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Viruses
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The Future of the Chronic Wasting Disease Epizootic
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The Future of the Chronic Wasting Disease Epizootic

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

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 19360

Special Issue Editors

Prof. Dr. Holger Wille

E-Mail Website
Guest Editor
Department of Biochemistry & Centre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB T6G 2M8, Canada
Interests: prions; amyloid; protein misfolding; neurodegenerative diseases; structure-based vaccine design; immunotherapy; conformation-specific antibodies; electron microscopy; X-ray fiber diffraction; biochemistry; biophysics
Prof. Dr. Debbie McKenzie

E-Mail Website
Guest Editor
Department of Biological Sciences & Centre for Prions and Protein Folding Diseases, University of Alberta, 204 Brain and Aging Research Building, Edmonton, AB T6G 2M8, Canada
Interests: prions; prion strains; protein misfolding; neurodegenerative diseases; chronic wasting disease; cell tropism; prion disease transmission; PRNP genetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue represents a collection of scientific review articles on the future of the chronic wasting disease (CWD) outbreak in North America, Europe, and South Korea. The reviews should be based on the published literature concerning the past and present situation of the CWD outbreak, with a well-justified, speculative section on future outcomes based on the author’s views (including discussions of the best possible outcome, most likely outcome/realistic scenarios, and worst possible outcome). Since this Special Issue is intended to assemble a comprehensive view of the CWD epizootic in North America, Europe, and South Korea, great emphasis will be placed on the scientific justification of the speculative portion of the reviews. Moreover, in the years to come, the predictions will undoubtedly be measured against the future developments and judged against the knowledge that is available to date.

Prof. Holger Wille
Prof. Debbie McKenzie
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cervids
  • disease abatement
  • environmental contamination
  • food security
  • game farming
  • genetic drift
  • hunting
  • livestock
  • prion
  • protein misfolding disease
  • transmissible spongiform encephalopathy
  • vaccine development
  • wildlife disease
  • zoonosis

Published Papers (5 papers)

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Research

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12 pages, 4005 KiB  
Article
Transmission of Raccoon-Passaged Chronic Wasting Disease Agent to White-Tailed Deer
by Eric D. Cassmann, Alexis J. Frese, S. Jo Moore and Justin J. Greenlee
Viruses 2022, 14(7), 1578; https://0-doi-org.brum.beds.ac.uk/10.3390/v14071578 - 20 Jul 2022
Cited by 1 | Viewed by 2180
Abstract
The transmission characteristics of prion diseases are influenced by host prion protein sequence and, therefore, the host species. Chronic wasting disease (CWD), a prion disease of cervids, has widespread geographical distribution throughout North America and occurs in both wild and farmed populations. CWD [...] Read more.
The transmission characteristics of prion diseases are influenced by host prion protein sequence and, therefore, the host species. Chronic wasting disease (CWD), a prion disease of cervids, has widespread geographical distribution throughout North America and occurs in both wild and farmed populations. CWD prions contaminate the environment through scattered excrement and decomposing carcasses. Fresh carcasses with CWD prions are accessible by free-ranging mesopredators such as raccoons and may provide a route of exposure. Previous studies demonstrated the susceptibility of raccoons to CWD from white-tailed deer. In this study, we demonstrate that white-tailed deer replicate raccoon-passaged CWD prions which results in clinical disease similar to intraspecies CWD transmission. Six white-tailed deer were oronasally inoculated with brain homogenate from a raccoon with CWD. All six deer developed clinical disease, had widespread lymphoid distribution of misfolded CWD prions (PrPSc), and had neuropathologic lesions with PrPSc accumulation in the brain. The presence of PrPSc was confirmed by immunohistochemistry, enzyme-linked immunoassay, and western blot. The western blot migration pattern of raccoon-passaged CWD was different from white-tailed deer CWD. Transmission of raccoon CWD back to white-tailed deer resulted in an interposed molecular phenotype that was measurably different from white-tailed deer CWD. Full article
(This article belongs to the Special Issue The Future of the Chronic Wasting Disease Epizootic)
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18 pages, 477 KiB  
Article
Chronic Wasting Disease Transmission Risk Assessment for Farmed Cervids in Minnesota and Wisconsin
by James M. Kincheloe, Amy R. Horn-Delzer, Dennis N. Makau and Scott J. Wells
Viruses 2021, 13(8), 1586; https://0-doi-org.brum.beds.ac.uk/10.3390/v13081586 - 11 Aug 2021
Cited by 4 | Viewed by 3034
Abstract
CWD (chronic wasting disease) has emerged as one of the most important diseases of cervids and continues to adversely affect farmed and wild cervid populations, despite control and preventive measures. This study aims to use the current scientific understanding of CWD transmission and [...] Read more.
CWD (chronic wasting disease) has emerged as one of the most important diseases of cervids and continues to adversely affect farmed and wild cervid populations, despite control and preventive measures. This study aims to use the current scientific understanding of CWD transmission and knowledge of farmed cervid operations to conduct a qualitative risk assessment for CWD transmission to cervid farms and, applying this risk assessment, systematically describe the CWD transmission risks experienced by CWD-positive farmed cervid operations in Minnesota and Wisconsin. A systematic review of literature related to CWD transmission informed our criteria to stratify CWD transmission risks to cervid operations into high-risk low uncertainty, moderate-risk high uncertainty, and negligible-risk low uncertainty categories. Case data from 34 CWD-positive farmed cervid operations in Minnesota and Wisconsin from 2002 to January 2019 were categorized by transmission risks exposure and evaluated for trends. The majority of case farms recorded high transmission risks (56%), which were likely sources of CWD, but many (44%) had only moderate or negligible transmission risks, including most of the herds (62%) detected since 2012. The presence of CWD-positive cervid farms with only moderate or low CWD transmission risks necessitates further investigation of these risks to inform effective control measures. Full article
(This article belongs to the Special Issue The Future of the Chronic Wasting Disease Epizootic)
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Review

