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Kevin M. De Cock, MD, MRCP, DTM&H; Sugantha Govindarajan, MD; Neville Sandford, MB, BS, BScMed, FRACP; Allan G. Redeker, MD

JAMA. 1986;256(10):1329-1331.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

THE NATURAL history of chronic hepatitis B virus (HBV) infection is one of progression from a replicative to a nonreplicative stage.¹ The 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 from the 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 . . . [Full Text PDF of this Article]

Author Affiliations
From the University of Southern California Liver Unit (Drs De Cock, Stanford, and Redeker) and Liver Unit Pathology (Dr Govindarajan), Rancho Los Amigos Medical Center, Downey, Calif. Dr De Cock is now with the Centers for Disease Control, Atlanta.

Footnotes
Reprints not available.

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