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From: TSS ()
Subject: Breaking an Absolute Species Barrier: Transgenic Mice Expressing the Mink PrP Gene Are Susceptible to TME
Date: November 10, 2005 at 12:35 pm PST

Journal of Virology, December 2005, p. 14971-14975, Vol. 79, No. 23
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.23.14971-14975.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Breaking an Absolute Species Barrier: Transgenic Mice Expressing the Mink PrP Gene Are Susceptible to Transmissible Mink Encephalopathy
O. Windl ,1,, M. Buchholz,2,, A. Neubauer,3 W. Schulz-Schaeffer,2 M. Groschup,4 S. Walter,1 S. Arendt,2 M. Neumann,1 A. K. Voss,5,¶ and H. A. Kretzschmar1*
University of Munich, Institute of Neuropathology, Feodor-Lynen-Strasse 23, 81377 München, Germany,1 University of Göttingen, Institute of Neuropathology, Robert-Koch-Strasse 40, 37077 Göttingen, Germany,2 University of Munich, Institute for Medical Microbiology, Infectious and Epidemic Diseases, Veterinärstrasse 13, 80539 Munich, Germany,3 Federal Research Centre for Virus Diseases of Animals, Institute for New and Emerging Diseases, Isle of Riems, Germany,4 Max Planck Institute for Biophysical Chemistry, Department of Molecular Cell Biology, Göttingen, Germany5

Received 28 December 2004/ Accepted 24 August 2005

Transmissible mink encephalopathy (TME) is a rare disease of the North American mink, which has never been successfully transmitted to laboratory mice. We generated transgenic mice expressing the mink prion protein (PrP) and inoculated them with TME or the mouse-adapted scrapie strain 79A. TME infected mink PrP-transgenic mice on a murine PrP knockout background. The absolute species barrier between the infectious agent of TME and mice was therefore broken. Following TME and 79A infection of mice carrying both mink and murine PrPC, only proteinase-resistant PrP homologous to the incoming agent was detectable. The presence of the murine PrPC prolonged the incubation time of TME substantially.

* Corresponding author. Mailing address: Center for Neuropathology and Prion Research, Ludwig-Maximilians-Universität Munich, Feodor-Lynen-Strasse 23, D-81377 Munich, Germany. Phone: 49-89-2180-78000. Fax: 49-89-2180-78037. E-mail:

O.W. and M.B. contributed equally to this work.

Present address: Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, United Kingdom.

Present address: University of Ulm, Department of Internal Medicine I, Robert-Koch-Str. 8, 89081 Ulm, Germany.

¶ Present address: Walter and Eliza Hall Institute, IG Royal Parade, Parkville, Victoria 3050, Australia.


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