Prions Adhere to Soil Minerals and Remain Infectious

Abstract

An unidentified environmental reservoir of infectivity contributes to the natural transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter soil environments via shedding from diseased animals and decomposition of infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of disposal has resulted in unintentional introduction of prions into subsurface environments. We examined the potential for soil to serve as a TSE reservoir by studying the interaction of the disease-associated prion protein (PrPSc) with common soil minerals. In this study, we demonstrated substantial PrPSc adsorption to two clay minerals, quartz, and four whole soil samples. We quantified the PrPSc-binding capacities of each mineral. Furthermore, we observed that PrPSc desorbed from montmorillonite clay was cleaved at an N-terminal site and the interaction between PrPSc and Mte was strong, making desorption of the protein difficult. Despite cleavage and avid binding, PrPSc bound to Mte remained infectious. Results from our study suggest that PrPSc released into soil environments may be preserved in a bioavailable form, perpetuating prion disease epizootics and exposing other species to the infectious agent.

A prion disease of cervids: Chronic wasting disease

“…Modelling studies have provided further support that environmental contamination is likely playing a significant role in transmitting CWD [53,56]. Additionally, infectious prions have been demonstrated to bind soil particles and remain infectious to animals by both intracerebral and oral exposure routes [37,38]. Prion infectivity has been recovered from soil more than two years after experimental exposure to prions, suggesting the soil may serve as a reservoir for CWD prions [75].…”

Influence of the geographic distribution of prion protein gene sequence variation on patterns of chronic wasting disease spread in white-tailed deer (Odocoileus virginianus)

“…The disease is transmitted horizontally by contact with pathogenic prions shed in bodily fluids [6,7] and vertically from mother to offspring [8,9]. Once shed, prions have been shown to persist in the environment, potentially remaining infectious and furthering disease spread long after affected deer have dispersed [10–12]. If left unchecked CWD prevalence will increase slowly over time [13–16] and deer population densities will decline [17,18], possibly to the point of extirpation [19,20].…”

Caprine PrP variants harboring Asp-146, His-154 and Gln-211 alleles display reduced convertibility upon interaction with pathogenic murine prion protein in scrapie infected cells

“…Affected animals, apart from suffering from this fatal disorder, pose the risk of transmitting the disease within a flock/herd, either though milk (transmission from scrapieaffected mothers to offsprings 31,32 or via infectious agent dissemination in the environment through affected animals' placenta sheds 33 and/ or excretions). 34 Moreover, binding of the scrapie agent to the soil and preservation of its infectivity for a long time, 35 constitutes a further source of disease dissemination to animals (sheep and goats) sharing the same pasture.…”