Virus Dataset Sample Info

> Dataset: 11472634 Search Result


Summary
Item Summary
Project 11472634
Virus Name HBV
Sample Number 19
Disease HBV infection
Country Brazil
Data Link https://www.ncbi.nlm.nih.gov/nuccore/?term=AF389988:AF390016[pacc]

Sample
ID Sample ID Age Gender Origin Detail
1 A1 55 M Brazil View
2 A2 41 F Brazil View
3 A3 45 M Brazil View
4 A4 40 F Brazil View
5 A5 10 F Brazil View
6 A6 52 M Brazil View
7 A7 38 M Brazil View
8 A8 54 M Brazil View
9 A9 52 M Brazil View
10 A10 39 M Brazil View
11 D1 36 M Brazil View
12 D2 54 F Brazil View
13 D3 56 F Brazil View
14 D4 35 M Brazil View
15 D5 55 M Brazil View
16 D6 47 M Brazil View
17 D7 53 M Brazil View
18 F1 10 M Brazil View
19 F2 35 M Brazil View

Literature
Item Summary
PMID 11472634
Title Low frequency of mutations in the core promoter and precore regions of hepatitis B virus in anti-HBe positive Brazilian carriers.
Abstract BACKGROUND: Mutations in the core promoter and precore regions of the hepatitis B virus (HBV) genome, notably the double substitution (AGG to TGA) at nt positions 1762-1764 in the core promoter, and the precore stop codon mutation G to A at nt 1896, can often explain the anti-HBe phenotype in chronic carriers. However, the A1896 mutation is restricted to HBV isolates that have T at nt 1858. The double substitution at positions 1762-1764 has been described to occur preferentially in patients infected with strains showing C instead of T at nt 1858. RESULTS: HBV DNAs from 29 anti-HBe Brazilian samples were characterized by nucleotide sequencing of PCR products from precore region. Among them, 18 isolates presented C at nt 1858 (mostly genotype A strains). The 11 remaining isolates (genotypes D and F) had T1858. The stop codon mutation at nt 1896 was found in seven isolates (24% of the total and 63% of the isolates that had T1858). The frequency of the double substitution at positions 1762-1764 was surprisingly low (20%) among C1858 isolates. An association between A1896 and TGA 1762-1764 mutations was observed among genotype D isolates: these showed either none of the two mutations or both. Furthermore, strains mutated at positions 1896 and/or 1762-1764 also presented an elevated number of other, less common substitutions in the core promoter and precore regions. CONCLUSIONS: The data reported here are not in accordance with some reports from other parts of the world. In half of the isolates, none of the mutations previously described could explain the anti-HBe phenotype.