Expression of the X Gene of Hepatitis B Virus

Pugh, J C; Weber, Christian; Houston, Heather; Murray, Kenneth

doi:10.1002/jmv.1890200305

Cited by 35 publications

(17 citation statements)

References 45 publications

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“…PCR ampli®cation of serum HBV DNA and direct sequencing of the region encompassing the a determinant between codons 109±164 [reference sequence; Pugh et al, 1986] of the surface gene was carried out on both pre-and post-transplant samples, as described previously [Hawkins et al, 1994].…”

Section: Ampli®cation Of Hbv Dna and Sequencing Of The Hbv Surface Genementioning

confidence: 99%

Novel immunoassay for the detection of hepatitis B surface ?escape? mutants and its application in liver transplant recipients

et al. 2001

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Hepatitis B virus (HBV) strains with mutations in the surface gene are responsible for the failure of prophylaxis with hepatitis B immunoglobulin (HBIG) in a proportion of patients transplanted for HBsAg positive cirrhosis. So far, the emergence and evolution of these 'surface antibody escape' mutants have been studied by DNA sequencing. In this study the use of an immunoassay is described for diagnosis and characterisation of HBV recurrence after liver transplantation (OLT), based on a monoclonal antibody able to recognise both wild-type and mutant HBsAg. Pre- and post-transplant samples from 22 patients transplanted for HBsAg positive cirrhosis were studied: Group A: 12 patients who reinfected the graft despite receiving HBIG; Group B: 6 patients with no HBV recurrence with continuous HBIG; Group C: 4 patients with HBV recurrence without prophylaxis. By running the new assay in parallel with an immunoassay that is susceptible to HBsAg mutants, 4 of 12 cases were identified in Group A with HBV recurrence due to surface antibody escape mutants, whereas in 8 patients this was due to the wild-type HBV. The results from the immunoassays were confirmed in all cases by HBV DNA sequencing. The surface gene mutations in the 4 patients affected codons 144 and 145 and in one of these 4 patients HBV strains with mutations in both codons were detected before and after transplantation. The epitope recognised by the new monoclonal antibody that reacts with both wild-type and mutant HBsAg seems to remain stable in the HBIG-induced HBV mutants. This serological approach allows rapid and cost-effective screening for HBsAg escape mutants in the liver transplant setting and may be helpful in the selection of appropriate prophylaxis.

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Section: Ampli®cation Of Hbv Dna and Sequencing Of The Hbv Surface Genementioning

confidence: 99%

Novel immunoassay for the detection of hepatitis B surface ?escape? mutants and its application in liver transplant recipients

et al. 2001

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“…The 13 HBV sequences are identified with their serotypes as follows: 1.adr (Fujiyama et al 1983), 2.adr (Kobayashi and Koike 1984), 3.adr (Gan et al 1987), 4.adr (Rho et al 1989, 5.ayr (Okamoto et al 1986), 6.adw (Ono et al 1983), Zadw (Valenzuela et aI. 1981), 8.adw (Estacio et al 1988), 9.adw (Okamoto et al 1987, lO.adw (Iswari et al 1985), 11.ayw (Galibert et al 1979), 12.ayw (Bichko et al 1985), and 13.adyw (Pugh et al 1986). Branch lengths (×10 -4) in the tree were estimated under the REV + C + dG model and were measured as the expected numbers of substitutions per site at the first codon position.…”

Section: Data and Modelsmentioning

confidence: 99%

Molecular evolution of the hepatitis B virus genome

Yang¹,

Lauder

Lin

1995

J Mol Evol

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The hepatitis B virus (HBV) has a circular DNA genome of about 3,200 base pairs. Economical use of the genome with overlapping reading frames may have led to severe constraints on nucleotide substitutions along the genome and to highly variable rates of substitution among nucleotide sites. Nucleotide sequences from 13 complete HBV genomes were compared to examine such variability of substitution rates among sites and to examine the phylogenetic relationships among the HBV variants. The maximum likelihood method was employed to fit models of DNA sequence evolution that can account for the complexity of the pattern of nucleotide substitution. Comparison of the models suggests that the rates of substitution are different in different genes and codon positions; for example, the third codon position changes at a rate over ten times higher than the second position. Furthermore, substantial variation of substitution rates was detected even after the effects of genes and codon positions were corrected; that is, rates are different at different sites of the same gene or at the same codon position. Such rates after the correction were also found to be positively correlated at adjacent sites, which indicated the existence of conserved and variable domains in the proteins encoded by the viral genome. A multiparameter model validates the earlier finding that the variation in nucleotide conservation is not random around the HBV genome. The test for the existence of a molecular clock suggests that substitution rates are more or less constant among lineages. The phylogenetic relationships among the viral variants were examined. Although the data do not seem to contain sufficient information to resolve the details of the phylogeny, it appears quite certain that the serotypes of the viral variants do not reflect their genetic relatedness.

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“…8 In a proportion of the samples, the entire HBsAg-coding region was amplified (1013 bp, positions 1292-2306). 9 Genomic positioning is according to Pugh et al 10 …”

Section: Pcr Amplification Of Hbv Dnamentioning

confidence: 99%