Imperial College London
Alternate

DrStathisGiotis

Faculty of Medicine, Department of Infectious Disease

Honorary Senior Research Fellow
 
 
 
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Contact

 

+44 (0)20 7594 9057e.giotis

 
 
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Location

 

Medical SchoolSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@unpublished{Liu:2020:10.1101/2020.03.27.011841,
author = {Liu, PJ and Harris, JM and Marchi, E and DArienzo, V and Michler, T and Wing, PAC and Magri, A and Ortega-Prieto, AM and van, de Klundert M and Wettengel, J and Durantel, D and Dorner, M and Klenerman, P and Protzer, U and Giotis, S and McKeating, JA},
doi = {10.1101/2020.03.27.011841},
title = {Hypoxic gene expression in chronic hepatitis B infected patients is not observed in state-of-art <i>in vitro</i> and mouse infection models},
url = {http://dx.doi.org/10.1101/2020.03.27.011841},
year = {2020}
}
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RIS format (EndNote, RefMan)

TY  - UNPB
AB  - <jats:title>ABSTRACT</jats:title><jats:p>Hepatitis 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 <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic> 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 <jats:italic>de novo</jats:italic> 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.</jats:p>
AU  - Liu,PJ
AU  - Harris,JM
AU  - Marchi,E
AU  - DArienzo,V
AU  - Michler,T
AU  - Wing,PAC
AU  - Magri,A
AU  - Ortega-Prieto,AM
AU  - van,de Klundert M
AU  - Wettengel,J
AU  - Durantel,D
AU  - Dorner,M
AU  - Klenerman,P
AU  - Protzer,U
AU  - Giotis,S
AU  - McKeating,JA
DO  - 10.1101/2020.03.27.011841
PY  - 2020///
TI  - Hypoxic gene expression in chronic hepatitis B infected patients is not observed in state-of-art <i>in vitro</i> and mouse infection models
UR  - http://dx.doi.org/10.1101/2020.03.27.011841
ER  -
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