Genetic variants associated with susceptibility to mother-to-child transmission of hepatitis B virus

Objective The mechanisms of immune tolerance to hepatitis B virus (HBV) in children infected perinatally or early in infancy still remain unclarified. We aimed to study the genetic variants of immune factors implicated in viral-host interaction in children who were born to HBV-positive mothers and who had different clinical outcome. Methods Mannose-binding lectin gene (mbl2) codon 54, codon 57, and promoter 221 variants, tumor necrosis factor a (TNF-alpha) 308G/A, and vitamin D receptor (VDR) ApaI and TaqI genotypes were analyzed in three groups of children born to HBV-positive mothers: children with chronic infection (n=33), those with resolved infection (n=36), and those naive for HBV (n=33). Results TNF-alpha - 308G allele frequency was found to be increased in children with chronic infection compared with children who were not affected by HBV [risk ratio (RR) 1.12, 95% confidence interval (CI) 1.0-1.25; P=0.050]. The VDR ApaI A allele tended to be more frequent in children with chronic infection than in those with resolved HBV infection (RR 1.27, 95% CI 0.95-1.67; P=0.071). The VDR ApaI a allele in ApaI and TaqI joint haplotype alpha T was more frequent in children with resolved infection than in those with chronic infection (RR 1.74, 95% CI 0.97-3.13; P=0.049). Conclusion Our results suggest that TNF-alpha and vitamin D pathways may be involved in the susceptibility to and outcome of HBV infection acquired early in life. Eur J Gastroenterol Hepatol 24: 1185-1190 (c) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.