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Basic Characteristics of Mutations
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Mutation Site
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M204V |
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Mutation Site Sentence
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The distribution of pre-treatment LAM-resistant YMDD variants was: rtM204I:18 (62.1%) and rtM204V:11 (37.9%). |
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Mutation Level
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Amino acid 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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B;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
|
Lamivudine(LAM) |
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Location
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China |
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Literature Information
|
|
PMID
|
17400303
|
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Title
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Adefovir dipivoxil treatment of lamivudine-resistant chronic hepatitis B
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Author
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Dai CY,Chuang WL,Hsieh MY,Lee LP,Huang JF,Hou NJ,Lin ZY,Chen SC,Hsieh MY,Wang LY,Tsai JF,Chang WY,Yu ML
|
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Journal
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Antiviral research
|
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Journal Info
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2007 Aug;75(2):146-51
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Abstract
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Adefovir dipivoxil (ADV)-resistant mutations have been identified in treating hepatitis B virus (HBV) infection. This study aimed to analyze the response, the incidence of ADV resistance and the virologic characteristics of ADV therapy. A total of 29 CHB patients with confirmed lamivudine (LAM)-resistant HBV were treated with ADV for more than 52 weeks. Serum HBV DNA, HBV genotypes and sequences of HBV polymerase reverse-transcriptase domain were determined. Rates for the biochemical response, HBeAg loss, HBeAg seroconversion and virologic response (< 200 copies/mL of HBV DNA) were 82.8, 23.5, 11.8, and 48.3%, respectively, at week 52 of treatment. Lower pre-treatment mean HBV DNA level was the only significant factor associated with negative HBV DNA after ADV therapy. Six (20.7%) patients had clearance of LAM-resistant YMDD variants with replacement by the wild type HBV at week 52. The rtN236T, rtA181V/T and rtI233V were not identified before ADV therapy and the genotypic mutation of rtN236T was detected in one (3.4%) patient. In conclusion, the 52-week ADV treatment for patients with LAM-resistant HBV variants significantly achieved normalization of ALT levels, reduced serum HBV DNA levels and induced HBeAg loss and seroconversion. The emergence of ADV-resistant mutations seemed rare at weeks 52.
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Sequence Data
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-
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