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Journal of Virology, November 2008, p. 10532-10542, Vol. 82, No. 21
0022-538X/08/$08.00+0     doi:10.1128/JVI.00422-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Duck Hepatitis B Virus Requires Cholesterol for Endosomal Escape during Virus Entry{triangledown} ,{dagger}

Anneke Funk,1,{ddagger} Mouna Mhamdi,1 Heinz Hohenberg,1 Jörg Heeren,2 Rudolph Reimer,1 Carsten Lambert,3 Reinhild Prange,3 and Hüseyin Sirma1*

Heinrich-Pette-Institute for Experimental Immunology and Virology, Hamburg, Germany,1 Institut für Biochemie und Molekularbiologie II, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany,2 Institute for Medical Microbiology and Hygiene, Johannes-Gutenberg-University, Mainz, Germany3

Received 26 February 2008/ Accepted 11 August 2008

The identity and functionality of biological membranes are determined by cooperative interaction between their lipid and protein constituents. Cholesterol is an important structural lipid that modulates fluidity of biological membranes favoring the formation of detergent-resistant microdomains. In the present study, we evaluated the functional role of cholesterol and lipid rafts for entry of hepatitis B viruses into hepatocytes. We show that the duck hepatitis B virus (DHBV) attaches predominantly to detergent-soluble domains on the plasma membrane. Cholesterol depletion from host membranes and thus disruption of rafts does not affect DHBV infection. In contrast, depletion of cholesterol from the envelope of both DHBV and human HBV strongly reduces virus infectivity. Cholesterol depletion increases the density of viral particles and leads to changes in the ultrastructural appearance of the virus envelope. However, the dual topology of the viral envelope protein L is not significantly impaired. Infectivity and density of viral particles are partially restored upon cholesterol replenishment. Binding and entry of cholesterol-deficient DHBV into hepatocytes are not significantly impaired, in contrast to their release from endosomes. We therefore conclude that viral but not host cholesterol is required for endosomal escape of DHBV.

* Corresponding author. Mailing address: Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie, Postfach 201652, 20206 Hamburg, Germany. Phone: 49 (40) 48051-226. Fax: 49 (40) 48051-222. E-mail: sirhus{at}rocketmail.com

{triangledown} Published ahead of print on 3 September 2008.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

{ddagger} Present address: RNA Virology Laboratory, School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Australia.

Journal of Virology, November 2008, p. 10532-10542, Vol. 82, No. 21
0022-538X/08/$08.00+0     doi:10.1128/JVI.00422-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Macovei, A., Radulescu, C., Lazar, C., Petrescu, S., Durantel, D., Dwek, R. A., Zitzmann, N., Nichita, N. B. (2010). Hepatitis B Virus Requires Intact Caveolin-1 Function for Productive Infection in HepaRG Cells. J. Virol. 84: 243-253 [Abstract] [Full Text]  


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