|
Basic Characteristics of Mutations
|
|
Mutation Site
|
Q215H |
|
Mutation Site Sentence
|
Other mutational patterns (rtV173M, rtA181S/V, rtM204I, rtQ215H, rtL229M, rtN238H, rtV84M+rtA181S+rtM204I, rtV84M+rtM204I, rtA181S+rtM204I, rtA181V+rtL229M, rtQ215H+rtN238H) reduced viral replication capacity to different extents. |
|
Mutation Level
|
Amino acid level |
|
Mutation Type
|
Nonsynonymous substitution |
|
Gene/Protein/Region
|
RT |
|
Standardized Encoding Gene
|
P
|
|
Genotype/Subtype
|
B;C |
|
Viral Reference
|
-
|
|
Functional Impact and Mechanisms
|
|
Disease
|
Hepatitis B, Chronic
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
- |
|
Treatment
|
- |
|
Location
|
China |
|
Literature Information
|
|
PMID
|
21056552
|
|
Title
|
Variable influence of mutational patterns in reverse-transcriptase domain on replication capacity of hepatitis B virus isolates from antiviral-experienced patients
|
|
Author
|
Ji D,Liu Y,Si LL,Li L,Chen GF,Xin SJ,Zhao JM,Xu D
|
|
Journal
|
Clinica chimica acta; international journal of clinical chemistry
|
|
Journal Info
|
2011 Jan 30;412(3-4):305-13
|
|
Abstract
|
BACKGROUND: Various mutations in reverse-transcriptase domain (RT) of hepatitis B virus (HBV) polymerase may develop during antiviral therapy. The influence of these mutational patterns on HBV replication capacity remains to be fully clarified. METHODS: Nine clones containing complete HBV genomes were isolated from 5 patients with chronic hepatitis B who had received antiviral treatment. Viral replication capacity was measured by quantitation of HBV replicative intermediates using vector-free transfer of paired mutant and wild-type HBV genomes into human hepatoma cell lines HepG2 and Huh7. HBV pgRNA was quantitated by real-time PCR and Southern blot analysis. RESULTS: A real-time PCR assay with high sensitivity and small variation was developed for quantitation of HBV replicative intermediates. Compared to wild-type counterpart, mutant rtL217P produced 1.98-fold higher replicative intermediate level, and mutant rtM204I+rtL217P increased the replicative intermediate level to 1.20 fold. Other mutational patterns (rtV173M, rtA181S/V, rtM204I, rtQ215H, rtL229M, rtN238H, rtV84M+rtA181S+rtM204I, rtV84M+rtM204I, rtA181S+rtM204I, rtA181V+rtL229M, rtQ215H+rtN238H) reduced viral replication capacity to different extents. CONCLUSIONS: The study offers a practical measurement assay and novel information for replication features of mutant strains; especially, rtL217P substitution likely represents an energetic replication-compensatory mutation.
|
|
Sequence Data
|
EU589344;EU589346;EU570073;EU589335;EU570075;EU560440;EU560441;EU579442;FJ032337
|
|
|