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Volume 20, Number 1—January 2014

Research

Molecular Barriers to Zoonotic Transmission of Prions

Marcelo A. Barria, Aru Balachandran, Masanori Morita, Tetsuyuki Kitamoto, Rona Barron, Jean Manson, Richard Knight, James W. Ironside, and Mark W. HeadComments to Author 
Author affiliations: The University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, R. Knight, J.W. Ironside, M.W Head); Canadian Food Inspection Agency, Ottawa, Ontario, Canada (A. Balachandran); Japan Blood Products Organization, Kobe, Japan (M. Morita); Tohoku University Graduate School of Medicine, Sendai, Japan (T. Kitamoto); University of Edinburgh, Easter Bush, Scotland, UK (R. Barron, J. Manson)

Main Article

Figure 5

Properties of C-BSE, CWD, and vCJD amplification products in a second round of PMCA. Hu-C-BSE, hu-vCJD, and hu-CWD (from a previous round of PMCA) were supplemented with fresh human brain homogenate and subjected to a second round of PMCA. The reactions were normalized by PrPres level and the product diluted (1:3, 1:6, 1:12, 1:24) in fresh human brain homogenate (PRNP codon 129MM) before PMCA. Odd numbers correspond to samples without PMCA; even numbers correspond to the reactions after PMCA (A,

Figure 5. . Properties of C-BSE, CWD, and vCJD amplification products in a second round of PMCA. Hu-C-BSE, hu-vCJD, and hu-CWD (from a previous round of PMCA) were supplemented with fresh human brain homogenate and subjected to a second round of PMCA. The reactions were normalized by PrPres level and the product diluted (1:3, 1:6, 1:12, 1:24) in fresh human brain homogenate (PRNP codon 129MM) before PMCA. Odd numbers correspond to samples without PMCA; even numbers correspond to the reactions after PMCA (A, B, and C). The PrP detection antibody was 3F4. C-BSE, C-type bovine spongiform encephalopathy; CWD, chronic wasting disease; vCJD variant Creutzfeldt-Jakob disease; PMCA, protein misfolding cyclic amplification; hu, human; PrPres, protease-resistant prion protein; M, molecular marker.

Main Article

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