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Division of Virus-associated Carcinogenesis

Prof. Dr. Dr. h. c. Ralf Bartenschlager

Chronic infections with Hepatitis B virus (HBV), Hepatitis D virus (HDV) 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 host cell homeostasis, most notably 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.
© dkfz.de

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), Hepatitis D virus (HDV) 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: 240 million in case of HBV, an estimated 10-20% being co-infected with HDV, and around 70 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, HDV, HCV and related viruses. In addition, given the similarities in important cell biology aspects, we have integrated studies focusing on the replication cycle of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) with the ultimate goal to develop broadly active antiviral drugs to increase future pandemic preparedness. Building on this expertise, within the division “Virus-Associated Carcinogenesis” at the German Cancer Research Center our research is centered on the following main topics:

  • The mechanisms how persistent hepatitis virus infections are established, how chronic infection contributes to the development of liver cancer and to devise novel concepts to break viral persistence, thus reducing the cancer risk
  • The basic principles how virus infections are sensed, how viruses overcome these antiviral strategies and the role of cell-intrinsic antiviral signaling in tumor development and therapy
  • The role of iron-regulatory networks in infection and inflammation-induced liver tumor Formation
  • The establishment of a portfolio of oncolytic parvoviruses and the analysis of virus-host cell interactions associated with virus-induced cell disturbances
In the course of the COVID-19 pandemic, we established a research network called CoViPa that aims to decipher the virological and immunological determinants of COVID-19 pathogenesis and to use gained knowledge to get better prepared for future pandemics. For further details see https://www.dkfz.de/en/covipa/covipa.html

Detailed information about the research conducted in the individual research groups of our division are available on their websites:

Research Group Ralf Bartenschlager
Research Group Marco Binder
Research Group Bruno Galy
Research Group Jürg Nüesch
Research Group Stefan Seitz

CoViPa research consortium

Contact

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

Selected Publications

  • Cadena C. et al. (2019). Ubiquitin-Dependent and -Independent Roles of E3 Ligase RIPLET in Innate Immunity. Cell pii: S0092-8674(19)30279-X. doi: 10.1016/j.cell.2019.03.017.
  • Mutz P. et al. (2018) HBV Bypasses the Innate Immune Response and Does Not Protect HCV From Antiviral Activity of Interferon. Gastroenterology 154 (6), 1791-1804.e22. doi: 10.1053/j.gastro.2018.01.044.
  • Lauber C. et al. (2017). Deciphering the Origin and Evolution of Hepatitis B Viruses by Means of a Family of Non-enveloped Fish Viruses. Cell Host Microbe, 22(3):387-399.e6. doi: 10.1016/j.chom.2017.07.019.
  • Nairz M. et al. (2015) Iron Regulatory Proteins mediate host resistance to Salmonella infection. Cell Host Microbe, 18,1-8. doi: 10.1016/j.chom.2015.06.017.
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