FOR 1202
Welcome to the homepage of the research unit 1202 (FOR 1202) „Mechanisms of persistence of hepatotropic viruses”.
The research unit is formed by scientists and clinicians from the University Clinical Center Heidelberg and the University Hospital Freiburg and it aims at a detailed understanding of the mechanisms underlying the establishment of persistence upon infections with the hepatitis B virus (HBV) and the hepatitis C virus (HCV). The FOR 1202 started in October 2009 and is supported by a grant from the German Research Foundation (DFG).
Six project teams have been united within this research unit with three projects carried out by groups of the Department of Infectious Diseases, Molecular Virology at the University Clinical Center Heidelberg and three groups located in Freiburg at the Department of Medicine II at the University Hospital Freiburg. The central aim of the research unit is to decipher the molecular and immunological mechanisms leading to persistence of HBV and HCV infections as well as HBV-HCV coinfections. In order to meet this challenge, members of this research group have combined their expertise in the field of molecular and cell biology, immunology, biochemistry and virology. Results obtained from these fundamental studies should help to develop prophylactic vaccines and to improve therapy of patients that are chronically infected with these viruses.
Speaker
Prof. Dr. Ralf Bartenschlager
Department of Infectious Diseases, Molecular Virology University Clinical Center Heidelberg
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Co-Speaker
Prof. Dr. Robert Thimme Department of Medicine II University Hospital Freiburg
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Project Coordinator and contact information
Dr. Sandra Bühler
Department of Infectious Diseases, Molecular Virology
University Clinical Center Heidelberg
Im Neuenheimer Feld 345
69120 Heidelberg
Tel.: +49-6221-56-4225
Fax.: +49-6221-56-4570
E-Mail: sandra_buehler@med.uni-heidelberg.de
© Dep. of Infectious Diseases, Molecular Virology. University of Heidelberg
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NEWS
09.01.2012
Schulze A, Mills K, Weiss TS, Urban S. Hepatocyte polarization is essential for the productive entry of the hepatitis B virus.
Hepatology. 2011 Sep 27. doi: 10.1002/hep.24707. [Epub ahead of print]
Publications
Thimme R, Binder M, Bartenschlager R. Failure of innate and adaptive immune responses in controlling hepatitis C virus infection.
FEMS Microbiol Rev. 2011 Dec 5. doi: 10.1111/j.1574-6976.2011.00319.x. [Epub ahead of print]
Publications
Neumann-Haefelin C, Oniangue-Ndza C, Kuntzen T, Schmidt J, Nitschke K, Sidney J, Caillet-Saguy C, Binder M, Kersting N, Kemper MW, Power KA,
Ingber S, Reyor LL, Hills-Evans K, Kim AY, Lauer GM, Lohmann V, Sette A, Henn MR, Bressanelli S, Thimme R, Allen TM.
Human leukocyte antigen B27 selects for rare escape mutations that significantly impair hepatitis C virus replication and require compensatory mutations.
Hepatology. 2011 Oct;54(4):1157-66. doi: 10.1002/hep.24541.
Publications
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