|
Basic Characteristics of Mutations
|
|
Mutation Site
|
G1896A |
|
Mutation Site Sentence
|
The G1896A pre-core mutation were detected in 29 (57%) which was significantly associated with higher concentration of serum TLR2 in comparison with patients without this mutation (4.8 ± 2.9 versus 3.4 ± 2.2 ng/mL, P = 0.03). |
|
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
|
Hepatitis B, Chronic
|
|
Immune
|
- |
|
Target Gene
|
TLR2
|
|
Clinical and Epidemiological Correlations
|
|
Clinical Information
|
- |
|
Treatment
|
- |
|
Location
|
Iran |
|
Literature Information
|
|
PMID
|
24187552
|
|
Title
|
The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation
|
|
Author
|
Moradzadeh M,Tayebi S,Poustchi H,Sayehmiri K,Shahnazari P,Naderi E,Montazeri G,Mohamadkhani A
|
|
Journal
|
Advances in virology
|
|
Journal Info
|
2013;2013:780319
|
|
Abstract
|
Recognition mechanisms of innate immune response help to improve immunotherapeutic strategies in HBeAg-negative chronic hepatitis B (CHB). Toll-like receptor 2 (TLR2) is an important component of innate immunity. In this study, the frequency of precore mutations of the hepatitis B virus (HBV) and serum TLR2 were evaluated in CHB patients. Fifty-one patients with chronic hepatitis B, negative for HBeAg and detectable HBV DNA, were examined for the presence of mutations in pre-core region of HBV genome by direct sequencing. Serum TLR2 was measured by enzyme-linked immunosorbent assay. Interactions of truncated HBeAg and TLR2 proteins were evaluated with molecular docking software. The G1896A pre-core mutation were detected in 29 (57%) which was significantly associated with higher concentration of serum TLR2 in comparison with patients without this mutation (4.8 +/- 2.9 versus 3.4 +/- 2.2 ng/mL, P = 0.03). There was also a significant correlation between serum ALT and TLR-2 (r = 0.46; P = 0.01). Docking results illustrated residues within the N-terminus of truncated HBeAg and TLR2, which might facilitate the interaction of these proteins. These findings showed the dominance of G1896A pre-core mutation of HBV variants in this community which was correlated with serum TLR2. Moreover TLR2 is critical for induction of inflammatory cytokines and therefore ALT elevation.
|
|
Sequence Data
|
-
|
|
|