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Journal of Virology, May 2007, p. 5014-5023, Vol. 81, No. 10
0022-538X/07/$08.00+0     doi:10.1128/JVI.02290-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Entry of Duck Hepatitis B Virus into Primary Duck Liver and Kidney Cells after Discovery of a Fusogenic Region within the Large Surface Protein{triangledown}

Claudia Maenz,1 Shau-Feng Chang,2 Alicja Iwanski,1 and Michael Bruns1*

Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie an der Universität Hamburg, 20251 Hamburg, Germany,1 Biomedical Engineering Center, Industrial Technology Research Institute, 31000 Chutung Hsinchu, Taiwan, Republic of China2

Received 19 October 2006/ Accepted 5 March 2007

Hepatitis B viruses exhibit a narrow host range specificity that is believed to be mediated by a domain of the large surface protein, designated L. For duck hepatitis B virus, it has been shown that the pre-S domain of L binds to carboxypeptidase D, a cellular receptor present in many species on a wide variety of cell types. Nonetheless, only hepatocytes become infected. It has remained vague which viral features determine host range specificity and organotropicity. By using chymotrypsin to treat duck hepatitis B virus, we addressed the question of whether a putative fusogenic region within the amino-terminal end of the small surface protein may participate in viral entry and possibly constitute one of the determinants of the host range of the virus. Addition of the enzyme to virions resulted in increased infectivity. Remarkably, even remnants of enzyme-treated subviral particles proved to be inhibitory to infection. A noninfectious deletion mutant devoid of the binding region for carboxypeptidase D could be rendered infectious for primary duck hepatocytes by treatment with chymotrypsin. Although because of the protease treatment mutant and wild-type viruses may have become infectious in an unspecific and receptor-independent manner, their host range specificity was not affected, as shown by the inability of the virus to replicate in different hepatoma cell lines, as well as primary chicken hepatocytes. Instead, the organotropicity of the virus could be reduced, which was demonstrated by infection of primary duck kidney cells.

* Corresponding author. Mailing address: Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie an der Universität Hamburg, Martinistrasse 52, D-20251 Hamburg, Germany. Phone: 49-40-48051 231. Fax: 49-40-48051 117. E-mail: mbruns{at}hpi.uni-hamburg.de

{triangledown} Published ahead of print on 14 March 2007.

Journal of Virology, May 2007, p. 5014-5023, Vol. 81, No. 10
0022-538X/07/$08.00+0     doi:10.1128/JVI.02290-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Maenz, C., Loscher, C., Iwanski, A., Bruns, M. (2008). Inhibition of duck hepatitis B virus infection of liver cells by combined treatment with viral e antigen and carbohydrates. J. Gen. Virol. 89: 3016-3026 [Abstract] [Full Text]  


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