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dc.contributor.authorLiu, PJ
dc.contributor.authorHarris, JM
dc.contributor.authorMarchi, E
dc.contributor.authorD'Arienzo, V
dc.contributor.authorMichler, T
dc.contributor.authorWing, PAC
dc.contributor.authorMagri, A
dc.contributor.authorOrtega-Prieto, Ana Maria
dc.contributor.authorvan de Klundert, M
dc.contributor.authorWettengel, J
dc.contributor.authorDurantel, D
dc.contributor.authorDorner, M
dc.contributor.authorKlenerman, P
dc.contributor.authorProtzer, U
dc.contributor.authorGiotis, ES
dc.contributor.authorMcKeating, JA
dc.date.accessioned2024-12-11T11:23:55Z
dc.date.available2024-12-11T11:23:55Z
dc.date.issued2020
dc.identifier.citationLiu, P.J., Harris, J.M., Marchi, E. et al. Hypoxic gene expression in chronic hepatitis B virus infected patients is not observed in state-of-the-art in vitro and mouse infection models. Sci Rep 10, 14101 (2020). https://doi.org/10.1038/s41598-020-70865-7es_ES
dc.identifier.urihttps://hdl.handle.net/10630/35591
dc.description.abstractHepatitis B virus (HBV) is the leading cause of hepatocellular carcinoma (HCC) worldwide. The prolyl hydroxylase domain (PHD)-hypoxia inducible factor (HIF) pathway is a key mammalian oxygen sensing pathway and is frequently perturbed by pathological states including infection and inflammation. We discovered a significant upregulation of hypoxia regulated gene transcripts in patients with chronic hepatitis B (CHB) in the absence of liver cirrhosis. We used state-of-the-art in vitro and in vivo HBV infection models to evaluate a role for HBV infection and the viral regulatory protein HBx to drive HIF-signalling. HBx had no significant impact on HIF expression or associated transcriptional activity under normoxic or hypoxic conditions. Furthermore, we found no evidence of hypoxia gene expression in HBV de novo infection, HBV infected human liver chimeric mice or transgenic mice with integrated HBV genome. Collectively, our data show clear evidence of hypoxia gene induction in CHB that is not recapitulated in existing models for acute HBV infection, suggesting a role for inflammatory mediators in promoting hypoxia gene expression.es_ES
dc.language.isoenges_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectViruses_ES
dc.subjectExpresión génicaes_ES
dc.subject.otherVirologyes_ES
dc.subject.otherHepatitises_ES
dc.titleHypoxic gene expression in chronic hepatitis B virus infected patients is not observed in state-of-the-art in vitro and mouse infection modelses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.centroFacultad de Cienciases_ES
dc.identifier.doi10.1038/s41598-020-70865-7
dc.rights.ccAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones_ES


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