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Variability in the precore and core promoter region of the hepatitis B virus genome.

Nordin, Maria LU ; Ingman, Mikael LU ; Lindqvist, Beata LU and Kidd-Ljunggren, Karin LU (2014) In Journal of Medical Virology 86(3). p.437-445
Abstract
There is increasing evidence that hepatitis B virus (HBV) infections with different genotypes and subgenotypes differ in response to treatment and long-term prognosis. The differences emerge from variability within the genomes that leads to structural deviations at the pregenomic level and to changes at the translational level. Naturally occurring HBV strains covering the four major genotypes A-D were obtained from 393 patients and part of the genome was amplified using polymerase chain reaction (PCR), sequenced, and analyzed for mutational differences in the precore and core promoter regions. The study confirmed that core promoter and precore mutations occur at key positions (A1762T, G1764A, G1896A, and G1899A), and that the proportions... (More)
There is increasing evidence that hepatitis B virus (HBV) infections with different genotypes and subgenotypes differ in response to treatment and long-term prognosis. The differences emerge from variability within the genomes that leads to structural deviations at the pregenomic level and to changes at the translational level. Naturally occurring HBV strains covering the four major genotypes A-D were obtained from 393 patients and part of the genome was amplified using polymerase chain reaction (PCR), sequenced, and analyzed for mutational differences in the precore and core promoter regions. The study confirmed that core promoter and precore mutations occur at key positions (A1762T, G1764A, G1896A, and G1899A), and that the proportions of strains with seroconvertion in patients differ between the four HBV genotypes. A rare double mutation (C1857T together with G1897A) was observed, and C1856T was found together with the emerging G1898A mutation, which itself was found to be more widespread geographically than previously described. We found a novel mutation (T1850C), never before observed in human HBV strains but known from woodchuck hepatitis virus (WHV). A novel association of mutation C1773T with G1764T, C1766A, and G1757A was also found within a site already suggested to be a putative binding site for HNF-3. This novel association is proposed by us to be of importance for additional binding of HNH-2 to this site and is a better indicator of the emergence of the double mutation G1764T and C1766A than the G1757A mutation proposed previously. J. Med. Virol. © 2013 Wiley Periodicals, Inc. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
Journal of Medical Virology
volume
86
issue
3
pages
437 - 445
publisher
John Wiley & Sons
external identifiers
  • wos:000329461000010
  • pmid:24249691
  • scopus:84891950046
ISSN
1096-9071
DOI
10.1002/jmv.23839
language
English
LU publication?
yes
id
741cb641-e18b-4436-97f5-24fc30e56c05 (old id 4179196)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24249691?dopt=Abstract
date added to LUP
2013-12-06 15:00:36
date last changed
2017-05-21 03:13:26
@article{741cb641-e18b-4436-97f5-24fc30e56c05,
  abstract     = {There is increasing evidence that hepatitis B virus (HBV) infections with different genotypes and subgenotypes differ in response to treatment and long-term prognosis. The differences emerge from variability within the genomes that leads to structural deviations at the pregenomic level and to changes at the translational level. Naturally occurring HBV strains covering the four major genotypes A-D were obtained from 393 patients and part of the genome was amplified using polymerase chain reaction (PCR), sequenced, and analyzed for mutational differences in the precore and core promoter regions. The study confirmed that core promoter and precore mutations occur at key positions (A1762T, G1764A, G1896A, and G1899A), and that the proportions of strains with seroconvertion in patients differ between the four HBV genotypes. A rare double mutation (C1857T together with G1897A) was observed, and C1856T was found together with the emerging G1898A mutation, which itself was found to be more widespread geographically than previously described. We found a novel mutation (T1850C), never before observed in human HBV strains but known from woodchuck hepatitis virus (WHV). A novel association of mutation C1773T with G1764T, C1766A, and G1757A was also found within a site already suggested to be a putative binding site for HNF-3. This novel association is proposed by us to be of importance for additional binding of HNH-2 to this site and is a better indicator of the emergence of the double mutation G1764T and C1766A than the G1757A mutation proposed previously. J. Med. Virol. © 2013 Wiley Periodicals, Inc.},
  author       = {Nordin, Maria and Ingman, Mikael and Lindqvist, Beata and Kidd-Ljunggren, Karin},
  issn         = {1096-9071},
  language     = {eng},
  number       = {3},
  pages        = {437--445},
  publisher    = {John Wiley & Sons},
  series       = {Journal of Medical Virology},
  title        = {Variability in the precore and core promoter region of the hepatitis B virus genome.},
  url          = {http://dx.doi.org/10.1002/jmv.23839},
  volume       = {86},
  year         = {2014},
}