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Correlations of HBV Genotypes, Mutations Affecting HBeAg Expression and HBeAg/ anti-HBe Status in HBV Carriers

This study was carried out to determine the effects of hepatitis B virus genotypes, core promoter mutations (A(1762)G(1764)→T(1762)A(1764)) as well as precore stop codon mutations (TGG→TAG) on HBeAg expression and HBeAg/ anti-HBe status. Study was also performed on the effects of codon 15 variants (...

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Detalles Bibliográficos
Autores principales: Lim, Chee Kent, Tan, Joanne Tsui Ming, Khoo, Jason Boo Siang, Ravichandran, Aarthi, Low, Hsin Mei, Chan, Yin Chyi, Ton, So Har
Formato: Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1332200/
https://www.ncbi.nlm.nih.gov/pubmed/16421626
Descripción
Sumario:This study was carried out to determine the effects of hepatitis B virus genotypes, core promoter mutations (A(1762)G(1764)→T(1762)A(1764)) as well as precore stop codon mutations (TGG→TAG) on HBeAg expression and HBeAg/ anti-HBe status. Study was also performed on the effects of codon 15 variants (C(1858)/ T(1858)) on the predisposition of precore stop codon mutations (TGG→TAG). A total of 77 sera samples were analyzed. Fifty one samples were successfully genotyped of which the predominant genotype was genotype B (29/ 51, 56.9 %), followed by genotype C (16/ 51, 31.4 %). Co-infections by genotypes B and C were observed in four samples (7.8 %). To a lesser degree, genotypes D and E (2.0 % each) were also observed. For core promoter mutations, the prevalence was 68.8 % (53/ 77) for A(1762)G(1764) wild-type and 14.3 % (11/ 77) for T(1762)A(1764 )mutant while 9.1 % (7/ 77) was co-infected by both strains. The prevalence of codon 15 variants was found to be 42.9 % (33/ 77) for T(1858 )variant and 16.9 % (13/ 77) for C(1858) variant. No TAG mutation was found. In our study, no associations were found between genotypes (B and C) and core promoter mutations as well as codon 15 variants. Also no correlation was observed between HBeAg/ anti-HBe status with genotypes (B and C) and core promoter mutations.