We investigated the effect of lamivudine on de novo Hepatitis B infection after pediatric LT. 51 liver transplanted children were included to the study. Eight patients (15.6%) aged 1-13 years, developed de-novo HBV infection median14 months (5-36 months) after LT. Five of them received a liver from antiHBcIgG (+) donor. None of the patients received lamivudine or HBIG prophylaxis after LT. At the time of de novo hepatitis B infection AST and ALT were higher than normal (40 IU/mL) in 3 patients. AntiHbcIgM was positive in 2 of 6 patients tested. HBV viral loads ranged between 7x105 IU/mL-4.2x109 IU/mL. Liver biopsy was available in 4/8 patients. Two patients had chronic portal inflammation, 1 patient had portal mixed type inflammatory cell infiltration, and 1 patient had acute hepatitis histologically. Lamivudine treatment (5 mg/kg/day) was given all 8 patients for median 26 months (7-39 months) following the diagnosis of denovo hepatitis B infection. Only 1 patient out of 8 who received lamivudine for 10 months cleared HBV DNA and HBsAg, and became AntiHBs and AntiHBe positive. This patient had acute hepatitis characterized by elevated AST/ALT (400/500 IU/mL), positive AntiHBcIgM, and acute hepatitis findings in her liver biopsy. Although lamivudine was stopped, this patient remained negative for HBsAg after 1.5 years. In the remaining 7 patients HBV DNA decreased 1-3 Log10 in 4 patients and increased 1-2Log10 in 3 patients. Lamivudine resistance (YMDD mutation) was detected in 2 out of 3 patients whose HBV DNA level increased on 30th and 22nd months of treatment. Lamivudine combined to adefovir dipivoxil in these patients and HBV-DNA decreased 4 Log10. However all these 7 patients remained positive for HBsAg, HBeAg, and negative for AntiHBs and AntiHBe. In conclusion, lamivudine treatment during acute phase of de novo hepatitis B infection was beneficial. Antiviral treatment was not effective in most of our patients who had chronic de novo hepatitis B infection.