Lack of Association between Hepatitis B Virus Infection and Polymorphism of Mannose-Binding Lectin Gene in Korean Population
Lack of Association between Hepatitis B Virus Infection and Polymorphism of Mannose-Binding Lectin Gene in Korean Population
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.
- Catholic University of Korea Korea (Republic of)
- Ajou University Korea (Republic of)
Adult, Male, Hepatitis B virus, Heterozygote, Korea, Polymorphism, Genetic, Genotype, Middle Aged, Hepatitis B, Fibrosis, Mannose-Binding Lectin, Polymorphism, Single Nucleotide, Hepatitis, Lectins, Disease Progression, Humans, Original Article, Female, Codon, Alleles
Adult, Male, Hepatitis B virus, Heterozygote, Korea, Polymorphism, Genetic, Genotype, Middle Aged, Hepatitis B, Fibrosis, Mannose-Binding Lectin, Polymorphism, Single Nucleotide, Hepatitis, Lectins, Disease Progression, Humans, Original Article, Female, Codon, Alleles
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