Chronic hepatitis B virus infection in an anti-HBC–nonreactive blood donor: Variant virus or defective immune response?
Jae-Hag Lee
University of California–Davis Medical Center, Sacramento 95817
Search for more papers by this authorTeresa G. Paglieroni
Sacramento Medical Foundation Center for Blood Research Sacramento, California 95816–7089
Search for more papers by this authorCorresponding Author
Paul V. Holland M.D.
Sacramento Medical Foundation Center for Blood Research Sacramento, California 95816–7089
Medical Director/CEO, Sacramento Medical Foundation, Blood Center, 1625 Stockton Blvd., Sacramento, CA 95816–7089===Search for more papers by this authorJerome B. Zeldis
University of California–Davis Medical Center, Sacramento 95817
Search for more papers by this authorJae-Hag Lee
University of California–Davis Medical Center, Sacramento 95817
Search for more papers by this authorTeresa G. Paglieroni
Sacramento Medical Foundation Center for Blood Research Sacramento, California 95816–7089
Search for more papers by this authorCorresponding Author
Paul V. Holland M.D.
Sacramento Medical Foundation Center for Blood Research Sacramento, California 95816–7089
Medical Director/CEO, Sacramento Medical Foundation, Blood Center, 1625 Stockton Blvd., Sacramento, CA 95816–7089===Search for more papers by this authorJerome B. Zeldis
University of California–Davis Medical Center, Sacramento 95817
Search for more papers by this authorAbstract
Viral sequence and host immune response were investigated in an unusual, asymptomatic chronic hepatitis B virus carrier (human leukocyte antigen type A24, Bw61, Bw62, Bw6, DRw11, DRw52, DQw7) who was consistently nonreactive for antibody to HBc and had a normal ALT level over a 5-yr study period. The precore and core region DNA sequences of virus isolated from his serum had seven silent mutations that resulted in no changes in the amino acid sequence of the adr HBsAg subtype. He had no abnormalities in the number of peripheral blood T or B cells and no HBcAg-specific suppressor T cells. His lymphocytes proliferated in vitro in response to phytohemagglutinin, pokeweed mitogen, Staphylococcus aureus and tetanus toxoid but not to recombinant HBcAg. Unlike other HBsAg carriers and hepatitis B virus–immune individuals, his monocytes did not ingest beads coated with HBcAg. Failure to produce antibody to HBc was not due to an hepatitis B virus variant but to a selective immune system defect in this asymptomatic HBsAg carrier. (HEPATOLOGY 1992;16:24–30.)
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