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Absence of detectable hepatitis B virus DNA in sera and liver of chimpanzees with non‐A, non‐B hepatitis
Author(s) -
Yap S. H.,
Heilings J. A.,
Rijntjes P. J. M.,
van Loon A. M.,
Duermeyer W.,
Stute R.
Publication year - 1985
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.1890150404
Subject(s) - virology , hbsag , hepatitis b , hepatitis b virus , hepatitis , hepadnaviridae , viremia , antibody , immunology , hepatitis d virus , medicine , virus , antigen , hepatitis a , biology
The risk of hepatitis B infections has been reduced by screening of blood donors for hepatitis B surface antigen (HBsAg). However, recipients remain at significant risk of developing post‐transfusion hepatitis. Studies have shown that non‐A, non‐B hepatitis virus(es) are responsible for the majority of post‐transfusion hepatitis infections. In spite of many efforts, these non‐A, non‐B hepatitis viruses have not yet been identified. Epidemiological studies, however, suggest that non‐A, non‐B hepatitis shares many features with hepatitis B. Recently, Wands et al [1982] showed, in chimpanzees infected with non‐A, non‐B hepatitis agents, the presence of antigenemia or viremia by radioimmunoassay with monoclonal antibodies directed toward distinct determinants of HBsAg and by molecular hybridization analysis. They suggested that non‐A, non‐B hepatitis agents may be related, but distinct variant(s) of hepatitis B virus (HBV). In this study, five chimpanzees were inoculated with three different agents that have been shown to transmit non‐A, non‐B hepatitis. The following inocula were used (I) a factor VIII preparation kindly provided by D.W. Bradley, (II) acute phase serum from a chimpanzee infected with the F strain kindly provided by A.J. Zuckerman, and (III) a DS‐antigen serum previously shown by us to transmit non‐A, non‐B hepatitis [Duermeyer et al, 1983]. All chimpanzees developed a rise in transaminase levels between 8 and 10 weeks after inoculation. None of the chimpanzees was positive for any markers of HBV infection. No evidence was obtained of infection with hepatitis A, cytomegalovirus, or Epstein‐Barr virus. One chimpanzee developed chronic liver disease. The presence of HBV DNA in sera and in liver biopsies was studied. HBV DNA hybridizable sequences were not detected in any of the samples collected at different stages of the disease. These findings suggest that the non‐A, non‐B hepatitis agents in our study are not related to HBV.