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Changes of hepatitis B virus DNA in liver and serum caused by recombinant leukocyte interferon treatment: Analysis of intrahepatic replicative hepatitis B virus DNA
Author(s) -
Yokosuka Osamu,
Omata Masao,
Imazeki Fumio,
Okuda Kunio,
Summers Jesse
Publication year - 1985
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840050505
Subject(s) - virology , hepatitis b virus , virus , liver biopsy , hepatitis b virus dna polymerase , interferon , biology , hepatitis , hepatitis c virus , hepatitis b , viral transformation , hbeag , hepadnaviridae , hepatitis b virus pre beta , medicine , biopsy , pathology , hbsag
Twenty patients with HBeAg‐positive chronic liver disease were given large doses of recombinant leukocyte interferon for 4 weeks. Changes of hepatitis B virus DNA in livers and sera were analyzed by the molecular hybridization technique in paired biopsies obtained before and 2 weeks after treatment. Serum hepatitis B virus DNA was examined before, during and after the treatment until 4 weeks post‐interferon. Analysis of hepatic hepatitis B virus DNA revealed species that appeared to represent various forms of replicative hepatitis B virus DNA, i.e., relaxed circular, linear, supercoiled and single‐stranded hepatitis B virus DNA, respectively. No evidence of integration of hepatitis B virus DNA in genomic DNA was obtained. Of 15 cases which were positive for hepatic hepatitis B virus DNA before treatment and in which paired biopsies were obtained, hepatic hepatitis B virus DNA became negative in 4, decreased in 5 and unchanged in 6. Among several types of replicative viral DNA in liver tissue, supercoiled hepatitis B virus DNA tended to remain after other forms were reduced. A close correlation between hepatic and serum hepatitis B virus DNA was found in 37 liver biopsy samples and corresponding sera. These results indicate that interferon treatment reduces serum hepatitis B virus levels by inhibiting viral replication in the liver and that persistence or reappearance of hepatitis B virus in serum after interferon is associated with replication.