Birke Bartosch The Pathological Consequences Hepatitis C Virus Induced Metabolic Reprogramming

Course and current status

Current position

Chargé de Recherche at INSERM 1052, team 15 "Mechanisms of chronic hepatitis B and C and novel antiviral strategies" at the Cancer Research Center of Lyon, France


1995               Master of Philosophy at University of Cambridge, Cambridge, UK
1999               Doctor of Philosophy at University College London, London, UK
2005               Habilitation à Diriger des Recherches (HDR), UCBL, France

Training/Professional experience

1999-2001      Research Fellow, University College London, Wohl Virion Centre
                       Project: The isolation and molecular characterisation of endogenous retroviruses

2001-2004       Research Fellow, Laboratoire de Retrovirologie et Therapie Genique, INSERM
                        U412, Ecole Normale Superieure de Lyon, France

                        Project: Hepatitis C virus pseudo-particles - the first HCV infection system

2005 – 2008    Charge de Recherche 1, INSERM U758, Enveloppes Virales et Ingéniérie des
                         Rétrovirus, Ecole Normale Superieure de Lyon, IFR 128

                         Project: Hepatitis C virus cell entry and neutralization

Awards and Fellowships

1993                Stipend from the German Academic Exchange service
1995 - 1999    Scholarship from the Imperial Cancer Research Fund
2000 - 2001    MRC grant
2001 - 2004    Marie Curie Individual Fellowship
2004                Prix Scientifique et Technologique de l'Association des Etablissements du
Technopôle de Gerland
2007                Award of an Interface clinical research contract (INSERM, HCL)

Research grants

ANRS, FP7, ANR, Labex, Region Rhones Alpes


  • 44 Research papers
  • 4 patents
  • H factor: 26

Scientific summary

Hepatitis C virus (HCV) is the only virus that is known to perturb hepatic glucose and lipid metabolism with important patho-physiological consequences that predispose towards the development of liver cancer. Chronic carriers often develop steatosis, insulin resistance and type 2 diabetes. HCV seems to rely on these modifications of the liver metabolic microenvironment to replicate efficiently. Indeed, some HCV proteins have been shown to interfere directly with many factors of the lipogenic and glycolytic pathways. We study HCV-induced changes in glucose-signaling and –metabolism, ask whether these changes are a prerequisite for HCV replication / assembly and analyse their pathological consequences.
The targeted modulation of cellular factors or pathways that we have identified to be necessary and beneficial for HCV production will allow us to develop novel therapeutic targets and on the long term to develop novel in vitro and in vivo infection systems for HCV, which will be critical to understand the pathogenesis of HCV infection and its role in hepatocarcinogenesis.
In particular, the following objectives are being addressed: 1) HCV-induced changes to the cellular glucose & lipid metabolism; 2) Development of more relevant cellular system with physiological metabolism for studying HCV replication and assembly/morphogenesis; 3) Development of innovative anti-HCV drugs; 4) Validation of the new concepts by experiments performed on clinical samples.
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