Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

18
694
1
7

Year Published

1993
1993
2007
2007

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 1,123 publications
(720 citation statements)
references
References 17 publications
18
694
1
7
Order By: Relevance
“…1). HBV precore nucleotide 1,896 mutation from guanine (G) to adenine (A) as well as changes of two nucleotides, an adenine (A) to thymine (T) transversion at nucleotide 1,762 together with a guanine (G) to adenine (A) transition at nucleotide 1,764 within the BCP, lead to a proportion of HBeAg-negative patients who continue to have moderate levels of HBV replication and active liver disease [71][72][73]. Although these mutants can also be found in asymptomatic hepatitis B carriers, the BCP T1762/A1764 mutation has been shown to increase the risk of liver disease progression and HCC development for both genotypes B and C infection [74][75][76][77][78].…”
Section: Naturally Occurring Mutantsmentioning
confidence: 99%
“…1). HBV precore nucleotide 1,896 mutation from guanine (G) to adenine (A) as well as changes of two nucleotides, an adenine (A) to thymine (T) transversion at nucleotide 1,762 together with a guanine (G) to adenine (A) transition at nucleotide 1,764 within the BCP, lead to a proportion of HBeAg-negative patients who continue to have moderate levels of HBV replication and active liver disease [71][72][73]. Although these mutants can also be found in asymptomatic hepatitis B carriers, the BCP T1762/A1764 mutation has been shown to increase the risk of liver disease progression and HCC development for both genotypes B and C infection [74][75][76][77][78].…”
Section: Naturally Occurring Mutantsmentioning
confidence: 99%
“…[1][2][3][4][5][6][7] The predominant mutation involves a G-to-A change at nucleotide 1896 (A1896), which creates a premature stop codon at codon 28 ( Fig. 1).…”
mentioning
confidence: 99%
“…Employing overlapping synthetic peptides covering the entire amino acid sequences of the HBcAg and HBeAg to analyse specific cytotoxic T-cell responses (CTL) in hepatitis B patients, an HLA-A2 restricted CTL epitope was located in the amino-terminal part of HBcAg (peptides 11-27) [16]. This peptide overlaps with an immunodominant helper epitope (peptides [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20], and both epitopes are included in the HBeAg amino acid sequences. Cell-mediated immune responses against HBeAg have not been compared with those against HBcAg.…”
Section: Immune Responsementioning
confidence: 99%
“…In a sequential study of HBV genome analysis in a maternal-fetal-transmitted HBV carrier, the estimated rate of nucleotide substitution per site per year for HBV was 1.4-3.2 x similar to some RNA viruses, but 100-fold less than human immunodeficiency virus (HIV) [18]. A mutation of the HBV genome bearing clinical significance was described, locating a point mutation in the precore region (nucleotide 1896) [19]. In the wild-type HBV, codon 28 of the precore region is TGG; the point mutation guanidine to adenine (G to A), results in TAG, a translation stop codon.…”
Section: Mutationsmentioning
confidence: 99%