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dc.contributor.authorBrochado-Kith, Oscar 
dc.contributor.authorMartinez, Isidoro 
dc.contributor.authorBerenguer, Juan
dc.contributor.authorMedrano, Luz Maria 
dc.contributor.authorGonzález-García, Juan
dc.contributor.authorJimenez-Sousa, Maria Angeles 
dc.contributor.authorCarrero, Ana
dc.contributor.authorHontañón, Víctor
dc.contributor.authorNavarro, Jordi
dc.contributor.authorGuardiola, Josep M
dc.contributor.authorFernandez-Rodriguez, Amanda 
dc.contributor.authorResino, Salvador 
dc.date.accessioned2021-04-07T08:44:54Z
dc.date.available2021-04-07T08:44:54Z
dc.date.issued2021-03-30
dc.identifier.citationJ Biomed Sci. 2021 Mar 30;28(1):23.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/12539
dc.description.abstractTo evaluate the impact of hepatitis C virus (HCV) elimination via interferon (IFN)-based therapy on gene expression profiles related to the immune system in HIV/HCV-coinfected patients. We conducted a prospective study in 28 HIV/HCV-coinfected patients receiving IFN-based therapy at baseline (HIV/HCV-b) and week 24 after sustained virological response (HIV/HCV-f). Twenty-seven HIV-monoinfected patients (HIV-mono) were included as a control. RNA-seq analysis was performed on peripheral blood mononuclear cells (PBMCs). Genes with a fold-change (FC) ≥ 1.5 (in either direction) and false discovery rate (FDR) ≤ 0.05 were identified as significantly differentially expressed (SDE). HIV/HCV-b showed six SDE genes compared to HIV-mono group, but no significantly enriched pathways were observed. For HIV/HCV-f vs. HIV/HCV-b, we found 58 SDE genes, 34 upregulated and 24 downregulated in the HIV/HCV-f group. Of these, the most overexpressed were CXCL2, PDCD6IP, ATP5B, IGSF9, RAB26, and CSRNP1, and the most downregulated were IFI44 and IFI44L. These 58 SDE genes revealed two significantly enriched pathways (FDR < 0.05), one linked to Epstein-Barr virus infection and another related to p53 signaling. For HIV/HCV-f vs. HIV-mono group, we found 44 SDE genes that revealed 31 enriched pathways (FDR < 0.05) related to inflammation, cancer/cell cycle alteration, viral and bacterial infection, and comorbidities associated with HIV/HCV-coinfection. Five genes were overrepresented in most pathways (JUN, NFKBIA, PIK3R2, CDC42, and STAT3). HIV/HCV-coinfected patients who eradicated hepatitis C with IFN-based therapy showed profound gene expression changes after achieving sustained virological response. The altered pathways were related to inflammation and liver-related complications, such as non-alcoholic fatty liver disease and hepatocellular carcinoma, underscoring the need for active surveillance for these patients.es_ES
dc.description.sponsorshipThis study was supported by grants from Instituto de Salud Carlos III (ISCII; Grant Numbers PI20/00474 and PI17/00657 to JB, PI20/00507 and PI17/00903 to JGG, PI18CIII/00020 to AFR, and PI20CIII/00004 and PI17CIII/00003 to SR). The study was also funded by the RD16CIII/0002/0002 and RD16/0025/0017, and RD16/0025/0018 projects as part of the Plan Nacional R + D + I and co-funded by ISCIII- Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER). JB is an investigator from the Programa de Intensificación de la Actividad Investigadora en el Sistema Nacional de Salud (I3SNS), Ref. INT16/00100.es_ES
dc.language.isoenges_ES
dc.publisherBioMed Central (BMC) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectGene expressiones_ES
dc.subjectHCV clearancees_ES
dc.subjectHIV/HCV coinfectiones_ES
dc.subjectImmune systemes_ES
dc.subjectInterferon therapyes_ES
dc.subjectPBMCses_ES
dc.titleHCV eradication with IFN-based therapy does not completely restore gene expression in PBMCs from HIV/HCV-coinfected patients.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33785040es_ES
dc.format.volume28es_ES
dc.format.number1es_ES
dc.format.page23es_ES
dc.identifier.doi10.1186/s12929-021-00718-6es_ES
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.contributor.funderMinisterio de Ciencia e Innovación (España) 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1423-0127es_ES
dc.relation.publisherversionhttps://doi.org/10.1186/s12929-021-00718-6es_ES
dc.identifier.journalJournal of biomedical sciencees_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI20/00474es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI17/00657es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI20/00507es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI17/00903es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI18CIII/00020es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI20CIII/00004es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI17CIII/00003es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD16CIII/0002/0002es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD16/0025/0017es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/RD16/0025/0018es_ES
dc.rights.accessRightsopen accesses_ES


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Atribución 4.0 Internacional
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