<?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>2026-04-29T05:37:37Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/27173" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/27173</identifier><datestamp>2026-01-23T01:16:37Z</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">Fernandez-Rodriguez, Amanda</subfield>
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      <subfield code="a">Berenguer, Juan</subfield>
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      <subfield code="a">Rallón, Norma</subfield>
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      <subfield code="a">Jimenez-Sousa, Maria Angeles</subfield>
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      <subfield code="a">López, Juan Carlos</subfield>
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      <subfield code="a">Soriano, Vicente</subfield>
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      <subfield code="a">Garcia-Alvarez, Monica</subfield>
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      <subfield code="a">Cosín, Jaime</subfield>
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      <subfield code="a">Martínez, Paula</subfield>
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      <subfield code="a">Guzman-Fulgencio, Maria</subfield>
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      <subfield code="a">Miralles, Pilar</subfield>
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   <datafield ind2=" " ind1=" " tag="720">
      <subfield code="a">Miguel Benito, José</subfield>
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      <subfield code="a">Resino, Salvador</subfield>
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      <subfield code="c">2014-10-01</subfield>
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      <subfield code="a">Objectives: To analyze whether peroxisome proliferator-activated receptor gamma (PPARγ2) rs1801282 (Pro12Ala) polymorphism is associated with the response to pegylated-interferon-alpha plus ribavirin treatment in HIV/hepatitis C virus (HCV)-coinfected patients, and whether it is able to predict the outcome of HCV treatment. Design: Retrospective follow-up study. Methods: Two hundred eighty-five naive patients, who started HCV-treatment, were genotyped for PPARγ2 and interleukin 28B polymorphisms. Genetic data were analyzed under dominant inheritance model. Sustained virological response (SVR) was defined as undetectable HCV viremia through 24 weeks after the end of HCV treatment. Results: The variables significantly associated with SVR in a multivariate analysis were HCV-genotype (GT) 3 {adjusted odds ratio [aOR] = 7.66 [95% of confidence interval (95% CI): 3.96 to 14.81] P &lt; 0.001}, HCV-viremia &lt;500,000 IU/mL [aOR = 2.20 (95% CI: 1.16 to 4.15] P = 0.015), no/mild liver fibrosis (F &lt; 2) [aOR = 1.92 (95% CI: 1.08 to 3.42) P = 0.026], IL28B rs12980275 AA genotype [aOR = 2.70 (95% CI: 1.54 to 4.71) P &lt; 0.001], and PPARγ2 rs1801282 CG/GG genotype [aOR = 2.93 (95% CI: 1.27 to 6.72) P = 0.011]. When PPARγ2 rs1801282 genotype was included in a decision tree analysis, HCV-GT3 patients with CG/GG genotype had increased SVR from 80.3% to 100%. In GT1/4 patients, rs12980275 AA carriers had increased SVR from 58.7% to 78.6%, and rs12980275 AG/GG carriers had increased SVR from 28.7% to 35.7%. The overall percentage of patients correctly classified was 71.6% and the area under the receiver operating characteristic curves was 0.766 ± 0.028. Conclusions: The presence of PPARγ2 rs1801282 G allele (Ala variant) was associated with increased odds for achieving SVR in HIV/HCV-coinfected patients on HCV treatment.</subfield>
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      <subfield code="a">Fernández-Rodríguez, Amanda; Berenguer, Juan MD; Rallón, Norma; Jiménez-Sousa, María A.; López, Juan Carlos; Soriano, Vicente; García-Álvarez, Mónica; Cosín, Jaime MD; Martínez, Paula; Guzmán-Fulgencio, María; Miralles, Pilar; Miguel Benito, José; Resino, Salvador. PPARγ2 Pro12Ala Polymorphism Is Associated With Sustained Virological Response in HIV/HCV-Coinfected Patients Under HCV Therapy. JAIDS Journal of Acquired Immune Deficiency Syndromes 67(2):p 113-119, October 1, 2014. DOI: 10.1097/QAI.0000000000000282.</subfield>
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      <subfield code="a">https://hdl.handle.net/20.500.12105/27173</subfield>
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      <subfield code="a">25072612</subfield>
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      <subfield code="a">10.1097/QAI.0000000000000282</subfield>
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      <subfield code="a">Journal of Acquired Immune Deficiency Syndromes</subfield>
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   <datafield tag="653" ind2=" " ind1=" ">
      <subfield code="a">Chronic hepatitis C</subfield>
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      <subfield code="a">AIDS</subfield>
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      <subfield code="a">HCV therapy</subfield>
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      <subfield code="a">PPARγ2</subfield>
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      <subfield code="a">Single nucleotide polymorphism</subfield>
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      <subfield code="a">PPARγ2 Pro12Ala polymorphism is associated with sustained virological response in HIV/HCV-coinfected patients under HCV therapy.</subfield>
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