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AUTHORS: Gael A. Sanchez, Randall W. DeYoung, Damon L. Williford, David G. Hewitt, Timothy E. Fulbright, Humberto Perotto-Baldivideo – Texas A&M University-Kingsville; Louis A. Harveson, Sul Ross State University; Shawn S. Gray, Texas Parks and Wildlife Department
ABSTRACT: Chronic Wasting Disease (CWD) was discovered in North American cervids in 1980 and has become a major management concern in recent decades. Chronic wasting disease was detected in Texas mule deer (Odocoileus hemionus) in 2012, most likely spread to Texas from New Mexico via natural movements of mule deer in the Hueco Mountains. Management has focused on containment of the disease as the most realistic and economically viable option. There is no cure or evidence of resistance to CWD, but mutations in the prion protein (PrP) gene affect susceptibility, incubation time, and the ability to detect the disease. We amplified and sequenced the PrP gene from tissue samples collected at CWD check stations in the Trans-Pecos and Panhandle regions of Texas during 2012-2015. We observed both synonymous and nonsynonymous mutations in the PrP gene, including six not previously reported in cervids. Twenty deer phenotypically identified as mule deer had nucleotide substitutions at codon 96, mutations originally identified in the white-tailed deer (O. virginianus) PrP gene. Seven mule deer had mutations at codon 225, resulting in an amino acid substitution associated with CWD prevalence and progression in Colorado and Wyoming populations. Our preliminary results reveal a diverse set of PrP alleles in Texas mule deer, due to past hybridization and backcrossing with white-tailed deer, as well as novel nonsynonymous mutations, with unknown significance. Genetic variation in the PrP gene has implications for detection of CWD and future management decisions throughout the state aimed at controlling the spread of the disease.