HEPATITIS-B VIRUS-REPLICATION - AN UPDATE

Hepatitis B virus (HBV), the causative agent of type B hepatitis in hu mans, is the prototypic member of the hepadnaviridae, a family of smal l enveloped DNA-containing viruses with pronounced host and tissue spe cificity. This property has greatly hampered progress in understanding the initial events of infection, i.e. attachment, penetration and unc oating. After the discovery, originally made with the duck hepatitis B virus (DHBV), that hepadnaviruses replicate by reverse transcription, DNA transfection of cloned wild-type and mutant HBV genomes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 mechanis ms of the late steps of the infectious cycle in some detail. During th e last few years, such studies have emphasized the differences between hepadnaviral and retroviral replication. Very recent research, howeve r, 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 da ta, with particular emphasis on the initiation of reverse transcriptio n.