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Journal of Virology, December 2006, p. 12303-12311, Vol. 80, No. 24
0022-538X/06/$08.00+0     doi:10.1128/JVI.01120-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Strain Fidelity of Chronic Wasting Disease upon Murine Adaptation{triangledown} ,{dagger}

Christina J. Sigurdson,1 Giuseppe Manco,1 Petra Schwarz,1 Pawel Liberski,2 Edward A. Hoover,3 Simone Hornemann,4 Magdalini Polymenidou,1 Michael W. Miller,5 Markus Glatzel,1,{ddagger} and Adriano Aguzzi1*

University Hospital Zurich, Institute of Neuropathology, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland,1 Department of Molecular Pathology, Medical University Lodz, Czechoslowacka Street 8/10, Pl 92-216 Lodz, Poland,2 Department of Microbiology, Immunology, and Pathology, Colorado State University, Campus Delivery 1619, Fort Collins, Colorado, 80523-1619,3 Institute of Molecular Biology and Biophysics, HPK G4, ETH Zurich, CH-8093 Zürich, Switzerland,4 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, Colorado 80526-20975

Received 31 May 2006/ Accepted 21 September 2006

Chronic wasting disease (CWD), a prion disease of deer and elk, is highly prevalent in some regions of North America. The establishment of mouse-adapted CWD prions has proven difficult due to the strong species barrier between mice and deer. Here we report the efficient transmission of CWD to transgenic mice overexpressing murine PrP. All mice developed disease 500 ± 62 days after intracerebral CWD challenge. The incubation period decreased to 228 ± 103 days on secondary passage and to 162 ± 6 days on tertiary passage. Mice developed very large, radially structured cerebral amyloid plaques similar to those of CWD-infected deer and elk. PrPSc was detected in spleen, indicating that murine CWD was lymphotropic. PrPSc glycoform profiles maintained a predominantly diglycosylated PrP pattern, as seen with CWD in deer and elk, across all passages. Therefore, all pathological, biochemical, and histological strain characteristics of CWD appear to persist upon repetitive serial passage through mice. These findings indicate that the salient strain-specific properties of CWD are encoded by agent-intrinsic components rather than by host factors.

* Corresponding author. Mailing address: UniversitätsSpital Zürich, Institute of Neuropathology, Department of Pathology, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland. Phone: 41 (1) 255 2107. Fax: 41 (1) 255 4402. E-mail: adriano.aguzzi{at}usz.ch.

{triangledown} Published ahead of print on 4 October 2006.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

{ddagger} Present address: University Medical Center Hamburg-Eppendorf, Institute of Neuropathology, Martinistrasse 52, D-20246 Hamburg, Germany.

Journal of Virology, December 2006, p. 12303-12311, Vol. 80, No. 24
0022-538X/06/$08.00+0     doi:10.1128/JVI.01120-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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