Studies of GB hepatitis agent in tamarins
Article first published online: 6 DEC 2005
Copyright © 1989 American Association for the Study of Liver Diseases
Volume 9, Issue 2, pages 186–192, February 1989
How to Cite
Karayiannis, P., Petrovic, L. M., Fry, M., Moore, D., Enticott, M., McGarvey, M. J., Scheuer, P. J. and Thomas, H. C. (1989), Studies of GB hepatitis agent in tamarins. Hepatology, 9: 186–192. doi: 10.1002/hep.1840090204
- Issue published online: 6 DEC 2005
- Article first published online: 6 DEC 2005
- Manuscript Accepted: 30 JUN 1988
- Manuscript Received: 24 MAR 1988
- Wellcome Trust
Three tamarins (Saguinus labiatus), two of which had previously been infected with hepatitis A virus and parenteral non-A, non-B hepatitis, were inoculated intravenously with the agent of GB hepatitis. All three animals developed alanine aminotransferase abnormalities 2, weeks after inoculation. Peak alanine aminotransferase levels were recorded 4 weeks postinoculation. These declined thereafter but continued to fluctuate at abnormal levels for 32 weeks. Liver biopsies showed liver cell swelling and inflammation with focal necrosis. Portal tracts and areas around central veins were heavily infiltrated with mononuclear cells. A fourth animal (no previous exposure to hepatitis viruses) inoculated with GB was killed on Day 15 postinoculation. Serum and extracts of liver and feces from this day were used as inocula for three other animals. Only the serum and liver extract transmitted GB hepatitis. The fecal specimen did not transmit and a fecal extract taken at a later date from another animal was also noninfectious.
GB hepatitis virus is distinct from the viruses causing Type A and blood-borne non-A, non-B-hepatitis. Although the virus is present in serum and has previously been transmitted per os, it is not shed in feces.