AIM: To investigate the incidence of de novo hepatitis B virus(HBV) infection after pediatric living donor liver transplantation(LDLT) and to analyze the risk factors associated with this de novo HBV infection. METHODS: The clinical and laboratory data of children who underwent LDLT from June 2010 to September 2012 in First Center Hospital in Tianjin, China, were retrospectively included in the study. Intrahepatic HBV DNA in donors and recipients was quantified by realtime polymerase chain reaction using DNA extracted from formalin-fixed, paraffin-embedded tissues. RESULTS: Between June 2010 to September 2012, 32 consecutive pediatric patients underwent LDLT in our institute. Thirty LDLT patients(13 girls and 17 boys) were followed up for a median of 15 mo, of whom 53.3%(16/30) were hepatitis B core antibody(HBcAb) positive and 36.7%(11/30) were hepatitis B surface antibody(HBsAb)/HBcAb positive before transplantation. Sixteen of the children received HBcAb-positive allografts, and 43.7%(7/16) of the grafts were found to be intrahepatic HBV DNA positive. De novo HBV infection developed in 16.1%(5/30) of the children within a median of 11 mo after transplantation. All five of the HBV-infected children had received HBcAb-positive allografts, four of which were intrahepatic HBV DNA positive. Two of the children developed de novo HBV infection despite the preoperative presence of both HBsAb and HBcAb CONCLUSION: In pediatric recipients, positive intrahepatic HBV DNA in allografts could be a risk factor for de novo HBV infection from HBcAb-positive allografts. HBsAb/HBcAb positivity in pediatric LDLT patients before transplantation exhibited only weak effectiveness in protecting them against de novo HBV infection from HBcAb-positive allografts. A: To investigate the incidence of no hepatitis hepatitis B virus (HBV) infection after pediatric living donor liver transplantation (LDLT) and to analyze the risk factors associated with this de novo HBV infection. METHODS: The clinical and laboratory data of children who underwent LDLT from June 2010 to September 2012 in First Center Hospital in Tianjin, China, were retrospectively included in the study. Intrahepatic HBV DNA in donors and recipients was quantified by realtime polymerase chain reaction using DNA extracted from formalin-fixed, paraffin-embedded tissues. RESULTS: Between June 2010 and September 2012, 32 consecutive pediatric patients underwent LDLT in our institute. Thirty LDLT patients (13 girls and 17 boys) were followed up for a median of 15 months, of whom 53.3% (16/30) were hepatitis Sixteen of the children received HBcAb-positive allografts, and 43.7% (11/30) were positive for B hepatitis B surface antibody (HBsAb) / HBcAb. 7% (7/16) of the grafts were found to be intrahepatic HBV DNA positive. De novo HBV infection developed in 16.1% (5/30) of the children within a median of 11 months after transplantation. All five of the HBV- Two of the children developed de novo HBV infection despite the preoperative presence of both HBsAb and HBcAb CONCLUSION: In pediatric recipients, positive intrahepatic HBV DNA in allografts could be a risk factor for de novo HBV infection from HBcAb-positive allografts. HBsAb / HBcAb positivity in pediatric LDLT patients before death plans only weak effectiveness in protecting them against de novo HBV infection from HBcAb-positive allografts.