Genotypic features of HBV, such as viral genotypes and mutations, were strongly associated with HBV pathogenesis as well as the pre- and post- LT clinical outcomes. To our knowledge, the present study was the largest series extensively evaluated the impact of HBV virological characteristics on viral relapse after LT. In contrast to pre-S deletions, the other virological factor, such as precore/core variants, was not found to be associated with hepatitis B relapse in this study. Similar findings were reported by Lo et al and Gaglio et al, indicating that precore/core mutations did not influence hepatitis B relapse or outcome. On the other hand, the viral genotype has been reported to have impact on patient’s outcome in LT. In view of HBV relapse after LT, Lo et al reported that the cumulative rate of viral breakthrough due to LAM-resistance at 3 years was 4% for genotype B and 21% for genotype C. However, Gaglio et al reported one of 8 patients with genotype B had HBV relapse compared to one of 18 patients with genotype C. Our data also supported that genotype did not influence the outcome of HBV relapse after LT. The major concern in the presented study is the relatively high rate of HBV relapse after LT. In this study, hepatitis B relapse was defined as reappearance of HBsAg. As such, 33 over 150 patients met the criteria during a median follow-up period of more than 3 years. However, if a more stringent definition was adopted, such as reappearance of both HBsAg and HBV-DNA, only 12% of our patients were considered hepatitis B relapse. The high incidence of HBV relapse might be related to our antiviral prophylaxis. In the present study, only short-term HBIG was used during the first week after LT. The viral DNA was not detected initially because viral replication was effectively inhibited by LAM. Fifteen of 33 patients with HBsAg relapse remained HBV-DNA negative at the end of follow-up with normal liver function. Unfortunately, prolonged usage of LAM resulted in drug resistance in 15 of 18 HBV-DNA relapse patients. According to the presented study, two independent risks were identified for HBV relapse after LT. As such, only 6.6% of our patients in the low risk group experienced hepatitis B relapse, suggesting the current strategy might be adequate for the low risk patients. However, more aggressive prophylactic protocol should be applied for those patients with one or more risks, such as long-term HBIG or replacement of LAM by Entecavir. Additionally, with the availability of a more potent and state-of the-art antiviral regimen, such as tenofovir or entecavir, the need for continuous HBIG-prophylaxis is heavily challenged. In conclusion, by analyzing preoperative clinical, virological and histopathological factors, we discovered that high viral load and LFpreSDel mutation were two independent predictors for hepatitis B relapse after LT. In patients presented with neither risk factor, it might be adequate to use short-term HBIG and life-long LAM prophylaxis, whereas more aggressive prophylactic strategy should be considered if patients were presented with one or both risk factors. Increased survival of very premature infants has been accompanied by an increased incidence of bronchopulmonary dysplasia. In the ‘‘new BPD,’’ there are larger and fewer alveoli, as well as poorly formed secondary crests, indicating interference with septation. Alveolar septa are thickened with collagen and a-smooth muscle actin, transforming growth factor -b-positive myofibroblasts. Adenoviral transfer of the TGF-b gene to newborn rat lungs induces changes consistent with BPD, including excess matrix deposition and large undeveloped pre-alveolar saccules.