Association of Mannose Binding Lectin Polymorphism with Hepatitis C Infection in Northwest of Iran

authors:

avatar Mohammad H. Somi 1 , * , avatar Mohammad Asgharzadeh 2 , avatar Sara Farhang 2 , avatar Rasoul Estakhry 2 , avatar Ali A. Pouri 2

Associate Professor of Gastroenterology, Liver and Gastrointestinal Disease Research Center, Tabriz University of Medical Sciences, mhosseinsina@yahoo.com, Azarbayejan-e-Sharghi, IR.Iran
Associate Professor of Gastroenterology, Liver and Gastrointestinal Disease Research Center, Tabriz University of Medical Sciences, Azarbayejan-e-Sharghi, IR.Iran
Hepatitis Monthly: Vol.6, issue 2; 53-57
article type: Research Article
received: April 7, 2006
accepted: April 28, 2006

How To Cite Somi M, Asgharzadeh M, Farhang S, Estakhry R, Pouri A. Association of Mannose Binding Lectin Polymorphism with Hepatitis C Infection in Northwest of Iran. Hepat Mon. 2006;6(2): 53-57. 

Abstract

Background and Aims: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.
Methods: 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.
Results: 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.
Conclusions: 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.

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