Mitigation of prion infectivity and conversion capacity by a simulated natural process--repeated cycles of drying and wetting.

Qi Yuan,Shannon Bartelt-Hunt,Thomas Eckland,Glenn Telling,Jason Bartz,Surachai Supattapone

doi:10.1371/journal.ppat.1004638

Qi Yuan, Shannon Bartelt-Hunt + Show 4 more

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https://doi.org/10.1371/journal.ppat.1004638

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Abstract

Prions enter the environment from infected hosts, bind to a wide range of soil and soil minerals, and remain highly infectious. Environmental sources of prions almost certainly contribute to the transmission of chronic wasting disease in cervids and scrapie in sheep and goats. While much is known about the introduction of prions into the environment and their interaction with soil, relatively little is known about prion degradation and inactivation by natural environmental processes. In this study, we examined the effect of repeated cycles of drying and wetting on prion fitness and determined that 10 cycles of repeated drying and wetting could reduce PrPSc abundance, PMCA amplification efficiency and extend the incubation period of disease. Importantly, prions bound to soil were more susceptible to inactivation by repeated cycles of drying and wetting compared to unbound prions, a result which may be due to conformational changes in soil-bound PrPSc or consolidation of the bonding between PrPSc and soil. This novel finding demonstrates that naturally-occurring environmental process can degrade prions.

Highlights

Prion diseases, known as transmissible spongiform encephalopathies (TSEs), are a group of fatal neurodegenerative diseases which impact a number of species including cattle, sheep and goats, deer, elk and moose, and humans (Creutzfeldt-Jakob disease, CJD, and others) [1]
Prion diseases such as chronic wasting disease and scrapie are emerging in North America at an increasing rate
Infectious prions are introduced into the environment from both living and dead animals where they can bind to soil

Summary

Introduction

Known as transmissible spongiform encephalopathies (TSEs), are a group of fatal neurodegenerative diseases which impact a number of species including cattle (bovine spongiform encephalopathy, BSE), sheep and goats (scrapie), deer, elk and moose (chronic wasting disease, CWD), and humans (Creutzfeldt-Jakob disease, CJD, and others) [1]. CWD and scrapie prions can remain infectious over long time periods [2,3,4,5] in the environment. Prions enter the environment from infected hosts. Prions enter the environment through decomposition of infected animal carcasses [5]. Prions can be present in these excreta during the presymptomatic phase of disease, infected animals can shed prions into the environment over wide areas of the host’s home range. The amount of infectivity that is introduced into the environment is difficult to assess since prion titer is operationally defined with the route of infection, the age of the animal, the number of doses, and the PrP genotype of the host all making significant contributions in establishment of infection [14,15,16,17]

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