The goals of treatment of hepatitis B are to prevent progression of the disease or to slow the disease process. Hepatitis B virus (HBV) is a DNA virus which integrates into the host genome. Thus it is difficult to eradicate viraemia. However, it is possible, albeit in a minority, to reduce levels of viraemia to relatively low threshold levels after finite courses of treatment with either interferon alpha or nucleoside analogues, and to lessen the induced necroinflammatory and immune response.¹ Two major forms of active chronic hepatitis B are recognised: wild-type (or hepatitis B e antigen (HBeAg) positive chronic HBV infection) and anti-HBe positive or precore mutant disease. The latter disease is caused by variants of HBV that contain nucleotide substitutions in the core promoter/precore regions of the viral genome.²

Wild-type (HBeAg positive) chronic hepatitis B can be treated with either interferon alpha or nucleoside analogues. Loss of HBeAg and associated suppression of viral replication with pegylated interferon alpha and new nucleoside analogues such as lamivudine, adefovir, tenofovir, telbuvidine, entecavir, and emtricitabine leads to biochemical remission, histological improvement, and in a small percentage, loss of HBsAg.^3–5 Durable responses can occur. Continuous therapy is frequently required for the majority of anti-HBe positive patients with chronic hepatitis B. Thus in most patients, longer term therapy is required to suppress viral replication and …