Date of Award

Spring 2006

Document Type

Thesis

Department

Life & Environmental Sciences

Abstract

The mechanism of prion shedding in prion disease is currently unknown. The purpose of this study was to determine if the nasal cavity is a site of prion infection. Hamsters were intracerebrally inoculated with the hyper strain of transmissible mink encephalopathy agent. Once clinically ill, the hamsters were euthanized and their skulls were removed and examined for prion infection using immunohistochemical and dual immunofluorescence staining techniques. In infected hamsters, the infectious agent (PrP50) was shown to be present in the olfactory receptor neurons of the olfactory sensory epithelium (OSE) as well as in the nasal-associated lymphoid tissue and the vomeronasal receptor neurons in the vomeronasal sensory epithelium (VSE) of the vomeronasal organ. PrPSc infection was specific to sensory and not to non-sensory epithelium in both the OSE and the VSE.

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