Fate of Prions in Soil: A Review

Abstract

Prions are the etiological agents of transmissible spongiform encephalopathies (TSEs), a class of fatal neurodegenerative diseases affecting humans and other mammals. The pathogenic prion protein is a misfolded form of the host-encoded prion protein and represents the predominant, if not sole, component of the infectious agent. Environmental routes of TSE transmission are implicated in epizootics of sheep scrapie and chronic wasting disease (CWD) of deer, elk, and moose. Soil represents a plausible environmental reservoir of scrapie and CWD agents, which can persist in the environment for years. Attachment to soil particles likely influences the persistence and infectivity of prions in the environment. Effective methods to inactivate TSE agents in soil are currently lacking, and the effects of natural degradation mechanisms on TSE infectivity are largely unknown. An improved understanding of the processes affecting the mobility, persistence, and bioavailability of prions in soil is needed for the management of TSE-contaminated environments.

Potential role of soil properties in the spread of CWD in western Canada

“…PrP CWD has changed by binding with HA but the exact mechanism of this process is still unclear. 40 In other studies, 44 it was suggested that negativelycharged HA could encapsulate positively-charged proteins and preserve their activity. A more recent study 20 has shown HA-like substances copolymerize with recPrP and irreversibly involve the PrP in their structure creating complexes which decrease recPrP recovery.…”

“…Prion-SOM interactions are not well characterized. 40 In studies where the ability of SOM compounds to bind uninfectious recombinantly generated PrP was investigated, the affinity of SOM for recPrP was almost equivalent to that offered by the clay mineral surfaces. [17][18][19][20] In addition, pure HA not only exhibited the strongest affinity for recPrP but also increased (about 10×) the sorption capacity of kaolinite and Mte clays.…”

“…19 However, differences in the structure of infectious and non-infectious prion proteins require more judicious analyses of these results to estimate SOM-infectious prion interactions. 40 The binding mechanism of SOM and its influence on prion infectivity is still poorly understood. Some results suggest that dissolved organic matter influences inactivation of infectious prions (PrP Sc ) in water; 41 and that soil humic acids inhibit the transformation of PrP c into PrP Sclike structure.…”

Supercritical Water Gasification of Municipal Sludge: A Novel Approach to Waste Treatment and Energy Recovery

“…The pathogens are a result of normal, human metabolic wastes as well as additional loading from medical effluents (Arthurson, 2008;Deblonde et al, 2011;Lewis et al, 2002;Mathney, 2011;Reilly, 2001;Straub et al, 1993;USEPA, 2009;Verlicchi et al, 2010). There are fewer than two dozen pathogens (e.g., fecal coliforms, Salmonella, enteric viruses, and parasites) monitored in sewage sludge (Mathney, 2011;NASNRC, 2002;Reilly, 2001;Snyder, 2005;USEPA, , 2002bUSEPA, , 2003, and many dangerous pathogens (e.g., prions) are neither affected by sewage treatment nor detected by standard analytical methods (Gale & Stanield, 2001;NASNRC, 2002;Peterson et al, 2008b;Saunders et al, 2008;Smith et al, 2011;Snyder, 2005).…”

Metals in obex and retropharyngeal lymph nodes of Illinois white-tailed deer and their variations associated with CWD status

“…[27][28][29][30] However, other soil characteristics, such as natural oxidants like manganese oxides (MnO 2 ), appear to interfere with the conversion of PrP C to PrP Sc . 31 To our knowledge there is no data regarding the concentration of Mn, Cu, Fe and Mg in obex and RLN of white-tailed deer even though these tissues are the preferred sites for diagnostic sampling and testing for CWD, and target sites for PrP Sc accumulation during infection.…”