Guest guest Posted June 27, 2006 Report Share Posted June 27, 2006 J Viral Hepat. 2006 Jul;13(7):427-34. Related Articles, Links Mutations affecting the replication capacity of the hepatitis B virus. Sheldon J, Rodes B, Zoulim F, Bartholomeusz A, Soriano V. Department of Infectious Diseases, Hospital III, Madrid, Spain. The genetic variability of the hepatitis B virus (HBV) encounters two compounding forces: a high viral copy number produced during active replication and the lack of proofreading activity in the HBV polymerase, resulting in a high mutational rate. A large pool of quasispecies is generated in which the fittest virus, i.e. the virus that replicates best, becomes the dominant species. Immune and antiviral selection pressures result in vaccine/immunoglobulin escape mutants and antiviral resistant variants. Viruses encoding changes associated with antiviral resistance often have reduced replication in vitro, but the accumulation of additional mutations helps restore viral fitness. These compensatory mutations may occur not only in the polymerase gene but also in other genes such as the overlapping envelope gene, the precore gene, or in regulatory regions such as the basal core promoter. In this report we aim to review the new findings that have appeared in recent months. PMID: 16792535 [PubMed - in process] _________________________________________________________________ Don’t just search. Find. Check out the new MSN Search! http://search.msn.click-url.com/go/onm00200636ave/direct/01/ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 27, 2006 Report Share Posted June 27, 2006 J Viral Hepat. 2006 Jul;13(7):427-34. Related Articles, Links Mutations affecting the replication capacity of the hepatitis B virus. Sheldon J, Rodes B, Zoulim F, Bartholomeusz A, Soriano V. Department of Infectious Diseases, Hospital III, Madrid, Spain. The genetic variability of the hepatitis B virus (HBV) encounters two compounding forces: a high viral copy number produced during active replication and the lack of proofreading activity in the HBV polymerase, resulting in a high mutational rate. A large pool of quasispecies is generated in which the fittest virus, i.e. the virus that replicates best, becomes the dominant species. Immune and antiviral selection pressures result in vaccine/immunoglobulin escape mutants and antiviral resistant variants. Viruses encoding changes associated with antiviral resistance often have reduced replication in vitro, but the accumulation of additional mutations helps restore viral fitness. These compensatory mutations may occur not only in the polymerase gene but also in other genes such as the overlapping envelope gene, the precore gene, or in regulatory regions such as the basal core promoter. In this report we aim to review the new findings that have appeared in recent months. PMID: 16792535 [PubMed - in process] _________________________________________________________________ Don’t just search. Find. Check out the new MSN Search! http://search.msn.click-url.com/go/onm00200636ave/direct/01/ Quote Link to comment Share on other sites More sharing options...
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