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15 pages, 1659 KiB  
Review
Transmission, Strain Diversity, and Zoonotic Potential of Chronic Wasting Disease
by Sandra Pritzkow
Viruses 2022, 14(7), 1390; https://0-doi-org.brum.beds.ac.uk/10.3390/v14071390 - 25 Jun 2022
Cited by 5 | Viewed by 4560
Abstract
Chronic wasting disease (CWD) is a prion disease affecting several species of captive and free-ranging cervids. In the past few decades, CWD has been spreading uncontrollably, mostly in North America, resulting in a high increase of CWD incidence but also a substantially higher [...] Read more.
Chronic wasting disease (CWD) is a prion disease affecting several species of captive and free-ranging cervids. In the past few decades, CWD has been spreading uncontrollably, mostly in North America, resulting in a high increase of CWD incidence but also a substantially higher number of geographical regions affected. The massive increase in CWD poses risks at several levels, including contamination of the environment, transmission to animals cohabiting with cervids, and more importantly, a putative transmission to humans. In this review, I will describe the mechanisms and routes responsible for the efficient transmission of CWD, the strain diversity of natural CWD, its spillover and zoonotic potential and strategies to minimize the CWD threat. Full article
(This article belongs to the Special Issue The Future of the Chronic Wasting Disease Epizootic)
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23 pages, 1189 KiB  
Review
Gene-Edited Cell Models to Study Chronic Wasting Disease
by Simrika Thapa, Cristobal Marrero Winkens, Waqas Tahir, Maria I. Arifin, Sabine Gilch and Hermann M. Schatzl
Viruses 2022, 14(3), 609; https://0-doi-org.brum.beds.ac.uk/10.3390/v14030609 - 15 Mar 2022
Viewed by 2686
Abstract
Prion diseases are fatal infectious neurodegenerative disorders affecting both humans and animals. They are caused by the misfolded isoform of the cellular prion protein (PrPC), PrPSc, and currently no options exist to prevent or cure prion diseases. Chronic wasting [...] Read more.
Prion diseases are fatal infectious neurodegenerative disorders affecting both humans and animals. They are caused by the misfolded isoform of the cellular prion protein (PrPC), PrPSc, and currently no options exist to prevent or cure prion diseases. Chronic wasting disease (CWD) in deer, elk and other cervids is considered the most contagious prion disease, with extensive shedding of infectivity into the environment. Cell culture models provide a versatile platform for convenient quantification of prions, for studying the molecular and cellular biology of prions, and for performing high-throughput screening of potential therapeutic compounds. Unfortunately, only a very limited number of cell lines are available that facilitate robust and persistent propagation of CWD prions. Gene-editing using programmable nucleases (e.g., CRISPR-Cas9 (CC9)) has proven to be a valuable tool for high precision site-specific gene modification, including gene deletion, insertion, and replacement. CC9-based gene editing was used recently for replacing the PrP gene in mouse and cell culture models, as efficient prion propagation usually requires matching sequence homology between infecting prions and prion protein in the recipient host. As expected, such gene-editing proved to be useful for developing CWD models. Several transgenic mouse models were available that propagate CWD prions effectively, however, mostly fail to reproduce CWD pathogenesis as found in the cervid host, including CWD prion shedding. This is different for the few currently available knock-in mouse models that seem to do so. In this review, we discuss the available in vitro and in vivo models of CWD, and the impact of gene-editing strategies. Full article
(This article belongs to the Special Issue The Future of the Chronic Wasting Disease Epizootic)
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12 pages, 1361 KiB  
Review
Exposure Risk of Chronic Wasting Disease in Humans
by Satish K. Nemani, Jennifer L. Myskiw, Lise Lamoureux, Stephanie A. Booth and Valerie L. Sim
Viruses 2020, 12(12), 1454; https://0-doi-org.brum.beds.ac.uk/10.3390/v12121454 - 17 Dec 2020
Cited by 8 | Viewed by 5888
Abstract
The majority of human prion diseases are sporadic, but acquired disease can occur, as seen with variant Creutzfeldt–Jakob disease (vCJD) following consumption of bovine spongiform encephalopathy (BSE). With increasing rates of cervid chronic wasting disease (CWD), there is concern that a new form [...] Read more.
The majority of human prion diseases are sporadic, but acquired disease can occur, as seen with variant Creutzfeldt–Jakob disease (vCJD) following consumption of bovine spongiform encephalopathy (BSE). With increasing rates of cervid chronic wasting disease (CWD), there is concern that a new form of human prion disease may arise. Currently, there is no evidence of transmission of CWD to humans, suggesting the presence of a strong species barrier; however, in vitro and in vivo studies on the zoonotic potential of CWD have yielded mixed results. The emergence of different CWD strains is also concerning, as different strains can have different abilities to cross species barriers. Given that venison consumption is common in areas where CWD rates are on the rise, increased rates of human exposure are inevitable. If CWD was to infect humans, it is unclear how it would present clinically; in vCJD, it was strain-typing of vCJD prions that proved the causal link to BSE. Therefore, the best way to screen for CWD in humans is to have thorough strain-typing of harvested cervids and human CJD cases so that we will be in a position to detect atypical strains or strain shifts within the human CJD population. Full article
(This article belongs to the Special Issue The Future of the Chronic Wasting Disease Epizootic)
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