Advances in the understanding of hepatitis B viral infection are a major accomplishment in modern hepatology. In three decades we have progressed from rather vague clinical concepts to a remarkably complete virology of hepatitis B virus (HBV), primary prevention with recombinant vaccines, and some effective antiviral treatments. This progress is especially important for children because it provides hope for preventing severe HBV associated liver disease. It is already evident that the best way to deal with hepatitis B infection is to avoid it altogether. The effectiveness of neonatal active with passive vaccination in preventing vertical transmission of HBV infection is on the order of 90–95%. Studies from Taiwan show that universal immunisation leads to reduced prevalence of HBV infection and a significantly lower incidence of hepatocellular carcinoma (HCC) in childhood.1

What about children who already have chronic HBV infection? Treatment with interferon α is effective in approximately one-third, where success denotes that active viral replication has ceased, HBeAg (hepatitis B e antigen) to anti-HBe (antibody to HBeAg) seroconversion has taken place, and serum HBV DNA is undetectable by hybridisation techniques. In a large randomised controlled paediatric clinical trial,2 18 of 70 (26%) children had HBeAg seroconversion during the 24 weeks of treatment or within 24 weeks of stopping treatment. Over the same 48 weeks, eight of 74 untreated control patients had spontaneous HBeAg seroconversion. An additional five children in the original treatment group had seroconversion 49–72 weeks after starting treatment: thus the overall response rate was 35%. There were no late spontaneous responses in the control group but the numbers were very small due to trial design. Drug induced and spontaneous HBeAg seroconversion were equally durable.

Interferon α treatment has limitations. It is most effective if commenced when serum alanine aminotransferase …