Short communicationAssociation of hepatitis B viral precore mutations with fulminant hepatitis B in Japan
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Cited by (69)
Fatal fulminant primary hepatitis B virus infections with G1896A precore viral mutants in southeastern France
2012, Clinics and Research in Hepatology and GastroenterologyCitation Excerpt :In the four fulminant and non-fulminant AHB reported here, it can be outlined that HBV genotype was D or E in AHB. The question of whether or not fulminant outcome after HBV infection is linked to precore G1896A HBV mutants has been raised in several studies, starting from initial descriptions of these viral strains in FHB [31,35,38,45,46]. Four studies conducted in Japan, where patients are mostly infected by HBV genotypes B or C, reported statistically significantly higher frequencies of G1896A mutants in FHB than in ASLHB.
Advances in hepatitis B virus infection
2003, Transplantation ProceedingsHigh hepatitis B virus (HBV) DNA viral load as the most important risk factor for HBV reactivation in patients positive for HBV surface antigen undergoing autologous hematopoietic cell transplantation
2002, BloodCitation Excerpt :Other HBV viral factors that might be involved in HBV reactivation are the presence of variants, notably, the G→A mutation at nucleotide 1896 in the precore region (A1896), which converts codon 28 for tryptophan to a stop codon23; and the double mutation in the basic core promoter (BCP) that consists of the A→T mutation at nucleotide 1762 and the G→A mutation at nucleotide 1764 (T1762/A1764).24 The precore A1896 stop mutation was reported to be an Andromeda strain that markedly increased HBV virulence and contributed to the development of fulminant hepatitis.25, 26 On the other hand, the BCP regulates transcription of pregenomic RNA, encodes core protein and HBV polymerase, and serves as a replicative intermediate for the synthesis of viral DNA.27
Viral genotype and hepatitis B virus DNA levels are correlated with histological liver damage in HBeAg-negative chronic hepatitis B virus infection
2002, American Journal of GastroenterologyCitation Excerpt :In vitro studies (1–3) suggest that precore stop codon mutation (G to A mutation at nucleotide 1896—i.e., G1896 to A1896) and a dual-nucleotide mutation at the core promoter region (A to T and G to A at nucleotides 1762 and 1764, respectively—i.e., A1762/G1764 to T1762/A1764) abolish and reduce the production of HBeAg, respectively, but at the same time they facilitate more efficient viral replication. These HBV mutants have been reported to be associated with fulminant hepatitis (4–7), chronic active hepatitis (8, 9), and hepatocellular carcinoma (10–12) among HBeAg-negative patients. However, others, including our group, have found these HBV mutants in a large number of HBeAg-negative patients who had inactive liver disease (13–17).