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Published on: July 6, 2016
Prion infection of oral and nasal mucosa
Crista DeJoia1, Brian Moreaux, Kimberly O'Connell
1Department of Veterinary Molecular Biology, P.O. Box 173610, Montana State University, Bozeman, Montana 59717, USA.
Abstract:
Centrifugal spread of the prion agent to peripheral tissues is postulated to occur by axonal transport along nerve fibers. This study investigated the distribution of the pathological isoform of the protein (PrP(Sc)) in the tongues and nasal cavities of hamsters following intracerebral inoculation of the HY strain of the transmissible mink encephalopathy (TME) agent. We report that PrP(Sc) deposition was found in the lamina propria, taste buds, and stratified squamous epithelium of fungiform papillae in the tongue, as well as in skeletal muscle cells. Using laser scanning confocal microscopy, PrP(Sc) was localized to nerve fibers in each of these structures in the tongue, neuroepithelial taste cells of the taste bud, and, possibly, epithelial cells. This PrP(Sc) distribution was consistent with a spread of HY TME agent along both somatosensory and gustatory cranial nerves to the tongue and suggests subsequent synaptic spread to taste cells and epithelial cells via peripheral synapses. In the nasal cavity, PrP(Sc) accumulation was found in the olfactory and vomeronasal epithelium, where its location was consistent with a distribution in cell bodies and apical dendrites of the sensory neurons. Prion spread to these sites is consistent with transport via the olfactory nerve fibers that descend from the olfactory bulb. Our data suggest that epithelial cells, neuroepithelial taste cells, or olfactory sensory neurons at chemosensory mucosal surfaces, which undergo normal turnover, infected with the prion agent could be shed and play a role in the horizontal transmission of animal prion diseases.
Insights
Prion diseases spread to the tongue and nasal cavity via nerve fibers. This study shows pathological prion protein (PrP(Sc)) in hamster tongues and noses, suggesting a route for horizontal transmission.
Area of Science:
- Neuroscience
- Pathology
- Veterinary Medicine
Background:
- Prion diseases are fatal neurodegenerative disorders.
- Centrifugal spread of prions to peripheral tissues is thought to occur via axonal transport.
- The distribution of pathological prion protein (PrP(Sc)) in peripheral tissues is not fully understood.
Purpose of the Study:
- To investigate the distribution of PrP(Sc) in the tongues and nasal cavities of hamsters after intracerebral inoculation with the HY strain of the transmissible mink encephalopathy (TME) agent.
- To determine the potential routes of prion spread to these peripheral sites.
Main Methods:
- Intracerebral inoculation of hamsters with the HY TME agent.
- Tissue analysis of tongues and nasal cavities for PrP(Sc) deposition.
- Laser scanning confocal microscopy to localize PrP(Sc) within nerve fibers and cells.
Main Results:
- PrP(Sc) deposition was detected in the tongue's lamina propria, taste buds, stratified squamous epithelium of fungiform papillae, and skeletal muscle.
- PrP(Sc) was localized to nerve fibers, neuroepithelial taste cells, and possibly epithelial cells in the tongue.
- PrP(Sc) accumulation was found in the olfactory and vomeronasal epithelium of the nasal cavity, associated with sensory neurons.
Conclusions:
- Prion spread to the tongue occurs along somatosensory and gustatory cranial nerves, with potential synaptic spread to taste and epithelial cells.
- Prion spread to the nasal cavity is consistent with transport via olfactory nerve fibers.
- Infected epithelial cells, taste cells, or olfactory neurons at mucosal surfaces may play a role in the horizontal transmission of animal prion diseases.
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