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Mutations in precore and core promoter region of HBV in patients with hepatic failure |
Lan-Juan Li, Bing Ruan, Reinhard H. Dennin, Jian-Er Wo, Zhi Chen and Ya-Gang Chen |
From the first Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China (Li LJ, Ruan B, Wo JE, Chen Z and Chen YG); Institute of Microbiology, Luebeck Medical College, Germany (Dennin RH)
Correspondence: Lan-Juan Li, MD (Tel: 86-571-87236752; Fax: 86-571-87236628; Email: my-bing@mail.hz.zj.cn) |
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Abstract Objective: To clarify the association of hepatitis B virus mutants in precore and core promoter regions in patients with hepatic failure and HBeAg state.
Methods: precore and core promoter regions of 25 HBV isolates from the patients with hepatic failure were analyzed by polymerase chain reaction (PCR) direct sequencing approach.
Results: precore G-to-A1896 mutants were iden tified in 16 (64%) of the 25 isolates. The “hot spot” mutations at A-to-T1762 and G-to-A1764 were present together in 19 (76%) of the 25 isolates, while C-to-T1653 and T-to-C1753 eXisted in a mutually exclusive manner and more frequently in hepatic failure with liver cirrhosis group than in hepatic failure with chronic hepatitis group (100% vs 50%). Both A1896 and T1762-A1764 could be found frequently in HBeAg-positive subjects (77.8% and 88.9%), whereas T1653/C1753 was more prevalent in anti-HBe-positive subjects than in HBeAg-positive subjects (93.8% vs 33.3%).
Conclusions: The whole frequency of mutations in precore and core promoter gene will become more frequent as HBV infection is to be persistent. Mutation to T1653/C1753 may be useful as a marker for hepatic failure. It requires further study whether the mixed infection of mutants and wilds will develop and affect the condition of HBeAg in serum along the progression of liver disease.
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