SEQUENTIAL-CHANGES IN FULL-LENGTH GENOMES OF HEPATITIS-B VIRUS ACCOMPANYING ACUTE EXACERBATION OF CHRONIC HEPATITIS-B

Background/Aim: During the course of persistent hepatitis B virus infe ction, viral replication markedly decreases after acute exacerbation o f liver inflammation accompanied by emergence of antihepatitis B e ant ibody (anti-HBe) and/or anti-hepatitis B surface antibody (anti-HBs), In some cases, however, persistent viral replication continues even af ter such exacerbation with or without HBeAg/anti-HBe seroconversion, T he aim of the present study was to investigate the extent of genetic v ariations of HBV in this phenomenon, Methods: Full-length HBV genomes were amplified by polymerase chain reaction from sera of three patient s before and after acute exacerbation and were directly sequenced, Res ults: In the whole genomes of 3215 nucleotides, only six nucleotide mu tations for six amino acid substitutions (2 in the surface gene, 2 in the X gene, 1 in the core gene and 1 in the polymerase gene) were obse rved in patient 1, 15 mutations for 14 amino acid substitutions (1 in the pre-core codon 28, 4 in the surface gene, 4 in the core gene and 5 in the polymerase gene) were observed in patient 2, and 5 mutations f or 6 amino acid substitutions (2 in the surface gene, 2 in the X gene, pre-core stop codon mutation and 1 in the polymerase gene) were obser ved in patient 3, Substitutions in the a determinant of the surface ge ne, which encodes target epitopes for neutralizing antibodies, as well as those in the pre-core/core gene, which encodes epitopes for cytoto xic T cells, were mainly found, Conclusion: HBV that remained after th e emergence of anti-HBe and anti-HBs are considered to possess mutatio ns in epitopes for both humoral and cellular immunity, These mutant HB V may be involved in the pathogenesis of persistent hepatic injury aft er acute exacerbation.