Abstract
THE NATURAL history of chronic hepatitis B virus (HBV) infection is one of progression from a replicative to a nonreplicative stage.1The former is characterized by high serum titers of hepatitis B surface antigen (HBsAg), DNA polymerase and HBV-DNA, and by the presence of hepatitis B e antigen (HBeAg). Patients in this stage of infection have significant inflammatory activity on liver biopsy specimen and usually demonstrate elevated serum aminotransferase levels. The nonreplicative stage is associated with low levels or absence of HBV-DNA, with the presence of antibody to HBeAg, and quiescent biochemical test values and liver histology. Conversion fromthe replicative to the nonreplicative phase of HBV infection is generally a function of time, HBeAg-positive patients losing HBeAg at the rate of about 5% per year.2 It has recently been recognized that remission of active viral turnover in chronic hepatitis B need not be permanent, and that reactivation
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