Mannose-Binding Lectin Polymorphisms in Patients with Hepatitis C Virus Infection

• Published in: Scandinavian journal of gastroenterology 2000, Vol.35 (9), p.960-965
• Main Authors: SASAKI, K, TSUTSUMI, A, WAKAMIYA, N, OHTANI, K, SUZUKI, Y, WATANABE, Y, NAKAYAMA, N, KOIKE, T
• Format: Article
• Language: English
• Subjects: Aged; Biological and medical sciences; Carrier Proteins - genetics; Case-Control Studies; Codon - genetics; Collectins; Female; Hepatitis C, Chronic - genetics; Hepatitis C, Chronic - metabolism; Human viral diseases; Humans; Immunoenzyme Techniques; Infectious diseases; Lectins - genetics; Liver Cirrhosis - metabolism; Liver Cirrhosis - virology; Male; Medical sciences; Middle Aged; Mutation; Polymorphism, Genetic; Polymorphism, Restriction Fragment Length; Viral diseases; Viral hepatitis
• ISSN: 0036-5521; 1502-7708
• DOI: 10.1080/003655200750023039

Background: Persistent infection with hepatitis C virus (HCV) leads to liver cirrhosis (LC) and often to liver cancer. Little is known about host factors that determine the variable natural history. Mannose-binding lectin (MBL) is an important constituent of the innate immune system. In white patients there is an association between codon 52 mutation of the MBL gene and persistent hepatitis B virus (HBV) infection. To determine whether MBL gene polymorphisms affect the course of HCV infection, we investigated the association between MBL gene polymorphisms and HCV infection in Japanese subjects. Methods: Fifty-two HCV-infected Japanese patients (8 with chronic inactive hepatitis (CIH), 31 with chronic active hepatitis (CAH), 13 with LC) and 50 normal controls were studied. MBL gene mutations were determined by means of polymerase chain reaction and restriction fragment length polymorphism analyses. Results: Codon 52 and codon 57 mutations were absent in all subjects. Homozygous mutation in codon 54 was present in one (0.9%) patient. Heterozygous codon 54 mutation was present in 17 (32%) of the 52 patients and in 21 (41%) of the controls. No significant difference in the frequency of codon 54 mutation was observed between patient and control groups. However, although no significant relationship was observed between MBL polymorphisms and the levels of HCV RNA, all patients with heterozygous or homozygous codon 54 mutations had CAH or LC. In contrast, 8 of the 34 patients without codon 54 mutation remained at CIH. (P = 0.0405). Conclusion: MBL may be one of the factors that influence the course of HCV infection.