|
Basic Characteristics of Mutations
|
|
Mutation Site
|
G1896A |
|
Mutation Site Sentence
|
Precore (G1896A) and core-promoter (A1762T/G1764A) mutations were more frequent in patients with fulminant than acute self-limited hepatitis (53% vs. |
|
Mutation Level
|
Nucleotide level |
|
Mutation Type
|
Nonsense mutation |
|
Gene/Protein/Region
|
PreC |
|
Standardized Encoding Gene
|
C
|
|
Genotype/Subtype
|
- |
|
Viral Reference
|
-
|
|
Functional Impact and Mechanisms
|
|
Disease
|
Acute Hepatitis B
|
|
Immune
|
- |
|
Target Gene
|
-
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
Y |
|
Treatment
|
- |
|
Location
|
Japan |
|
Literature Information
|
|
PMID
|
16871568
|
|
Title
|
Influence of genotypes and precore mutations on fulminant or chronic outcome of acute hepatitis B virus infection
|
|
Author
|
Ozasa A,Tanaka Y,Orito E,Sugiyama M,Kang JH,Hige S,Kuramitsu T,Suzuki K,Tanaka E,Okada S,Tokita H,Asahina Y,Inoue K,Kakumu S,Okanoue T,Murawaki Y,Hino K,Onji M,Yatsuhashi H,Sakugawa H,Miyakawa Y,Ueda R,Mizokami M
|
|
Journal
|
Hepatology (Baltimore, Md.)
|
|
Journal Info
|
2006 Aug;44(2):326-34
|
|
Abstract
|
The outcome of acute hepatitis B virus (HBV) infection is variable, influenced by host and viral factors. From 1982 through 2004, 301 patients with acute HBV infection entered a multi-center cross-sectional study in Japan. Patients with fulminant hepatitis (n = 40) were older (44.7 +/- 16.3 vs. 36.0 +/- 14.3 years, P < .0017), less predominantly male (43% vs. 71%, P = .0005), less positive for hepatitis B e antigen (HBeAg) (23% vs. 60%, P < .0001), less infected with subgenotype Ae (0% vs. 13%, P < .05), and more frequently with Bj (30% vs. 4%, P < .0001) than those with acute self-limited hepatitis (n = 261). Precore (G1896A) and core-promoter (A1762T/G1764A) mutations were more frequent in patients with fulminant than acute self-limited hepatitis (53% vs. 9% and 50% vs. 17%, P < .0001 for both). HBV infection persisted in only three (1%) patients, and they represented 2 of the 23 infected with Ae and 1 of the 187 with the other subgenotypes (9% vs. 0.5%, P = .032); none of them received antiviral therapy. In multivariate analysis, age 34 years or older, Bj, HBeAg-negative, total bilirubin 10.0 mg/dL or greater, and G1896A mutation were independently associated with the fulminant outcome. In in vitro transfection experiments, the replication of Bj clone was markedly enhanced by introducing either G1896A or A1762T/G1764A mutation. In conclusion, persistence of HBV was rare (1%) and associated with Ae, whereas fulminant hepatitis was frequent (13%) and associated with Bj and lack of HBeAg as well as high replication due to precore mutation in patients with acute HBV infection.
|
|
Sequence Data
|
-
|
|
|