Abstract
In individual animals affected by transmissible spongiform encephalopathies, different disease phenotypes can be identified which are attributed to different strains of the agent. In the absence of reliable technology to fully characterise the agent, classification of disease phenotype has been used as a strain typing tool which can be applied in any host. This approach uses standardised data on biological parameters, established for a single host, to allow comparison of different prion sources. Traditionally prion strain characterisation in wild type mice is based on incubation periods and lesion profiles after the stabilisation of the agent into the new host which requires serial passages. Such analysis can take many years, due to prolonged incubation periods. The current study demonstrates that the PrPSc patterns produced by one serial passage in wild type mice of bovine or ovine BSE were consistent, stable and showed minimal and predictable differences from mouse-stabilised reference strains. This biological property makes PrPSc deposition pattern mapping a powerful tool in the identification and definition of TSE strains on primary isolation, making the process of characterisation faster and cheaper than a serial passage protocol. It can be applied to individual mice and therefore it is better suited to identify strain diversity within single inocula in case of co-infections or identify strains in cases where insufficient mice succumb to disease for robust lesion profiles to be constructed. The detailed description presented in this study provides a reference document for identifying BSE in wild type mice.
Highlights
Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases that affect humans and animals
Despite the disagreement in the scientific community regarding the exact nature of the infectious agent, proteinaceous infectious particles consisting of abnormal isoforms (PrPSc) is considered to be a ubiquitous marker of TSE disease and it accumulates in the brains of affected subjects from the very early stages of the disease before any
Stabilization of a TSE agent in a wild type murine host requires serial passages within this host which have a significant effect on incubation period and lesion profiles [26,41]
Summary
Transmissible spongiform encephalopathies (TSEs) are fatal neurodegenerative diseases that affect humans and animals. The hallmark lesion of TSEs is spongiform changes in the brains of affected subjects. Despite the disagreement in the scientific community regarding the exact nature of the infectious agent, PrPSc is considered to be a ubiquitous marker of TSE disease and it accumulates in the brains of affected subjects from the very early stages of the disease before any Scrapie, the archetypal TSE which affects small ruminants, is not considered to be a public health risk and is known for centuries [11,12,13]. Bovine spongiform encephalopathy (BSE) is a TSE of cattle first recognised in 1986 [14]. Novel spongiform encephalopathies in captive ruminants [15] and cats [1618] and a variant of Creutzfeldt-Jakob disease (vCJD) in humans [19,20,21] were identified. A link between BSE and these new emerging TSEs was established and wild type mouse bioassay contributed in determining this association [22]
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