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  • Hepatitis B virus  (2)
  • Tree shrews  (1)
  • Springer  (2)
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  • Springer  (2)
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  • 1
    ISSN: 1432-1335
    Keywords: Hepatitis B virus ; Infection, experimental ; Tree shrews ; HB vaccine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tree shrews (Tupaia belangeri chinenesis) can be experimentally infected with human hepatitis B virus (HBV) by inoculation with human serum positive for HBV, the experimental infection rate being 55.21%. Successive infections have been passed through five generations among the tree shrews inoculated with HBV-positive sera from the infected animals, the average infection rate being 94.0%. The experimental infection of tree shrews with HBV may be prevented by immunization with hepatitis B vaccine, the protection rate being 88.89%. Standard serum containing HBV at 108 CID (chimpanzee infection dose)/ml, was diluted 10−6, 10−7, 10−8, 10−9, and 10−10 and produced infection rates of 80.0%, 88.8%, 66.7%, 55.6% and 42.9% respectively. Thus the CID50 in tree shrews may reach a dilution of 10−9, which shows that tree shrews are sensitive to HBV infection. These results successfully establish tree shrews as a reliable and useful animal model for research on HBV infection and its relation to hepatocarcinogenesis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1335
    Keywords: Hepatocellular carcinoma ; Hepatitis B virus ; Aflatoxin B1 ; Tree shrew
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract On the basis of the successful establishment of an animal model in tree shrews experimentally infected with human hepatitis B virus (HBV), a study on the hepatocarcinogenic effects of HBV and/or aflatoxin B1 (AFB1) was conducted. The results showed that the incidence of hepatocellular carcinoma (HCC) was significantly higher in the animals both infected with HBV and exposed to AFB1 (52.94%) than in those solely infected with HBV (11.11%) or exposed to AFB1 (12.50%). No HCC of precancerous lesions were found in the controls that were neither HBV-infected nor AFB1-exposed. Precancerous lesions, including liver cell dysplasia and enzyme-altered hyperplastic hepatocyte foci, were observed before the occurrence of HCC, and the frequency of their appearance correlated well with the incidence of HCC. HBV DNA and the protein it encodes were detected in the cancer cells and/or the surrounding hepatocytes. Integration of HBV DNA inot the host liver genome was found during hepatocarcinogenesis among the animals infected by HBV. These results suggest that exposure to HBV and AFB1 may play a synergistic role in the development of HCC, and support the viewpoint of an aetiological relationship between HBV and HCC.
    Type of Medium: Electronic Resource
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