|
Basic Characteristics of Mutations
|
|
Mutation Site
|
G1899A |
|
Mutation Site Sentence
|
There were 30 patients in all with the latter mutation, nine of whom had the G1899A change also. All G1862T variants were free from either the BCP or precore stop codon mutations. l with the latter mutation, nine of whom had the G1899A change also. |
|
Mutation Level
|
Nucleotide level |
|
Mutation Type
|
Nonsynonymous substitution |
|
Gene/Protein/Region
|
PreC |
|
Standardized Encoding Gene
|
C
|
|
Genotype/Subtype
|
B |
|
Viral Reference
|
J02203; M38454;M54923
|
|
Functional Impact and Mechanisms
|
|
Disease
|
Fulminant Hepatitis B
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
Y |
|
Treatment
|
- |
|
Location
|
China |
|
Literature Information
|
|
PMID
|
12185284
|
|
Title
|
Detection and significance of a G1862T variant of hepatitis B virus in Chinese patients with fulminant hepatitis
|
|
Author
|
Hou J,Lin Y,Waters J,Wang Z,Min J,Liao H,Jiang J,Chen J,Luo K,Karayiannis P
|
|
Journal
|
The Journal of general virology
|
|
Journal Info
|
2002 Sep;83(Pt 9):2291-2298
|
|
Abstract
|
The prevalence of a G1862T variant of hepatitis B virus (HBV) has been investigated in patients with fulminant hepatitis and chronic liver disease, using primer mismatch amplification, followed by restriction fragment length polymorphism analysis. This variant was five times more common in patients with fulminant hepatitis (13.7%, 7 of 52) than in chronic carriers (2.5%, 2 of 81). The G-->T substitution at position 1862 leads to an amino acid change in codon 17 of the precore protein of the virus, which is part of a signal peptidase recognition motif. Variants with this mutation were only seen in patients infected with genotype B. In vitro translation experiments showed that this variant has greatly reduced capacity to produce hepatitis B e antigen (HBeAg) from its precore protein precursor. Furthermore, 88.5% of patients with fulminant hepatitis had mutations that are known to be associated with abrogated or reduced production of HBeAg. This suggests that, following HBV infection, the absence or reduced amounts of HBeAg may be a contributing factor in fulminant disease.
|
|
Sequence Data
|
AF495662–AF495713
|