PrP genotypes of captive and free-ranging Rocky Mountain elk (Cervus elaphus nelsoni) with chronic wasting disease

Authors

Katherine I. O'Rourke, U.S. Department of AgricultureFollow
T. E. Besser, Washington State UniversityFollow
M. W. Miller, Colorado Division of WildlifeFollow
T. F. Cline, South Dakota Animal Industry Board
T. R. Spraker, College of Veterinary Medicine and Biomedical Sciences
A. L. Jenny, U.S. Department of Agriculture
M. A. Wild, Colorado Division of Wildlife
G. L. Zebarth, North American Elk Breeders' Association

Document Type

Article

Date of this Version

1999

Comments

Published in Journal of General Virology (1999), 80, 2765–2679.

Abstract

The PrP gene encodes the putative causative agent of the transmissible spongiform encephalopathies (TSEs), a heterogeneous group of fatal, neurodegenerative disorders including human Creutzfeldt–Jakob disease, bovine spongiform encephalopathy, ovine scrapie and chronic wasting disease (CWD) of North American deer and elk. Polymorphisms in the PrP gene are associated with variations in relative susceptibility, pathological lesion patterns, incubation times and clinical course of TSEs of humans, mice and sheep. Sequence analysis of the PrP gene from Rocky Mountain elk showed only one amino acid change (Met to Leu at cervid codon 132). Homozygosity for Met at the corresponding polymorphic site (Met to Val) in humans (human codon 129) predisposes exposed individuals to some forms of Creutzfeldt–Jakob disease. In this study, Rocky Mountain elk homozygous for PrP codon 132 Met were over-represented in both free-ranging and farm-raised CWD-affected elk when compared to unaffected control groups.