Mannose-binding lectin gene polymorphism and chronic hepatitis B infection in children

Saudi J Gastroenterol. 2015 Mar-Apr;21(2):84-9. doi: 10.4103/1319-3767.153825.

Abstract

Background/aims: Mannose-binding lectin (MBL) is a member of innate immune system that activates complement system through lectin pathway. MBL deficiency is associated with susceptibility to infectious diseases. In this study, the relation between MBL gene polymorphism and chronic hepatitis B infection in children is evaluated.

Patients and methods: The study included 67 children with chronic hepatitis B and 99 healthy controls. The hepatitis B patients were divided into immuntolerant, chronic inactive, and treatment groups according to their laboratory findings. MBL gene codon 52, 54, and 57 polymorphisms were studied with polymerase chain reaction in all patients and controls. The associations of MBL gene polymorphism with clinical, laboratory, and histopathologic findings were evaluated.

Results: Homozygous codon 54 polymorphism of MBL was found significantly higher in chronic hepatitis B patients than controls. Rate of the polymorphism was similar in all groups and, responsive and nonresponsive patients in the treatment group.

Conclusions: The hepatitis B patients who are homozygous for codon 54 of MBL are prone to develop chronic infection. Longitudinal studies with larger groups are needed.

MeSH terms

  • Adolescent
  • Child
  • Child, Preschool
  • DNA / genetics*
  • Female
  • Gene Frequency
  • Genotype
  • Hepatitis B, Chronic / genetics*
  • Hepatitis B, Chronic / metabolism
  • Humans
  • Male
  • Mannose-Binding Lectin / genetics*
  • Mannose-Binding Lectin / metabolism
  • Polymerase Chain Reaction
  • Polymorphism, Genetic*

Substances

  • Mannose-Binding Lectin
  • DNA