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dc.contributor.author | Brochado-Kith, Oscar | |
dc.contributor.author | Martinez, Isidoro | |
dc.contributor.author | Berenguer, Juan | |
dc.contributor.author | Medrano, Luz Maria | |
dc.contributor.author | González-García, Juan | |
dc.contributor.author | Jimenez-Sousa, Maria Angeles | |
dc.contributor.author | Carrero, Ana | |
dc.contributor.author | Hontañón, Víctor | |
dc.contributor.author | Navarro, Jordi | |
dc.contributor.author | Guardiola, Josep M | |
dc.contributor.author | Fernandez-Rodriguez, Amanda | |
dc.contributor.author | Resino, Salvador | |
dc.date.accessioned | 2021-04-07T08:44:54Z | |
dc.date.available | 2021-04-07T08:44:54Z | |
dc.date.issued | 2021-03-30 | |
dc.identifier.citation | J Biomed Sci. 2021 Mar 30;28(1):23. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/12539 | |
dc.description.abstract | To 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.sponsorship | This 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.iso | eng | es_ES |
dc.publisher | BioMed Central (BMC) | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | Gene expression | es_ES |
dc.subject | HCV clearance | es_ES |
dc.subject | HIV/HCV coinfection | es_ES |
dc.subject | Immune system | es_ES |
dc.subject | Interferon therapy | es_ES |
dc.subject | PBMCs | es_ES |
dc.title | HCV eradication with IFN-based therapy does not completely restore gene expression in PBMCs from HIV/HCV-coinfected patients. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 33785040 | es_ES |
dc.format.volume | 28 | es_ES |
dc.format.number | 1 | es_ES |
dc.format.page | 23 | es_ES |
dc.identifier.doi | 10.1186/s12929-021-00718-6 | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1423-0127 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1186/s12929-021-00718-6 | es_ES |
dc.identifier.journal | Journal of biomedical science | es_ES |
dc.repisalud.centro | ISCIII::Centro Nacional de Microbiología | es_ES |
dc.repisalud.institucion | ISCIII | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI20/00474 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI17/00657 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI20/00507 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI17/00903 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI18CIII/00020 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI20CIII/00004 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/PI17CIII/00003 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/RD16CIII/0002/0002 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/RD16/0025/0017 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/RD16/0025/0018 | es_ES |
dc.rights.accessRights | open access | es_ES |