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Veterinary Laboratories Agency (VLA-Lasswade), Pentlands Science Park, Bush Loan, Penicuik, Midlothian EH26 0PZ, UK
Correspondence
Martin Jeffrey
m.jeffrey{at}vla.defra.gsi.gov.uk
Scrapie and bovine spongiform encephalopathy (BSE) are transmissible spongiform encephalopathies (TSEs) or prion diseases affecting domestic and exotic ruminants. In previous immunohistochemical studies, we have shown that different sheep TSE sources may be distinguished by both the proportion of disease-specific prion protein (PrPd) accumulation relative to different cell types in the brain (the ‘PrPd profile’) and by different labelling patterns for PrP peptide sequences within phagocytic cells. In the present study, we have further characterized the intracellular accumulation patterns of PrPd in the lymphoreticular system (LRS) and in the brain of sheep clinically affected with scrapie or BSE. BSE-infected PrPARQ/ARQ sheep of different breeds were compared with scrapie-infected sheep of different PrP genotypes. Cases of BSE infection could be distinguished from scrapie cases by a marked reduction in labelling of PrPd containing the 84–105 amino acid residues in phagocytic cells of the LRS and in neurones and glia of the brain. These results therefore indicate that TSE agent-dependent processing of PrP in specific cell types within the brain and LRS can be used to distinguish between BSE in PrPARQ/ARQ sheep and scrapie in sheep of several PrP genotypes. Three different N-terminal peptide antibody labelling patterns were recognized for different cell types in different tissues of BSE-infected sheep, suggesting that different truncated forms of PrPd are formed following infections with this agent strain. These variations in the cleavage sites of BSE PrPd may be due to cell-specific variation in endosomal–lysosomal digestion or to cell- and tissue-specific differences in BSE PrPd conformation.
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 S. Cronier, H. Laude, and J.-M. Peyrin Prions can infect primary cultured neurons and astrocytes and promote neuronal cell death PNAS, August 17, 2004; 101(33): 12271 - 12276. [Abstract] [Full Text] [PDF]
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K. M. Luhr, E. K. Nordstrom, P. Low, H.-G. Ljunggren, A. Taraboulos, and K. Kristensson Scrapie Protein Degradation by Cysteine Proteases in CD11c+ Dendritic Cells and GT1-1 Neuronal Cells J. Virol., May 1, 2004; 78(9): 4776 - 4782. [Abstract] [Full Text] [PDF]
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S. Lezmi, S. Martin, S. Simon, E. Comoy, A. Bencsik, J.-P. Deslys, J. Grassi, M. Jeffrey, and T. Baron Comparative Molecular Analysis of the Abnormal Prion Protein in Field Scrapie Cases and Experimental Bovine Spongiform Encephalopathy in Sheep by Use of Western Blotting and Immunohistochemical Methods J. Virol., April 1, 2004; 78(7): 3654 - 3662. [Abstract] [Full Text] [PDF]
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L. Gonzalez, S. Martin, and M. Jeffrey Distinct profiles of PrPd immunoreactivity in the brain of scrapie- and BSE-infected sheep: implications for differential cell targeting and PrP processing J. Gen. Virol., May 1, 2003; 84(5): 1339 - 1350. [Abstract] [Full Text] [PDF]
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