In a series of 325 HBV chronically infected children observed over an 18-year period, three developed HCC. These three children were born in southern Italy, a region characterized by a high endemic HBV infection rate; each had been infected perinatally, developed an acute hepatitis, and became a chronic carrier. Two of the three with cirrhosis were HBsAg positive at the time their HCC was detected. The remaining case had seroconverted to HBsAb but HBV-DNA integration could be demonstrated in the absence of cirrhosis; moreover HBV antigens were not expressed in the tissue of this case. The interval between HBV infection and HCC appearance in these three cases ranged from six to 11 years. A similarity between these three Italian cases and the majority of HCC arising in chronically infected children in the Far East is noted.

Thirty‐five children with chronic HBV infection, HBV‐DNA and eAg serum positivity, and HBcAg in liver tissue were treated with lymphoblastoid human interferon alpha with (16 cases) or without (19 cases) prednisolone pretreatment. The patients were double‐blind randomized to receive steroid or placebo for 4 weeks, followed after 2 weeks by 5 or 10 MU/m2 interferon for 12 weeks. The e anti‐e seroconversion rate reached 48%, which is much higher than the spontaneous seroconversion rate. The influence of “prednisolone priming” was not statistically significant. HBeAg clearance was similar in both groups (44% after prednisolone/interferon and 53% after interferon alone). The response to either treatment did not correlate with the pretreatment serum transaminase, HBV‐DNA or degree of histological activity. Interferon was well tolerated, the side effects being less severe than in adults, and never led to suspension of the treatment.

Integrated hepatitis B virus (HBV) DNA sequences were found in neoplastic liver tissue of a hepatitis B surface antigen (HBsAg)-negative child who had previously suffered from HBsAg-positive chronic active hepatitis and was anti-HBs and anti-hepatitis B core (HBc) positive at the time of tumor development. Reintegration pattern was consistent with the presence of a single integration site of the HBV genome into cellular DNA, and clonal proliferation of such infected cells. A normal liver, tested in the same experiment with the same amount of total DNA, was negative for viral DNA sequences. These findings support the possible oncogenic role of HBV in the development of liver cancer, not only in adults, but also in children, even in patients who are negative for HBsAg at the time of tumor diagnosis.