Hepatitis B virus replication--an update.
Hepatitis B virus (HBV), the causative agent of type B hepatitis in humans, is the prototypic member of the hepadnaviridae, a family of small enveloped DNA-containing viruses with pronounced host and tissue specificity. This property has greatly hampered progress in understanding the initial events of infection, i.e. attachment, penetration and uncoating. After the discovery, originally made with the duck hepatitis B virus (DHBV), that hepadnaviruses replicate by reverse transcription, DNA transfection of cloned wild-type and mutant HBV genomes into cell lines supporting virion formation has revealed the molecular mechanisms of the late steps of the infectious cycle in some detail. During the last few years, such studies have emphasized the differences between hepadnaviral and retroviral replication. Very recent research, however, indicates that the border separating the two viral families may not be as strict as previously thought. In this article, we will briefly summarize the pertinent differences, and will then focus on the new data, with particular emphasis on the initiation of reverse transcription.
Nassal
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Zentrum für Molekulare Biologie (ZMBH), University of Heidelberg, Germany.
Schaller
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H
D015684:Gene Products, pol / Q000502:physiology; D016679:Genome, Viral; D006515:Hepatitis B virus / Q000235:genetics* / Q000254:growth & development*; D006801:Humans; D018832:Molecular Chaperones / Q000502:physiology; D019251:Nucleocapsid / Q000737:chemistry / Q000235:genetics; D014176:Protein Biosynthesis; D012367:RNA, Viral / Q000502:physiology; D014158:Transcription, Genetic
D015684:Gene Products, pol; D018832:Molecular Chaperones; C066027:P protein, Hepatitis B virus; D012367:RNA, Viral