PMID- 16622876 OWN - NLM STAT- MEDLINE DCOM- 20060828 LR - 20220409 IS - 0146-6615 (Print) IS - 0146-6615 (Linking) VI - 78 Suppl 1 DP - 2006 TI - Hepatitis B virus genetic diversity. PG - S36-42 AB - Hepatitis B virus (HBV) is a human DNA virus, which replicates through an RNA intermediate because of the reverse-transcriptase (RT) activity of its DNA polymerase. As a result, the mutation rate for HBV is higher than the rate observed for most DNA viruses. HBVs are classified into genotypes based on genomic sequencing, and antigenic subtypes based on the antigenic properties of its major surface glycoprotein, the HBV surface antigen (HBsAg). Subgenotypes have been identified within most of the HBV genotypes. The HBV groups defined by the different genotype-HBsAg subtype associations found over the world display characteristic geographical distributions, reflecting the movements of human populations and other epidemiologically significant events. Such HBV groups constitute genetically stable viral populations sharing a common evolutionary history, but additional stable changes, originating from mutation and mutant selection, are observed within all of them. These viral sub-populations are known as the HBV variants, and some of which have medical and public health relevance. Pre-core (pre-C) defective variants have been shown to make HBV infection much less susceptible to interferon treatment, and treatment failures with other antiviral drugs have been associated with selection of resistant variants that display specific mutations in the genome region encoding the viral RT activity. Since the RT region of the genome overlaps the sequence encoding the HBsAg molecule, selection of drug resistant variants involves, in some cases, the indirect selection of HBsAg variants. Viral variants displaying changes in HBsAg seem to be very common among chronic HBV carriers; and some of these variants may emerge under the pressure of the neutralizing antibody response, leading to vaccine resistance and resistance to immunotherapy. Mutations conferring resistance to immunotherapy are noted often among liver transplant recipients and among babies born to HBV-carrier mothers. In addition, some of these HBsAg variants have been associated with lack of detection by HBsAg tests used for the diagnosis of HBV infection, for the identification of chronic carriers, for screening of blood donations for transfusion, and in the manufacture of therapeutic blood products. FAU - Echevarria, Jose M AU - Echevarria JM AD - Service of Diagnostic Microbiology, National Centre of Microbiology, Instituto de Salud Carlos III, Madrid, Spain. jmecheva@isciii.es FAU - Avellon, Ana AU - Avellon A LA - eng PT - Journal Article PL - United States TA - J Med Virol JT - Journal of medical virology JID - 7705876 RN - 0 (Antiviral Agents) RN - 0 (Hepatitis B Surface Antigens) RN - EC 2.7.7.49 (RNA-Directed DNA Polymerase) SB - IM MH - Antiviral Agents/pharmacology MH - Carrier State/virology MH - Drug Resistance, Viral MH - Evolution, Molecular MH - Genetic Variation MH - Genome, Viral MH - Hepatitis B/diagnosis/drug therapy/*virology MH - Hepatitis B Surface Antigens/classification/genetics MH - Hepatitis B virus/classification/drug effects/*genetics MH - Hepatitis B, Chronic/virology MH - Humans MH - Liver Transplantation/adverse effects MH - Mutation MH - RNA-Directed DNA Polymerase/genetics/metabolism EDAT- 2006/04/20 09:00 MHDA- 2006/08/29 09:00 CRDT- 2006/04/20 09:00 PHST- 2006/04/20 09:00 [pubmed] PHST- 2006/08/29 09:00 [medline] PHST- 2006/04/20 09:00 [entrez] AID - 10.1002/jmv.20605 [doi] PST - ppublish SO - J Med Virol. 2006;78 Suppl 1:S36-42. doi: 10.1002/jmv.20605.