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BSE Case Associated with Prion Protein Gene Mutation

Figure 1

Analysis of brainstem samples from BSE-infected animals employing various methods.

(A) Hybrid Immunoblot Analysis using enriched samples: Lanes 1–5: monoclonal antibody 6H4 (raised against human PrP residues 144–152), lanes 8–12 monoclonal antibody P4 (raised against ovine PrP residues 89–104): 1 = sheep scrapie control, 2 mg; 2 = classical BSE (2003 U.S. BSE case), 2 mg; 3 = H-type BSE case (2004 U.S. BSE case), 2 mg; 4 = U.S. BSE Alabama case, 1 mg; 5 = U.S. BSE Alabama case, 2.5 mg; 6,7 = protein weight maker; 8 = U.S. BSE Alabama case, 2.5 mg; 9 = U.S. BSE Alabama case, 1 mg; 10 = H-type BSE case (2004 U.S. BSE case), 2 mg; 11 = classical BSE (2003 U.S. BSE case), 2 mg; 12 = sheep scrapie control, 2 mg. (B) Immunohistochemistry of the U.S. BSE Alabama case (H-type BSE) using PrP-specific monoclonal antibody F99/97.6.1. Brainstem at the level of obex was examined. Bar = 35 µm. (C) Immunohistochemistry of a classical BSE case [4] using PrP-specific monoclonal antibody F99/97.6.1. Brainstem at the level of obex was examined. Spongiform changes are found in the area with highly PrPd-positive cells. Bar = 90 µm.

Figure 1

doi: https://doi.org/10.1371/journal.ppat.1000156.g001