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From: TSS ()
P03.138 According to biochemical and epidemiological findings bovine spongiform encephalopathy (BSE) was transmitted to humans causing variant Creutzfeldt Jakob disease (vCJD). Previous studies have shown intracerebral (i.c.) transmission of BSE affected brain from cattle can cause TSEs in cynomolgus macaques (M. fascicularis). The lesion profile resembles that of vCJD. Recently, oral infection of M. fascicularis with macaque-adapted BSE material was reported. In cooperation with five European partners a quantitative study for the transmission of the BSE agent to M. fascicularis was initiated to assess the risk of vCJD infection in humans through contaminated food products (EU study QLK1-CT-2002-01096). Titration was performed orally and intracerebrally to determine the minimal infectious dose for cynomolgus monkeys. Here we report the outcome of the intracerebral infection with 50 mg BSE brain homogenate in six non-human primates. All animals showed clinical symptoms of TSE after an average of 1100 days. Using immunohistological and biochemical methods prion protein (PrP) deposits were confirmed in the brains of all animals. Using Western blot analysis the glycosylation pattern was compared to the inoculum and to the pattern of different CJD subtypes. Simian PrPres was detected with the monoclonal anti prion antibody 11C6, which revealed a higher sensitivity in comparison to 12F10 http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
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