The same prion strain causes vCJD and BSE

被引：1113

作者：

Hill, AF

Desbruslais, M

Joiner, S

Sidle, KCL

Gowland, I

Collinge, J

Doey, LJ

Lantos, P

机构：

[1] ST MARYS HOSP,PRION DIS GRP,NEUROGENET UNIT,LONDON W2 1PG,ENGLAND

[2] INST PSYCHIAT,DEPT NEUROPATHOL,LONDON SE5 8AF,ENGLAND

[3] ST MARYS HOSP,DEPT NEUROL,LONDON W2 1NY,ENGLAND

来源：

NATURE | 1997年 / 389卷 / 6650期

关键词：

D O I：

10.1038/38925

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Epidemiological and clinicopathological studies, allied with pathological prion protein (PrPSc) analysis, strongly support the hypothesis that the human prion disease new variant Creutzfeldt-Jakob disease (vCJD) is causally related to bovine spongiform encephalopathy (BSE)1,2, but considerable controversy remains. Distinct prion strains are distinguished by their biological properties on transmission to laboratory animals and by physical and chemical differences in PrPSc strains. We now find that the biological and molecular transmission characteristics of vCJD are consistent with it being the human counterpart of BSE.

引用

页码：448 / 450

页数：3

共 16 条

[1] AMINO-ACID POLYMORPHISM IN HUMAN PRION PROTEIN AND AGE AT DEATH IN INHERITED PRION DISEASE
BAKER, HF
POULTER, M
CROW, TJ
FRITH, CD
LOFTHOUSE, R
RIDLEY, RM
COLLINGE, J
[J]. LANCET, 1991, 337 (8752) : 1286 - 1286
[2] SCRAPIE STRAIN VARIATION AND MUTATION
BRUCE, ME
[J]. BRITISH MEDICAL BULLETIN, 1993, 49 (04) : 822 - 838
[3] THE DISEASE CHARACTERISTICS OF DIFFERENT STRAINS OF SCRAPIE IN SINC CONGENIC MOUSE LINES - IMPLICATIONS FOR THE NATURE OF THE AGENT AND HOST CONTROL OF PATHOGENESIS
BRUCE, ME
MCCONNELL, I
FRASER, H
DICKINSON, AG
[J]. JOURNAL OF GENERAL VIROLOGY, 1991, 72 : 595 - 603
[4] Unaltered susceptibility to BSE in transgenic mice expressing human prion protein (vol 378, pg 779, 1995)
Collinge, J
Palmer, MS
Sidle, KCL
Hill, AF
Gowland, I
Meads, J
Asante, E
Bradley, R
Doey, LJ
Lantos, PL
[J]. NATURE, 1997, 389 (6650) : 526 - 526
[5] Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD
Collinge, J
Sidle, KCL
Meads, J
Ironside, J
Hill, AF
[J]. NATURE, 1996, 383 (6602) : 685 - 690
[6] TRANSMISSION OF FATAL FAMILIAL INSOMNIA TO LABORATORY-ANIMALS
COLLINGE, J
PALMER, MS
SIDLE, KCL
GOWLAND, I
MEDORI, R
IRONSIDE, J
LANTOS, P
[J]. LANCET, 1995, 346 (8974): : 569 - 570
[7] GENETIC PREDISPOSITION TO IATROGENIC CREUTZFELDT-JAKOB DISEASE
COLLINGE, J
PALMER, MS
DRYDEN, AJ
[J]. LANCET, 1991, 337 (8755) : 1441 - 1442
[8] UNALTERED SUSCEPTIBILITY TO BSE IN TRANSGENIC MICE EXPRESSING HUMAN PRION PROTEIN
COLLINGE, J
PALMER, MS
SIDLE, KCL
HILL, AF
GOWLAND, I
MEADS, J
ASANTE, E
BRADLEY, R
DOEY, LJ
LANTOS, PL
[J]. NATURE, 1995, 378 (6559) : 779 - 783
[9] Prion protein gene analysis in new variant cases of Creutzfeldt-Jakob disease
Collinge, J
Beck, J
Campbell, T
Estibeiro, K
Will, RG
[J]. LANCET, 1996, 348 (9019) : 56 - 56
[10] Transmission of the BSE agent to mice in the absence of detectable abnormal prion protein
Lasmezas, CI
Deslys, JP
Robain, O
Jaegly, A
Beringue, V
Peyrin, JM
Fournier, JG
Hauw, JJ
Rossier, J
Dormont, D
[J]. SCIENCE, 1997, 275 (5298) : 402 - 405

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