摘要
Objective: To clarify the association of hepatitis Bvirus mutants in precore and core promoter regions inpatients with hepatic failure and HBeAg state.Methods: Precore and core promoter regions of 25HBV isolates from the patients with hepatic failurewere analyzed by polymerase chain reaction (PCR)direct sequencing approach.Results: Precore G-to-A^(1896) mutants were identified in16 (64%) of the 25 isolates. The 'hot spot' mutationsat A-to-T^(1762) and G-to-A^(1764) were present together in19 (76%) of the 25 isolates, while C-to-T^(1653) and T-to-C^(1753) existed in a mutually exclusive manner andmore frequently in hepatic failure with liver cirrhosisgroup than in hepatic failure with chronic hepatitisgroup (100% vs 50%). Both A^(1896) and T^(1762)-A^(1764)could be found frequently in HBeAg-positive subjects(77.8% and 88.9%), whereas T^(1653)/C^(1753) was moreprevalent in anti-HBe-positive subjects than inHBeAg-positive subjects (93.8% vs 33.3%).Conclusions: The whole frequency of mutations in pre-core and core promoter gene will become more fre-quent as HBV infection is to be persistent. Mutationto T^(1653)/C^(1753) may be useful as a marker for hepaticfailure. It requires further study whether the mixedinfection of mutants and wilds will develop and affectthe condition of HBeAg in serum along the progres-sion of liver disease.
Objective: To clarify the association of hepatitis Bvirus mutants in precore and core promoter regions inpatients with hepatic failure and HBeAg state.Methods: Precore and core promoter regions of 25HBV isolates from the patients with hepatic failurewere analyzed by polymerase chain reaction (PCR)direct sequencing approach.Results: Precore G-to-A^(1896) mutants were identified in16 (64%) of the 25 isolates. The 'hot spot' mutationsat A-to-T^(1762) and G-to-A^(1764) were present together in19 (76%) of the 25 isolates, while C-to-T^(1653) and T-to-C^(1753) existed in a mutually exclusive manner andmore frequently in hepatic failure with liver cirrhosisgroup than in hepatic failure with chronic hepatitisgroup (100% vs 50%). Both A^(1896) and T^(1762)-A^(1764)could be found frequently in HBeAg-positive subjects(77.8% and 88.9%), whereas T^(1653)/C^(1753) was moreprevalent in anti-HBe-positive subjects than inHBeAg-positive subjects (93.8% vs 33.3%).Conclusions: The whole frequency of mutations in pre-core and core promoter gene will become more fre-quent as HBV infection is to be persistent. Mutationto T^(1653)/C^(1753) may be useful as a marker for hepaticfailure. It requires further study whether the mixedinfection of mutants and wilds will develop and affectthe condition of HBeAg in serum along the progres-sion of liver disease.
