Chronic Wasting Disease Research at the USGS-Wisconsin Cooperative Wildlife Research Unit

                                                                                               
Genetic variation in complement system genes and resistance to chronic wasting disease in free-ranging white-tailed deer

Increasingly, it appears that prion diseases such as CWD are influenced by components of the innate (non-adaptive) immune system also known as the complement system (Klein et al. 2001, Mabbott and Bruce 2001, Kovacs et al. 2004). The specific mechanisms by which prions activate the complement system are unknown. One hypothesized role of the complement system in early TSE pathogenesis is that prions are recognized and bound by complement components C3 and C1q that deliver prions to follicular dendritic cells (FDCs) where they are able to convert normal prion to the abnormal conformation and subsequently enter the central nervous system and spread to the brain. Support for this hypothesis comes from studies in mice demonstrating that deficiencies in C3 or C1q impede the accumulation of scrapie-prion in lymph tissue and delay spread of the disease into the brain (Klein et al. 2001, Mabbott and Bruce 2001). These complement components, therefore, are natural targets to examine as factors potentially modulating CWD pathogenesis in natural populations.

                                             
The objective of this study is to investigate the potential association between complement gene variation and susceptibility to CWD in free-ranging white-tailed deer in south-central Wisconsin. Given the important role of the complement system in immune function, free-ranging animals, unlike laboratory models, are unlikely to be completely deficient in particular components of the complement system. However, individuals within populations are often variable with respect to the specific genetic makeup of immune system genes. The goal of this study, therefore, is to examine whether genetic polymorphisms of complement components are associated with the presence or absence of CWD in a free-ranging population of white-tailed deer.

 

 

Co-Investigators: Dr. Dennis Heisey, USGS National Wildlife Health Center; Dr. Kim T. Scribner, Department of Fisheries and Wildlife, Michigan State University


Former Research Associate: Dr. Julie A. Blanchong

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