|
Basic Characteristics of Mutations
|
|
Mutation Site
|
G1896A |
|
Mutation Site Sentence
|
A mutation at nucleotide 1896 (G1896A) is the most common cause for the loss of HBeAg. |
|
Mutation Level
|
Nucleotide level |
|
Mutation Type
|
Nonsense mutation |
|
Gene/Protein/Region
|
PreC |
|
Standardized Encoding Gene
|
C
|
|
Genotype/Subtype
|
D |
|
Viral Reference
|
-
|
|
Functional Impact and Mechanisms
|
|
Disease
|
-
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
- |
|
Treatment
|
- |
|
Location
|
- |
|
Literature Information
|
|
PMID
|
26119876
|
|
Title
|
Hepatitis B "e" antigen-mediated inhibition of HBV replication fitness and transcription efficiency in vitro
|
|
Author
|
Samal J,Kandpal M,Vivekanandan P
|
|
Journal
|
Virology
|
|
Journal Info
|
2015 Oct;484:234-240
|
|
Abstract
|
A mutation at nucleotide 1896 (G1896A) is the most common cause for the loss of HBeAg. In contrast to clinical data, cell culture studies report a high-replicating phenotype for the G1896A mutant. Differences between the wild-type and the G1896A mutant in early steps of HBV replication including the synthesis of pre-genomic RNA and transcripts have not been investigated. The G1896A mutant is associated with higher replication fitness, transcription efficiency and higher levels of secreted HBsAg than the wild-type. Interestingly, trans-complementation of the G1896A mutant with HBeAg lowers the replication fitness and transcriptionefficiency to levels comparable to that of the wild-type. Our results highlight the role of HBeAg in modulating the early steps in HBV replication. In sum, our findings highlight the role of HBeAg in regulating hepatitis B virus replication fitness and transcription efficiency and new insights on the early steps of replication in the G1896A mutant.
|
|
Sequence Data
|
-
|