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. 2021 Feb 18;11:4058. doi: 10.1038/s41598-021-83630-1

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Detection of PrP^TSE in the CSF of CJD patients. CSF samples from 8 sCJD patients (§1–§8) and 1 definite vCJD patients were serially amplified by PMCA. The PrP^TSE signal was assessed by means of western blot analysis after proteinase K digestion using 9A2 antibody. For each sample, 20 µL of the product were loaded onto the gel. R refers to the number of rounds. M indicates the typical molecular mass of PrP^res in the range of 20–30 kDa. (a): Representation of the results according to CSF sample genotypes and number of rounds; (b): vCJD amplification in TgMet, TgVal and BV substrates; (c): sCJD amplification: MM subtypes in BV substrate; VV subtype in TgVal substrate. − 3na MM2/MM1/VV2 refer to non-amplified material (no PMCA) obtained from the 10⁻³ dilution (w/v) of the initial infectious brain samples from MM2, MM1 and VV2 subtypes, respectively.