title: The hepatitis B virus and common mutants.
abstract: Most biological systems have developed complex mechanisms to maintain the stability of their genetic information. Exceptions to this include viruses that can undergo rapid and substantial genetic sequence changes and alterations. The hepatitis B virus (HBV) has evolved a unique life cycle resulting in the production of enormous viral loads during active replication without actually directly killing the infected cell. Because the virus uses reverse transcription to copy its DNA genome, mutant viral genomes are frequently found. Particular selection pressures, both endogenous (host immune clearance) and exogenous (vaccines and antivirals), readily select out these escape mutants. It is still not known which particular viral mutations or combination of mutations directly affects the clinical presentation of the liver disease, the nature of the viral persistence, or the course and outcome of chronic infection. Further studies are needed to identify the pathogenic basis for the selection of these mutants. Such research should help improve the basic understanding of this unique virus-host relationship and provide new strategies for complete control of HBV infections.
authors.affiliation: Victorian Infectious Diseases Reference Laboratory, North Melbourne, Australia. stephenlocarnini@compuserve.com
authors.forename: Stephen
authors.initials: S
authors.lastname: Locarnini
authors.forename: Janine
authors.initials: J
authors.lastname: McMillan
authors.forename: Angeline
authors.initials: A
authors.lastname: Bartholomeusz
mesh_terms: D004279:DNA, Viral; D004351:Drug Resistance; D005838:Genotype; D006509:Hepatitis B / Q000821:virology*; D017325:Hepatitis B Vaccines / Q000494:pharmacology; D006515:Hepatitis B virus / Q000235:genetics* / Q000472:pathogenicity*; D006801:Humans; D009154:Mutation; D014158:Transcription, Genetic; D019562:Viral Load; D014771:Virion; D014779:Virus Replication
chemical_list: D004279:DNA, Viral; D017325:Hepatitis B Vaccines