressors (RPs). SPs pre-HAART showed higher CXCL10 levels compared to elite controllers and RPs under HAART (pc=0.009 and pc=0.007, respectively). CXCL10 levels were higher in SPs HAART CD4<350 (initiated HAART with <350 CD4+T-cells) when compared with SPs HAART CD4>350 (initiated HAART with >350 CD4+T-cells) (1096 vs. 360.33pg/mL, p=0.0101). Normalisation of CXCL10 levels seems to depend on the CD4+T-cell nadir at HAART initiation. CCL20 levels were higher in chronic SPs, SPs pre-HAART, SPs HAART and RPs HAART compared with the HIV-negative controls, indicating persistent CCL20 expression. In conclusion, our results indicate that CXCL10 levels are a hallmark in the clinical evolution of HIV infection. However, our results must be verified in a study evaluating a larger number of AIDS progressors."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.org/dc/terms/identifier"doi:10.1016/j.meegid.2017.11.002"xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/author"Chies J.A.B."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/author"Santos B.R."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/author"de Medeiros R.M."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/author"Almeida S.E.M."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/author"Ellwanger J.H."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/author"Valverde-Villegas J.M."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/author"Melo M.G."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/name"Infect Genet Evol"xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/pages"51-58"xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/title"High CXCL10/IP-10 levels are a hallmark in the clinical evolution of the HIV infection."xsd:string
http://purl.uniprot.org/citations/29122683http://purl.uniprot.org/core/volume"57"xsd:string
http://purl.uniprot.org/citations/29122683http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29122683
http://purl.uniprot.org/citations/29122683http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29122683
http://purl.uniprot.org/uniprot/#_P02778-mappedCitation-29122683http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29122683
http://purl.uniprot.org/uniprot/P02778http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/29122683