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REVIEW ARTICLE
Year : 2005  |  Volume : 2  |  Issue : 1  |  Page : 74-92

HBV variants: Clinical significance and public health implications


Research and Molecular Development, Victorian Infectious Diseases Reference Laboratory, 10 Wreckyn Street, North Melbourne, Victoria 3051, Australia

Correspondence Address:
Stephen Locarnini
Research and Molecular Development, Victorian Infectious Diseases Reference Laboratory, 10 Wreckyn Street, North Melbourne, Victoria 3051
Australia
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Source of Support: None, Conflict of Interest: None


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Inadequate and/or inappropriate host immune responses, are mainly responsible for the liver disease of chronic hepatitis B. Infection of the hepatocyte with the hepatitis B virus (HBV) results in very high levels of viral replication without actually killing the infected cell directly. The HBV uses reverse transcription to copy its DNA genome and because of a lack of proof-reading capability, mutant viral genomes or quasi species, emerge continually. All the selection pressures, both endogenous (host immune clearance) and exogenous (vaccines and antiviral drugs), readily select particular quasispecies with increased replication fitness, which then emerge as the new dominant population. The specific viral mutations or combination of mutations that play a role in the final clinical outcome of HBV infection are not fully known, but certain patterns and associations are starting to emerge. In particular, the expression of a novel protein, the hepatitis B splice protein (HBSP), has been linked to liver fibrosis and liver disease progression. Further studies are needed to identify the molecular pathological basis and subsequent clinical sequelae arising from the selection of these quasispecies in infected individuals.


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