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dc.contributor.authorCrowell, Jenna
dc.contributor.authorWiley, James A.
dc.contributor.authorBessen, Richard A.
dc.date.accessioned2015-10-20T20:32:40Z
dc.date.available2015-10-20T20:32:40Z
dc.date.issued2015-03
dc.identifier.citationCrowell, Jenna, James A. Wiley, and Richard A. Bessen. "Lesion of the Olfactory Epithelium Accelerates Prion Neuroinvasion and Disease Onset when Prion Replication Is Restricted to Neurons." PLoS ONE 10, no. 3 (March 2015): e0119863. DOI:https://dx.doi.org/10.1371/journal.pone.0119863.en_US
dc.identifier.issn1932-6203
dc.identifier.urihttps://scholarworks.montana.edu/xmlui/handle/1/9337
dc.description.abstractNatural prion diseases of ruminants are moderately contagious and while the gastrointestinal tract is the primary site of prion agent entry, other mucosae may be entry sites in a subset of infections. In the current study we examined prion neuroinvasion and disease induction following disruption of the olfactory epithelium in the nasal mucosa since this site contains environmentally exposed olfactory sensory neurons that project directly into the central nervous system. Here we provide evidence for accelerated prion neuroinvasion and clinical onset from the olfactory mucosa after disruption and regeneration of the olfactory epithelium and when prion replication is restricted to neurons. In transgenic mice with neuron restricted replication of prions, there was a reduction in survival when the olfactory epithelium was disrupted prior to intranasal inoculation and there was >25% decrease in the prion incubation period. In a second model, the neurotropic DY strain of transmissible mink encephalopathy was not pathogenic in hamsters by the nasal route, but 50% of animals exhibited brain infection and/or disease when the olfactory epithelium was disrupted prior to intranasal inoculation. A time course analysis of prion deposition in the brain following loss of the olfactory epithelium in models of neuron-restricted prion replication suggests that neuroinvasion from the olfactory mucosa is via the olfactory nerve or brain stem associated cranial nerves. We propose that induction of neurogenesis after damage to the olfactory epithelium can lead to prion infection of immature olfactory sensory neurons and accelerate prion spread to the brain.en_US
dc.rightsCC BY 4.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/legalcodeen_US
dc.titleLesion of the Olfactory Epithelium Accelerates Prion Neuroinvasion and Disease Onset when Prion Replication Is Restricted to Neuronsen_US
dc.typeArticleen_US
mus.citation.extentfirstpagee0119863en_US
mus.citation.issue3en_US
mus.citation.journaltitlePLoS ONEen_US
mus.citation.volume10en_US
mus.identifier.categoryHealth & Medical Sciencesen_US
mus.identifier.doi10.1371/journal.pone.0119863en_US
mus.relation.collegeCollege of Agricultureen_US
mus.relation.collegeCollege of Letters & Scienceen_US
mus.relation.departmentMicrobiology & Immunology.en_US
mus.relation.universityMontana State University - Bozemanen_US
mus.data.thumbpage6en_US


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