Ultraviolet-ozone treatment reduces levels of disease-associated prion protein and prion infectivity

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  • Background: Transmissible spongiform encephalopathies (TSEs) are a group of fatal neurodegenerative diseases caused by novel infectious agents referred to as prions. Prions appear to be composed primarily, if not exclusively, of a misfolded isoform of the cellular prion protein. TSE infectivity is remarkably stable and can resist many aggressive decontamination procedures, increasing human, livestock and wildlife exposure to TSEs. Findings: We tested the hypothesis that UV-ozone treatment reduces levels of the pathogenic prion protein and inactivates the infectious agent. We found that UV-ozone treatment decreased the carbon and prion protein content in infected brain homogenate to levels undetectable by dryashing carbon analysis or immunoblotting, respectively. After 8 weeks of ashing, UV-ozone treatment reduced the infectious titer of treated material by a factor of at least 105. A small amount of infectivity, however, persisted despite UV-ozone treatment. When bound to either montmorillonite clay or quartz surfaces, PrPTSE was still susceptible to degradation by UV-ozone. Conclusion: Our findings strongly suggest that UV-ozone treatment can degrade pathogenic prion protein and inactivate prions, even when the agent is associated with surfaces. Using larger UVozone doses or combining UV-ozone treatment with other decontaminant methods may allow the sterilization of TSE-contaminated materials.

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    Article (Published)
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    © 2009 Aiken et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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    • Johnson, C. J., Gilbert, P., McKenzie, D., Pedersen, J. A., & Aiken, J. M. (2009). Ultraviolet-ozone treatment reduces levels of disease-associated prion protein and prion infectivity. BMC research notes, 2, 121. BioMed Central. DOI: 10.1186/1756-0500-2-121