Figure 2.

Abundant PrP^Sc in heart of 1 bovine spongiform encephalopathy (BSE)–infected rhesus macaque. A) In sodium phosphotungstic acid precipitation of PrP^Sc, followed by Western blotting, highly abundant PrP^Sc was demonstrated in the heart of 1 BSE-infected primate. In this monkey, only the heart contained PrP^Sc. Controls include cardiac muscle spiked with minimal amounts brain of a healthy (–) and prion-diseased (+) primate. All analyses were prepared from 50 mg of tissue except the heart of 1 monkey 59 months postinoculation (mpi) (20 mg). PK, proteinase K. B) In protein-misfolding cyclic amplification, PrP^Sc was amplified only from the heart of 1 monkey 59 months postinoculation (mpi). As a positive control, brain tissue from a BSE-diseased monkey was used, and tissue from an uninfected control monkey served as a negative control. PK–digested hamster PrP^Sc (263 K) served as loading and digestion control for PrP^Sc. C) Paraffin-embedded tissue blotting of the entire heart of the 59 mpi monkey showed abundant deposition of PrP^Sc, mainly in the septum of the heart. Inset confirms the deposition pattern of PrP^Sc as amyloid. Scale bar = 0.25 mm. D) Histologic and immunohistochemical examination of heart tissue of the 59-mpi monkey by using hematoxylin and eosin (HE) staining and immunohistochemical staining against T-cell marker CD3 showed regularly configured cardiomyocytes and only single T-cells associated with blood vessels (arrow). Congo red staining showed Congo red–positive material in cardiomyocytes in a patch-like deposition pattern (arrows). Scale bar = 10 µm.