Mannose binding lectin gene haplotype in Iranian patients with hepatitis C infection

Persistent infection with hepatitis C virus [HCV] leads to liver cirrhosis [LC] and often to liverm cancer. Mannose binding lectin [MBL] is a C-type serum lectin, which plays an important role in innate immunity by activating the classical complement pathway. Variants of the MBL have been shown to be associated with low serum concentrations of the protein and to predispose to bacterial, fungal and viral infections. This study was undertaken to investigate the association between polymorphisms of MBL gene and hepatitis C virus infection. We determined genotypes of two promoters and three exon 1 SNPs in mbl2 by SSP-PSR and grouped these genotypes according to related amount of functional MBL production in 100 patients infected with hepatitis C virus and 100 healthy blood donors in Iranian population. MBL gene mutations were determined by means of polymerase chain reaction and restriction fragment length polymorphism analyses. genotypes XA/O or O/O were significantly more frequent among patients infected with hepatitis C virus, where YA/YA genotype was more common among donors. Frequency of alleles X, Y, H and L did not have a significant difference between the two groups as well as alleles HYA, LYA nor LXA. MBL may be one of the factors that influence the course of HCV infection. Additional study on subjects at a high risk for infection with hepatitis C may clarify the role of carriage for the variant allele of mbl2 in a life-long risk of infection

Association of mannose binding lectin polymorphism with hepatitis C infection in northwest of Iran

Persistent infection with hepatitis C virus leads to liver cirrhosis and often to liver cancer. Mannose binding lectin is a C-type serum lectin, which plays an important role in innate immunity by activating the classical complement pathway. Variants of the mannose binding lectin have been shown to be associated with low serum concentrations of the protein and to predispose the subjects to bacterial, fungal and viral infections. This study was undertaken to investigate the association between hepatitis C virus infection and polymorphisms of mannose binding lectin gene. We assessed the single nucleotide polymorphism of mannose binding lectin in exon 1, at codon 52, codon 54 and codon 57 in 100 patients infected with hepatitis C virus and 100 controls in Iranian population. Mannose binding lectin gene mutations were determined by means of polymerase chain reaction and restriction fragment length polymorphism analyses. The occurrence of the codon 54 mutation was significantly higher in patients [OR 3.53, CI 95%: 1.94-6.44, p<0.005]. No significant difference in the frequency of codon 52 and 57 mutations was observed between patient and control groups. Mannose binding lectin may be one of the factors that influence the course of HCV infection. Our results suggest that heterozygous carriage of the variant allele of codon 54 of mannose binding lectin is associated with hepatitis C virus infection in our cases. This may not be true about codons 52 and 57 mutations