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Basic Characteristics of Mutations
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Mutation Site
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C1589T |
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Mutation Site Sentence
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In HBV_w228, a total of 13 nt substitutions were found, as compared with HBV_w100, leading to 17 aa substitutions (five in HBsAg, 11 in polymerase including the nt substitutions A1588C/C1589T, leading to the rtT184L substitution, and one in the HBx protein). |
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Mutation Level
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Nucleotide level |
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Mutation Type
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Nonsynonymous substitution |
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Gene/Protein/Region
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RT |
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Standardized Encoding Gene
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P
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Genotype/Subtype
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C |
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Viral Reference
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-
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Functional Impact and Mechanisms
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Disease
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Hepatitis B, Chronic
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Immune
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- |
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Target Gene
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-
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Clinical and Epidemiological Correlations
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Clinical Information
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Y |
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Treatment
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- |
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Location
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- |
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Literature Information
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PMID
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19125938
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Title
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Spontaneous HBeAg seroconversion and loss of hepatitis B virus DNA after acute flare due to development of drug resistant mutants during entecavir monotherapy
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Author
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Mao RC,Yin YK,Qin YL,Wu XH,Weng XH,Zhang JM,Lu M
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Journal
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Hepatology research : the official journal of the Japan Society of Hepatology
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Journal Info
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2009 Jan;39(1):14-20
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Abstract
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AIMS: Patients with chronic hepatitis B virus (HBV) infection under entecavir (ETV) treatment develop resistant mutants with viral rebound. Here, we report an interesting case of spontaneous loss of HBV-DNA and seroconversion following an acute flare after the development of ETV-resistant mutants. This patient received ETV after lamivudine breakthrough. METHODS: Cloning and sequence analysis of the HBV reverse transcriptase (RT) region were performed with seven samples during ETV therapy. In addition, two full-length HBV genomes derived from samples before and after the emergence of ETV resistance were sequenced. RESULTS: ETV resistant mutants appeared at week 228, with virological and biochemical rebound at the same time. Unexpectedly, HBeAg seroconversion occurred 8 weeks later. The viral load decreased and became undetectable from week 252. Analysis of HBV isolates in the patient at week 124 revealed that wild-type HBV was predominant at that time and ETV resistant mutants were not found among 20 clones. Interestingly, a new mutant type with rtL180M+rtT184L was found alongside rtL180M+rtT184L+rtM204V/I at week 228 and appeared to develop independently, according to the sequence analysis. In contrast to the previously identified ETV resistant mutants, it did not carry the rtM204V/I mutations. CONCLUSION: The data presented here indicates that the flare following the emergence of ETV resistant mutants may reflect immune-mediated control of HBV infection, leading to a spontaneous loss of HBV-DNA and seroconversion.
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Sequence Data
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EF536065;EF536066
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