Hepatitis B virus (HBV) has evolved a unique life cycle that results in the production
of enormous viral loads during active replication without actually killing the infected
cell directly. Because HBV uses reverse transcription to copy its DNA genome, mutant
viral genomes emerge frequently. Particular selection pressures, both endogenous (host
immune clearance) and exogenous (vaccines and antiviral drugs), readily select out
these escape mutants. Which particular viral mutations or combination of mutations
directly affect the clinical outcome of infection are not known. Further studies are
clearly needed to identify the pathogenic basis and clinical sequelae arising from
the selection of these mutants.
Reverse transcription - covalently closed circular DNA - viral mutants - drug resistance
- vaccine escape