Division of Virus-associated Carcinogenesis

Prof. Dr. Ralf Bartenschlager

Chronic infections with Hepatitis B virus (HBV) and Hepatitis C virus (HCV) lead to chronic inflammation of the liver, which is driven by innate and adaptive immune responses. In addition, these viruses alter the metabolism of infected cells and vice versa, the metabolic status of the cell/host profoundly impacts the outcome of infection and ultimately, cancer development.
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Our division –established in March 2014– aims at deciphering the basic principles underlying tumor formation in the context of chronic viral infection. Our research centers on liver cancer, which is one of the most frequent causes of cancer-related deaths. Around 75% of all liver cancer cases are linked to infection with hepatitis B virus (HBV) or hepatitis C virus (HCV). Thus, liver cancer is a paradigm for infection-associated tumors. The medical relevance is very high as reflected by the high numbers of persistently infected individuals: 230 million in case of HBV and 130 million in case of HCV. These people have a high risk to develop serious liver damage, most notably liver cirrhosis and hepatocellular carcinoma. Important comorbidity factors are metabolic syndrome, alcohol consumption and chronic inflammation as induced and sustained by persistent virus infection. Since therapy of liver tumors still is very inefficient, there is an urgent need for preventive and therapeutic regimens as well as more sensitive diagnostics.

Together with our sister department “Molecular Virology” at University Hospital Heidelberg we already laid the ground to study the basic principles of the replication cycles of HBV, HCV and related viruses such as Dengue virus. Building on this expertise, within the division “Virus-Associated Carcinogenesis” at the German Cancer Research Center we focus on the molecular and cellular mechanisms leading to persistent infection and how chronic viral hepatitis contributes to liver cancer. Three main topics are studied:

  • The mechanisms how persistent hepatitis virus infections are established and how chronic infection contributes to the development of liver cancer
  • The basic principles how virus infections are sensed and how viruses overcome these antiviral strategies
  • The role of iron-regulatory networks in infection and inflammation-induced liver tumor Formation
More detailed information can be found on the pages of the individual research groups of our division:

Research Group Ralf Bartenschlager
Research Group Marco Binder
Research Group Bruno Galy

Prof. Dr. Bartenschlager receives Lasker~DeBakey Award 2016

Contact

Prof. Dr. Ralf Bartenschlager
Virus-associated Carcinogenesis (F170)
Deutsches Krebsforschungszentrum
Im Neuenheimer Feld 280
69120 Heidelberg
Tel: +49 6221 424970

Selected Publications

  • Lempp FA. et al. (2015). Evidence that hepatitis B virus replication in mouse cells is limited by the lack of a host cell dependency factor. J Hepatol. 2016 Mar;64(3):556-64. doi: 10.1016/j.jhep.2015.10.030.
  • Bender S. et al. (2015). Activation of Type I and III Interferon Response by Mitochondrial and Peroxisomal MAVS and Inhibition by Hepatitis C Virus. PLoS Pathog. 2015 Nov 20;11(11):e1005264. doi: 10.1371/journal.ppat.1005264.
  • Willemsen, J., Wicht, O., Wolanski, J.C., Baur, N., Bastian, S., Haas, D.A., Matula, P., Knapp, B., Meyniel-Schicklin, L., Wang, C., Bartenschlager, R., Lohmann, V., Rohr, K., Erfle, H., Kaderali, L., Marcotrigiano, J., Pichlmair, A. and Binder, M. (2017) Phosphorylation-Dependent Feedback Inhibition of RIG-I by DAPK1 Identified by Kinome-wide siRNA Screening. Molecular Cell 65 (3):403–415
  • Nairz M., D. Ferring-Appel D, D. Casarrubea, T. Sonnweber, L. Viatte, A. Schroll, D. Haschka, F.C. Fang, M.W. Hentze, G. Weiss, and B. Galy. (2015) Iron Regulatory Proteins mediate host resistance to Salmonella infection. Cell Host Microbe, 18,1-8.
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