Mannose-binding lectin polymorphisms and outcome of patients with chronic hepatitis C
Chronic infection with hepatitis C virus (HCV) often leads to chronic active inflammation and fibrosis of the liver. Host factors may contribute to the variable natural history and outcome. Deficiency of mannose-binding lectin (MBL) protein, a pattern recognition molecule involved in innate immunity, is determined by variant alleles in mbl2 gene promoter and exon-1 regions. To determine whether mbl2 gene polymorphisms affect the course of HCV infection we investigated the association between mbl2 gene polymorphisms and HCV infection in 80 Caucasian HCV-infected patients. Mannose-binding lectin (mbl2) gene mutations were determined by using polymerase chain reaction (PCR) and restriction fragment length polymorphisms (RFLPs) analysis. Non-A haplotype was found more frequently within chronic active hepatitis (CAH) patient genotypes rather than chronic inactive hepatitis (CIH) patient genotypes (p=0.0374, OR=0.3255, 95%CI=0.1172 to 0,9039). Five patients were found homozygous for codon #54 mutations and four of them had advanced grade of fibrosis (ISHAK index ≥4) (p=0.1774, OR=5.077, 95%CI=0.5344 to 48.233). In conclusion mbl2 gene polymorphisms may have a role in determining the progression of chronic HCV infection.