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Article

Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy

1
CEA, Institute of Emerging Diseases and Innovative Therapies (iMETI), Division of Prions and Related Diseases (SEPIA), Route du Panorama, BP6, 92265 Fontenay-aux-Roses, France
2
Istituto Zooprofilattico Sperimentale del Piemonte, Via Bologna 148, 10154 Torino, Italy
3
Kansas State University, College of Veterinary Medicine, K224B Mosier Hall, Manhattan, Kansas 66506-5601 USA
4
National Animal Disease Center, USDA, Agricultural Research Service, 1920 Dayton Ave, Ames, Iowa 50010 USA
5
Instituto Nacional de Investigacion y Tecnologia Agraria y Alimentaria, Madrid, Spain
*
Author to whom correspondence should be addressed.
Pathogens 2013, 2(3), 520-532; https://doi.org/10.3390/pathogens2030520
Received: 27 June 2013 / Revised: 28 July 2013 / Accepted: 30 July 2013 / Published: 30 July 2013
(This article belongs to the Special Issue Prions)
Successful transmission of Transmissible Mink Encephalopathy (TME) to cattle supports the bovine hypothesis for the still controversial origin of TME outbreaks. Human and primate susceptibility to classical Bovine Spongiform Encephalopathy (c-BSE) and the transmissibility of L-type BSE to macaques indicate a low cattle-to-primate species barrier. We therefore evaluated the zoonotic potential of cattle-adapted TME. In less than two years, this strain induced in cynomolgus macaques a neurological disease similar to L-BSE but distinct from c-BSE. TME derived from another donor species (raccoon) induced a similar disease with even shorter incubation periods. L-BSE and cattle-adapted TME were also transmissible to transgenic mice expressing human prion protein (PrP). Secondary transmissions to transgenic mice expressing bovine PrP maintained the features of the three tested bovine strains (cattle TME, c-BSE and L-BSE) regardless of intermediate host. Thus, TME is the third animal prion strain transmissible to both macaques and humanized transgenic mice, suggesting zoonotic potentials that should be considered in the risk analysis of animal prion diseases for human health. Moreover, the similarities between TME and L-BSE are highly suggestive of a link between these strains, and therefore the possible presence of L-BSE for many decades prior to its identification in USA and Europe. View Full-Text
Keywords: primate; prion; transgenic mice; TME; cattle; raccoon; zoonotic potential primate; prion; transgenic mice; TME; cattle; raccoon; zoonotic potential
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MDPI and ACS Style

Comoy, E.E.; Mikol, J.; Ruchoux, M.-M.; Durand, V.; Luccantoni-Freire, S.; Dehen, C.; Correia, E.; Casalone, C.; Richt, J.A.; Greenlee, J.J.; Torres, J.M.; Brown, P.; Deslys, J.-P. Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy. Pathogens 2013, 2, 520-532. https://doi.org/10.3390/pathogens2030520

AMA Style

Comoy EE, Mikol J, Ruchoux M-M, Durand V, Luccantoni-Freire S, Dehen C, Correia E, Casalone C, Richt JA, Greenlee JJ, Torres JM, Brown P, Deslys J-P. Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy. Pathogens. 2013; 2(3):520-532. https://doi.org/10.3390/pathogens2030520

Chicago/Turabian Style

Comoy, Emmanuel E.; Mikol, Jacqueline; Ruchoux, Marie-Madeleine; Durand, Valérie; Luccantoni-Freire, Sophie; Dehen, Capucine; Correia, Evelyne; Casalone, Cristina; Richt, Juergen A.; Greenlee, Justin J.; Torres, Juan M.; Brown, Paul; Deslys, Jean-Philippe. 2013. "Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy" Pathogens 2, no. 3: 520-532. https://doi.org/10.3390/pathogens2030520

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