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Prophylactic and Therapeutic Vaccination against Hepatitis C Virus (HCV): Developments and Future Perspectives
Viruses 2009, 1(2), 185-209; doi:10.3390/v1020185

HBV Life Cycle: Entry and Morphogenesis

1 Molecular Medical Virology, Institute of Infection Medicine, University of Kiel, D-24105 Kiel, Germany 2 Faculty of Biology, University of Freiburg, Schaenzlestrasse 1, D-79104 Freiburg, Germany
* Author to whom correspondence should be addressed.
Received: 13 June 2009 / Revised: 31 July 2009 / Accepted: 13 August 2009 / Published: 1 September 2009
(This article belongs to the Special Issue Hepatitis Viruses)
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Hepatitis B virus (HBV) is a major cause of liver disease. HBV primarily infects hepatocytes by a still poorly understood mechanism. After an endocytotic process, the nucleocapsids are released into the cytoplasm and the relaxed circular rcDNA genome is transported towards the nucleus where it is converted into covalently closed circular cccDNA. Replication of the viral genome occurs via an RNA pregenome (pgRNA) that binds to HBV polymerase (P). P initiates pgRNA encapsidation and reverse transcription inside the capsid. Matured, rcDNA containing nucleocapsids can re-deliver the RC-DNA to the nucleus, or be secreted via interaction with the envelope proteins as progeny virions.
Keywords: hepatitis B virus; entry; morphogenesis; liver disease hepatitis B virus; entry; morphogenesis; liver disease
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Schädler, S.; Hildt, E. HBV Life Cycle: Entry and Morphogenesis. Viruses 2009, 1, 185-209.

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