Association between CCR5 Promoter Polymorphisms and Hepatitis B Virus Infection.
- Author:
Hye Young CHANG
1
;
Sang Hoon AHN
;
Do Young KIM
;
Jeon Soo SHIN
;
Yong Soo KIM
;
Sun Pyo HONG
;
Hyun Jae CHUNG
;
Soo Ok KIM
;
Wang Don YOO
;
Kwang Hyub HAN
Author Information
1. Department of Internal Medicine, Yonsei University College of Medicine, Korea. gihankhys@yumc.yonsei.ac.kr
- Publication Type:Original Article ; English Abstract
- Keywords:
Chemokine receptor 5;
Hepatitis B virus;
Genetic polymorphism
- MeSH:
Adult;
English Abstract;
Female;
Genetic Predisposition to Disease;
Genotype;
Hepatitis B/*genetics;
Hepatitis B virus/genetics;
Humans;
Male;
Middle Aged;
*Polymorphism, Genetic;
Promoter Regions (Genetics)/*genetics;
Receptors, CCR5/*genetics
- From:The Korean Journal of Hepatology
2005;11(2):116-124
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: Immunogenetic factors may play a role in determining the susceptibility of an individual to viral infection. CCR5 promoter polymorphisms are known to be associated with HIV infection. However, there has been no report on the association between CCR5 promoter polymorphism and HBV infection. Therefore, we investigated the relationship between the CCR5 promoter polymorphism and HBV infection. METHODS: A total of 377 patients were classified into two groups according to their HBV infection status: (1)he spontaneous clearance group (SC); HBsAg (-), anti-HBc (+), anti-HBs (+) (2)he chronic HBsAg (+) carrier group (CC); HBsAg (+), anti-HBc (+), anti-HBs (-). CCR5 polymorphisms were detected by employing matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS)- based SNP scoring assay, termed Restriction Fragment Mass Polymorphism (RFMP), which exploits the differences in molecular masses between the common allele and rare allele bases of interest. RESULTS: We found that the genotype frequencies of CCR5 A59029G significantly differed between the SC group (n=138) and CC group (n=239) (P<0.05). The CCR5 59029A allelic genotype was associated with an increased risks of chronic infection rather than spontaneous clearance (P=0.002), and the presence of the CCR5 59029G allele was significantly associated with the spontaneous clearance of HBV (P=0.001). Strong linkage disequilibrium between the CCR5-59029 and the CCR5-59353 polymorphic variants was identified. None of the 377 subjects had the CCR5-32 bp deletion mutation. CONCLUSIONS: The CCR5 promoter polymorphisms at position 59029 might play a role in the clearance of HBV infection. This primary experimental evidence needs further studies to clarify the clinical usefulness of CCR5 promoter polymorphisms as a target for the screening or treatment of HBV infection.
