The ZMBH mourns the passing of Heinz Schaller on April 10, 2010

ZMBH, University of Heidelberg
Professor emeritus
since 1974
Professor of Microbiology, Univ. Heidelberg
Senior Scientist and Group Leader, MPI fuer Virusforschung, Tuebingen
Postdoc, University of Wisconsin Madison, USA
Dr. rer. nat. University of Heidelberg

Link to the Chica and Heinz Schaller Foundation:

Heinz Schaller
(Professor emeritus)

Control of Hepatitis B Virus Replication

Hepatitis B viruses (HBVs) represent a family of animal viruses that are characterized by carrying a very small, uniquely structured DNA genome, as well as by causing acute and chronic liver infections in their respective hosts. Their prototype, the human HBV, is the causative agent of a major public health problem with about 350 million chronic HBV carriers worldwide who are at high risk of developing liver cirrhosis and hepatocellular carcinoma. During the past 25 years, our research has contributed significantly to the development of a safe antiviral vaccine and, thereafter, to the elucidation of the mechanisms that govern the intracellular steps of the virus life cycle, in particular the unconventional mode of genome replication through reverse transcription of an RNA intermediate.
More recently, we have increasingly focused on the mechanisms that control virus entry and intracellular trafficking, mainly using the duck hepatitis B virus (DHBV) animal model where cultured primary hepatocytes are readily available for infection experiments. These studies have led to the functional characterization of a virus receptor which is apparently absent from the cell surface. They also revealed drastic variations in genome replication and gene expression as result of an intimate cross talk of virus and the host cell in response to the host defense system and other extracellular agents. In this context, our results demonstrated a wide heterogeneity of hepatocytes with respect to their competence to permit virus entry and establishment of hepadnavirus infection, not only in cultured cells but also in the liver. Realistically, we thus remain far from establishing a reproducibly efficient cell culture system that would allow to study, and to interfere with, all steps of the HBV replication cycle in vitro – which is in turn essential for targeted development of antiviral drugs.

Selected Publications

Breiner, K.M., Urban, S., and Schaller, H. (1998) Carboxypeptidase D (gp180), a Golgi-resident Protein, Functions in the Attachment and Entry of Avian Hepatitis B Viruses. J. Virol. 72, 8098-8104 (see Abstract),

Rothmann, K., et al (1998) Host cell - virus cross talk: phosphorylation of a hepatitis B virus envelope protein mediates intracellular signaling J. Virol. 72, 10138-10147 (see Abstract).

Protzer, U., et al. (1999) Interferon gene transfer by a novel hepatitis B virus vector efficiently suppresses wild-type virus infection. Proc. Natl. Acad. Sci. USA, 96, 10818-10823 (see Abstract).

Urban, S., et al. (2000) Receptor recognition by a hepatitis B virus reveals a novel mode of high affinity virus-receptor interaction. EMBO J. 19, 1217 – 1227 (see Abstract).

Breiner, K.M., Schaller, H., and Knolle, P. (2001) Endothelial Cell-Mediated uptake of a Hepatitis B Virus: A new concept of Liver-Targeting. Hepatology 34, 803-808 (see Abstract).

Mabit, H., et al. (2003) Nuclear Localization of the Duck Hepatitis B Vitrus Capsid Protein: Detection and Functional Implications of Distinct Subnuclear Bodies in a Compartment Coupled to RNA Synthesis and Maturation. J Virol. 77, 2157-2164 (see Abstract).


Nassal, M. and Schaller, H. (1996) Hepatitis B virus replication - an update. J. of Viral Hepatitis 3, 217 – 226 (see Abstract).