<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-30T02:01:35Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/17446" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/17446</identifier><datestamp>2024-09-27T20:48:47Z</datestamp><setSpec>com_20.500.12105_2052</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19609</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Berenguer, Juan</subfield>
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      <subfield code="a">Fernandez-Rodriguez, Amanda</subfield>
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      <subfield code="a">Jimenez-Sousa, Maria Angeles</subfield>
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      <subfield code="a">Cosín, Jaime</subfield>
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      <subfield code="a">Zarate, Paola</subfield>
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      <subfield code="a">Micheloud, Dariela</subfield>
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      <subfield code="a">López, Juan Carlos</subfield>
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      <subfield code="a">Miralles, Pilar</subfield>
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      <subfield code="a">Catalán, Pilar</subfield>
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      <subfield code="a">Resino, Salvador</subfield>
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      <subfield code="c">2012-01</subfield>
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      <subfield code="a">Background: CXCL10 may contribute to the host immune response against the hepatitis C virus (HCV), liver disease progression, and response to HCV antiviral therapy. The aim of our study was to analyze the relationship among virological, immunological, and clinical characteristics with plasma CXCL10 levels in human immunodeficiency virus (HIV)/HCV-coinfected patients. Methods: We carried out a cross-sectional study on 144 patients. CXCL10 and insulin were measured using an immunoassay kit. The degree of insulin resistance was estimated for each patient using the homeostatic model assessment (HOMA) method. Insulin resistance was defined as a HOMA index higher than or equal to 3.8. Aspartate aminotransferase (AST) to platelet ratio (APRI), FIB-4, Forns index, HGM1, and HGM2 were calculated. Results: The variables associated with log(10) CXCL10 levels by univariate analysis were age (b=0.013; p=0.023), prior AIDS-defining condition (b=0.127; p=0.045), detectable plasma HIV viral load (b=0.092; p=0.006), log(10) HOMA (b=0.216; p=0.002), HCV-genotype 1 (b=0.114; p=0.071), and liver fibrosis assessed by all non-invasive indexes (log(10) APRI (b=0.296; p=0.001), log(10) FIB-4 (b=0.436; p&lt;0.001), log(10) Forns index (b=0.591; p&lt;0.001), log(10) HGM1 (b=0.351; p=0.021), and log(10) HGM2 (b=0.215; p=0.018)). However, in multivariate analysis, CXCL10 levels were only associated with HOMA, detectable plasma HIV viral load, HCV-genotype 1 and FIB-4 (R-square=0.235; p&lt;0.001). Conclusion: Plasma CXCL10 levels were influenced by several characteristics of patients related to HIV and HCV infections, insulin resistance, and liver fibrosis, indicating that CXCL10 may play an important role in the pathogenesis of both HCV and HIV infections.</subfield>
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      <subfield code="a">Cytokine. 2012 Jan;57(1):25-9.</subfield>
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      <subfield code="a">10.1016/j.cyto.2011.10.020</subfield>
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      <subfield code="a">1096-0023</subfield>
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      <subfield code="a">Cytokine</subfield>
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      <subfield code="a">22136974</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/17446</subfield>
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      <subfield code="a">Chemokine</subfield>
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      <subfield code="a">HOMA</subfield>
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      <subfield code="a">AIDS</subfield>
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      <subfield code="a">Chronic hepatitis C</subfield>
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      <subfield code="a">Inflammation</subfield>
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      <subfield code="a">High plasma CXCL10 levels are associated with HCV-genotype 1, and higher insulin resistance, fibrosis, and HIV viral load in HIV/HCV coinfected patients</subfield>
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