The infection and its management A high proportion of hepatitis B virus (HBV) infections, which lead to chronicity rather than being resolved, are infections occuring at birth or early childhood[1]. Despite successful vaccination programs, the number of chronic carriers increases worldwide. Hepatocellular carcinoma (HCC) develops late in the course of a chronic infection, with its concomitant overall decrease in viral replication. However, stages associated with a particularly high risk to develop cancer are not described to this date. A still attractive model for the progression of infection points to a persistence of hepatocytes that contain chromosomally integrated, as well as free viral DNA, over hepatocytes containing only free replicating DNA[2]. Specifically, it is suggested that the process of integration depends on structural differences of replication complexes, whereby newly-synthesized viral DNA is rendered accessible to nucleases. Apart from integrated viral DNA, thus far identified only in tissue material, a marker characteristic of a chronic infection is still lacking. Stages of cryptic replicative or non-replicative HBV infection have been described[3], and are thought to represent either late stages of a chronic infection or cases of infection that has resolved without a preceding phase of chronicity[4].