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Viruses
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Prion Neuroinvasion 2.0
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Prion Neuroinvasion 2.0

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Prions".

Deadline for manuscript submissions: closed (15 June 2022) | Viewed by 5251

Special Issue Editor

Dr. Anthony E. Kincaid

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Guest Editor
Department of Pharmacy Sciences, School of Pharmacy and Health Professions, Creighton University, Omaha, NE, USA
Interests: prion pathogenesis;specifically the characterization of routes of entry and mechanisms of centripetal and centrifugal spread of prions in the nervous system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Prion diseases are a class of fatal neurodegenerative diseases that affect animals, including humans. The causative agent is a misfolded protein that is sometimes inherited and the result of an iatrogenic procedure, but more commonly, prions gain access to the interior of the body by crossing the epithelium of the gut, nasal cavity, or the skin.

While much work has been carried out on the pathogenesis of prion diseases, there are several questions that remain unanswered, including the cellular and molecular events of prions crossing the epithelial tissue, the role of blood in the spread of prions, the specific mechanism(s) of how prions enter and spread centripetally in the peripheral and central nervous systems, and how prions spread centrifugally to peripheral tissues where they are shed.

The focus of this Special Issue is the process of prion entry and neuroinvasion, the spread of prions in the central and peripheral nervous systems, and the mechanism(s) of neuronal cell death.

Dr. Anthony E. Kincaid
Guest Editor

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Keywords

  • prion pathogenesis
  • prion entry
  • prion neuroinvasion
  • transport in nerves
  • spread in the central nervous system
  • centrifugal and centripetal spread of prions
  • prionemia

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Published Papers (2 papers)

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Research

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17 pages, 4975 KiB  
Article
Multiple Factors Influence the Incubation Period of ALS Prion-like Transmission in SOD1 Transgenic Mice
by Jacob I. Ayers, Guilian Xu, Qing Lu, Kristy Dillon, Susan Fromholt and David R. Borchelt
Viruses 2023, 15(9), 1819; https://doi.org/10.3390/v15091819 - 26 Aug 2023
Viewed by 1290
Abstract
Mutations in superoxide dismutase 1 (SOD1) that are associated with amyotrophic lateral sclerosis (ALS) cause its misfolding and aggregation. Prior studies have demonstrated that the misfolded conformation of ALS-SOD1 can template with naïve SOD1 “host proteins” to propagate, spread, and induce paralysis in [...] Read more.
Mutations in superoxide dismutase 1 (SOD1) that are associated with amyotrophic lateral sclerosis (ALS) cause its misfolding and aggregation. Prior studies have demonstrated that the misfolded conformation of ALS-SOD1 can template with naïve SOD1 “host proteins” to propagate, spread, and induce paralysis in SOD1 transgenic mice. These observations have advanced the argument that SOD1 is a host protein for an ALS conformer that is prion-like and experimentally transmissible. Here, we investigated the propagation of different isolates of G93A-SOD1 ALS conformers using a paradigm involving transmission to mice expressing human G85R-SOD1 fused to yellow fluorescent protein (G85R-SOD1:YFP). In these studies, we also utilized a newly developed line of mice in which the G85R-SOD1:YFP construct was flanked by loxp sites, allowing its temporal and spatial regulation. We used methods in which the G93A ALS conformers were injected into the sciatic nerve or hindlimb muscle of adult transgenic mice. We observed that the incubation period to paralysis varied significantly depending upon the source of inoculum containing misfolded G93A SOD1. Serial passage and selection produced stable isolates of G93A ALS conformers that exhibited a defined minimum incubation period of ~2.5 months when injected into the sciatic nerve of young adult mice. As expected, neuronal excision of the transgene in loxpG85R-SOD1:YFP mice blocked induction of paralysis by transmission of G93A ALS conformers. Our findings indicate that G93A ALS conformers capable of inducing disease require neuronal expression of a receptive host SOD1 protein for propagation, with a defined incubation period to paralysis. Full article
(This article belongs to the Special Issue Prion Neuroinvasion 2.0)
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Review

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14 pages, 2106 KiB  
Review
Transport of Prions in the Peripheral Nervous System: Pathways, Cell Types, and Mechanisms
by Sam M. Koshy, Anthony E. Kincaid and Jason C. Bartz
Viruses 2022, 14(3), 630; https://doi.org/10.3390/v14030630 - 18 Mar 2022
Cited by 4 | Viewed by 3519
Abstract
Prion diseases are transmissible protein misfolding disorders that occur in animals and humans where the endogenous prion protein, PrPC, undergoes a conformational change into self-templating aggregates termed PrPSc. Formation of PrPSc in the central nervous system (CNS) leads [...] Read more.
Prion diseases are transmissible protein misfolding disorders that occur in animals and humans where the endogenous prion protein, PrPC, undergoes a conformational change into self-templating aggregates termed PrPSc. Formation of PrPSc in the central nervous system (CNS) leads to gliosis, spongiosis, and cellular dysfunction that ultimately results in the death of the host. The spread of prions from peripheral inoculation sites to CNS structures occurs through neuroanatomical networks. While it has been established that endogenous PrPC is necessary for prion formation, and that the rate of prion spread is consistent with slow axonal transport, the mechanistic details of PrPSc transport remain elusive. Current research endeavors are primarily focused on the cellular mechanisms of prion transport associated with axons. This includes elucidating specific cell types involved, subcellular machinery, and potential cofactors present during this process. Full article
(This article belongs to the Special Issue Prion Neuroinvasion 2.0)
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