| Item type |
文献 / Documents(1) |
| 公開日 |
2020-03-18 |
| アクセス権 |
|
|
アクセス権 |
open access |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 出版社版DOI |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1371/journal.pone.0216807 |
|
|
言語 |
ja |
|
|
関連名称 |
10.1371/journal.pone.0216807 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Tracking and clarifying differential traits of classical- and atypical L-type bovine spongiform encephalopathy prions after transmission from cattle to cynomolgus monkeys |
|
言語 |
en |
| タイトル別表記 |
|
|
その他のタイトル |
L-BSE prions after propagation in a non-human primate model |
|
言語 |
en |
| 著者 |
ハギワラ, ケンイチ
サトウ, ユウコ
ヤマカワ, ヨシオ
原, 英之
トビウメ, ミノル
オケモト ナカムラ, ユウコ
サタ, テツタロウ
ホリウチ, モトヒロ
シバタ, ヒロアキ
オノ, フミコ
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Classical- (C-) and atypical L-type bovine spongiform encephalopathy (BSE) prions cause different pathological phenotypes in cattle brains, and the disease-associated forms of each prion protein (PrPSc) has a dissimilar biochemical signature. Bovine C-BSE prions are the causative agent of variant Creutzfeldt-Jakob disease. To date, human infection with L-BSE prions has not been reported, but they can be transmitted experimentally from cows to cynomolgus monkeys (Macaca fascicularis), a non-human primate model. When transmitted to monkeys, C- and L-BSE prions induce different pathological phenotypes in the brain. However, when isolated from infected brains, the two prion proteins (PrPSc) have similar biochemical signatures (i.e., electrophoretic mobility, glycoforms, and resistance to proteinase K). Such similarities suggest the possibility that L-BSE prions alter their virulence to that of C-BSE prions during propagation in monkeys. To clarify this possibility, we conducted bioassays using inbred mice. C-BSE prions with or without propagation in monkeys were pathogenic to mice, and exhibited comparable incubation periods in secondary passage in mice. By contrast, L-BSE prions, either with or without propagation in monkeys, did not cause the disease in mice, indicating that the pathogenicity of L-BSE prions does not converge towards a C-BSE prion type in this primate model. These results suggest that, although C- and L-BSE prions propagated in cynomolgus monkeys exhibit similar biochemical PrPSc signatures and consist of the monkey amino acid sequence, the two prions maintain strain-specific conformations of PrPSc in which they encipher and retain unique pathogenic traits. |
|
言語 |
en |
| 書誌情報 |
en : PLOS ONE
巻 14,
号 5,
p. e0216807,
発行日 2019-05-16
|
| 収録物ID |
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収録物識別子タイプ |
ISSN |
|
収録物識別子 |
19326203 |
| 出版者 |
|
|
出版者 |
PLOS |
|
言語 |
en |
| 権利情報 |
|
|
言語 |
en |
|
権利情報 |
© 2019 Hagiwara et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
| EID |
|
|
識別子 |
362758 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
pone_14_5_e0216807.pdf (4.51 MB)
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