Research Topic Directory Prion Biology

Name E-mail Address Phone Department
970-491-3975Microbiology, Immunology, and Pathology
970-491-7587Microbiology, Immunology, and Pathology
970-491-1455Microbiology, Immunology, and Pathology
970-491-2968Microbiology, Immunology, and Pathology

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                    [ProfileText] => Dr. Mathiason is Associate Professor of Pathobiology and Director of the Office of Vice President for Research (OVPR) Program for Research and Scholarly Excellence (PRSE)- Infectious Disease and Rapid Response Network. Dr. Mathiason’s research focuses on the role blood and maternal infections play in disease pathogenesis and transmission dynamics.  Her laboratory combines use of native and rodent in vivo hosts with highly sensitive in vitro assays to assimilate an understanding of the biological mechanisms associated with covert transmission of infectious agents.  The intent of these works is to provide basic science principles for continued efforts to mitigate infectious agents via preventative, therapeutic and vaccine therapies. 
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                    [ProfileText] => Since 1982, Dr. Hoover's laboratory focused on the mechanisms of transmission, pathogenesis, and detection of especially feline retroviruses and more recently the transmission of the prion disease chronic wasting disease (CWD) of cervids (deer, elk, moose, reindeer).  Prions are important as the cause of fatal neurologic diseases of animals and models and humans disease--i.e. bovine spongiform encephalopathy (mad cow disease, BSE), sheep scrapes, and Creutzfeldt-Jakob disease.  Previous research in the Hoover laboratory led to development of the first successful and most widely used feline leukemia virus (FeLV) vaccine now used to immunize cats worldwide against leukemia, and the way in which feline immunodeficiency virus (FIV) infects and causes disease in cats.  Current work is focused on CWD, in particular: (1) the mechanisms whereby prions cross the mucous membranes and travel to the lymphoid tissues and then the brain to cause disease, (2) the mechanisms and cells involved in prion shedding transmission among deer, which appears to be much like the transmission of viruses; (3) the barriers to cross-species transmission of CWD to non-cervid species; and (4) experimental approaches to vaccination against this transmissible prion infection.
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                    [ProfileText] => Dr. Zabel is Professor of Prion Biology and Immunology.  Drawing on his background in both immunology and prion biology, Dr. Zabel’s research program focuses on the interaction of prions with cells and receptors of the immune system and lymphoid tissues in the early entry, trafficking, and pathogenesis phases of prion infections.  Little is known regarding the cell surface molecules and molecular co-factors that control these events.  Using mice engineered to transgenically express both the cervid or ovine normal prion protein gene and selected receptors of the innate immune system, the Zabel lab examines the early lymphoid system distribution of prions and employs vector systems expressing prion-targeted interfering RNA molecules as therapeutic strategies for prion infections.  
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                    [ProfileText] => Dr. Telling’s involvement in prion disease research began as a trainee with Nobel Laureate Stanley Prusiner. He subsequently worked as an independent investigator at the UK Medical Research Council Prion Unit, and at the Sanders Brown Center on Aging at the University of Kentucky. Since late 2011, Dr. Telling has Directed the Prion Research Center (PRC) at Colorado State University where he is also a Professor in the Department of Microbiology, Immunology and Pathology. While the Telling lab is particularly recognized for transgenic mouse modeling of prion diseases, it is one of only a handful of research groups with the resources and expertise for studying prion diseases using whole animal, transgenic, cell biological, biochemical, and molecular genetic approaches. The overarching goal of Dr. Telling’s research program is to study the mechanism of prion replication, prion species barriers and strain diversity, and the molecular basis of inherited human prion diseases. 
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