Lack of Association between Hepatitis B Virus Infection and Polymorphism of Mannose-Binding Lectin Gene in Korean Population.
10.3346/jkms.2005.20.1.65
- Author:
Jae Youn CHEONG
1
;
Sung Won CHO
;
Sun Kyo LIM
;
Do Hyun SHIN
;
Seung Kew YOON
;
Jong Eun LEE
;
Ki Baik HAHM
;
Jin Hong KIM
Author Information
1. Department of Gastroenterology, Ajou University School of Medicine, Suwon, Korea. sung_woncho@hotmail.com
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Mannose-Binding Lectin;
Hepatitis B;
Polymorphism, Genetic
- MeSH:
Adult;
Alleles;
Codon;
Disease Progression;
Female;
Fibrosis;
Genotype;
Hepatitis;
Hepatitis B/*genetics/*metabolism;
Hepatitis B virus/*metabolism;
Heterozygote;
Humans;
Korea;
*Lectins;
Male;
Mannose-Binding Lectin/*chemistry/*genetics;
Middle Aged;
*Polymorphism, Genetic;
Polymorphism, Single Nucleotide;
Research Support, Non-U.S. Gov't
- From:Journal of Korean Medical Science
2005;20(1):65-69
- CountryRepublic of Korea
- Language:English
-
Abstract:
Mannose-binding lectin (MBL) plays an important role in immune defense. This study was undertaken to investigate the association between hepatitis B virus infection and polymorphisms of MBL gene. We assessed the single nucleotide polymorphism at codon 54 in exon 1 of MBL in patients with hepatitis B virus infection and HBsAg negative controls in Korean population. A total of 498 enrolled subjects was classified into four groups. Group 1; Clearance, Group 2; Inactive healthy carrier, Group 3; Chronic hepatitis, Group 4; Liver cirrhosis. MBL gene polymorphisms at codon 54 led to three genotypes (G/G, G/A, A/A). When we divided subjects into clearance group (group 1) and persistence group (group 2-4), G/G genotype and A-allele carrier were observed in 55.6% and 44.4% in clearance group, 64.8% and 35.2% in persistence group (p=0.081), respectively. When hepatitis B virus persistent cases were divided into inactive healthy carrier (group 2) and disease progression group (group 3 and 4), MBL gene polymorphisms at codon 54 were not related to disease progression (p=0.166). MBL gene polymorphism at codon 54 was not associated with the clearance of hepatitis B virus infection nor progression of disease in chronic hepatitis B virus infection.
