Eminler, A. T.Karkucak, M.Gurel, S.Ayyildiz, T.Gulten, T.Irak, K.Yakut, T.2024-05-192024-05-1920230043-31442309-5830https://doi.org10.7727/wimj.2016.155https://hdl.handle.net/20.500.12713/5126Objective: Mannose-binding lectin (MBL) has become a popular molecule in investigations on basic and clinical gastroenterology and contributed to new approaches to the understanding of infectious and immune diseases associated with intestine and liver. The aim of the present study was to investigate the association between codon 54 polymorphisms in MBL2 gene coding MBL and predisposition to fibrosis in patients with viral hepatitis B and C. Methods: One hundred patients with chronic hepatitis (70 hepatitis B, 30 hepatitis C) who underwent liver biopsy and 100 healthy controls with no known chronic disease were included in the study. Patients in both viral hepatitis groups were divided into two groups according to their fibrosis scores with Ishak scoring system. The polymerase chain reaction-restriction fragment length polymorphism method was applied to determine the MBL2 codon 54 polymorphisms. For the statistical analysis, the level of significance was set at p < 0.05. Results: No significant differences in allele frequencies for any polymorphism were observed between patients and controls, although the G allele was more frequent in the patient groups (p > 0.05). In the comparison in terms of G and A alleles between two groups, hepatitis B patients in Group-II (group with high fibrosis score) were found to have a significantly higher frequency of A alleles (p = 0.027). Conclusion: Although it is accepted that MBL2 polymorphism plays a part during hepatitis B virus and hepatitis C virus infections, larger studies investigating the relation between MBL2 polymorphism and disease progression, and treatment are required.eninfo:eu-repo/semantics/openAccessFibrosisHepatitis BHepatitis CMbl2 GenePolymorphismAssociation between Mannose-Binding Lectin 2 Gene Polymorphism and Liver Fibrosis in Patients with Chronic Viral HepatitisArticle701712WOS:001111167400003N/A10.7727/wimj.2016.155