Sodium hydroxide treatment effectively inhibits PrP^CWD replication in farm soil

Abstract

Chronic wasting disease (CWD) agents are shed into biological samples, facilitating their horizontal transmission between cervid species. Once prions enter the environment, binding of PrP CWD by soil particles may maintain them near the soil surface, posing a challenge for decontamination. A 2 N sodium hydroxide (NaOH) or 2% sodium hypochlorite (NaClO) solution is traditionally recommended for prion decontamination of equipment and surfaces. Using protein misfolding cyclic amplification with beads and a bioassay with TgElk mice, we compared the effects of these disinfectants in CWD-contaminated soil for 1 or 16 h to those of controls of known infectious titres. Our results suggest that 2 N NaOH in a 1/5 farm soil volume provides a large decrease (>10 2-fold) in prion infectivity.

A Novel, Reliable and Highly Versatile Method to Evaluate Different Prion Decontamination Procedures

“…These prion-coated steel wires have been used to assess the efficacy of prion inactivation or elimination treatments by determining infectivity in vivo (Peretz et al, 2006;Giles et al, 2008;Berberidou et al, 2013) and by other criteria by ex vivo (Edgeworth et al, 2011) and in vitro (Fichet et al, 2004;Belondrade et al, 2016;Mori et al, 2016;Belondrade et al, 2020) methodologies also. Limited studies have been performed using other materials, mainly metallic or oxidized surfaces such as titanium (Berberidou et al, 2013), aluminum oxide and silicon dioxide (Jacobson et al, 2013), and non-metallic materials such as bricks (Gough et al, 2017) or farm soil (Sohn et al, 2019). These data, together with the results presented here, clearly demonstrate the relevance of the material prions are attached to with respect to the variability in efficacy of decontaminants, highlighting differences even between metallic surfaces such as steel and titanium (Berberidou et al, 2013).…”

In‐depth examination of PrP Sc in Holstein cattle carrying the E211K somatic mutation of the bovine prion protein gene ( PRNP )

“…Fragmented PrP Sc presents an increased number of seeds, and this technique provides an enhanced detection threshold (Murayama et al, 2016;Sohn et al, 2019). Thus, the detection of PrP Sc by western blot analysis was limited, and further in-depth examination is needed.…”

“…Prion diseases are malignant transmissible neurodegenerative diseases caused by misfolded prion protein (PrP Sc ) derived from normal prion protein (PrP C ), and these diseases show paramount host ranges, including Creutzfeldt‐Jakob disease (CJD), Gerstmann‐Straussler‐Scheinker syndrome (GSS) and fatal familial insomnia (FFI) in humans, bovine spongiform encephalopathy (BSE) in cattle, and chronic wasting disease (CWD) in the cervid family (Arifin et al., 2021; Jeong, M. J., Kim, & Jeong, 2021; Kim et al., 2018; Kim, D. J., Kim, Kim, & Jeong, 2020; Kim, H. H., Kim, Kim, Kim, Kim, & Jeong, 2020; Kim, Y. C. & Jeong 2020; Kim, Y. C., Kim, Won, Do, & Jeong, 2020; Kim, Y. C., Won, & Jeong, 2020; Kim, Y.C., Kim, Won, & Jeong, 2020; Lee et al., 2013; Prusiner, 1998; Roh et al., 2020; Sohn et al., 2019; Won, S.Y., Kim, Do, & Jeong, 2020).…”

“…In addition, protein misfolding cyclic amplification (PMCA) is based on the conversion of PrP C to PrP Sc by fragmented PrP Sc seeds using intermittent sonication, and the minimum PrP amount for detection is 1.3 attogram. Fragmented PrP Sc presents an increased number of seeds, and this technique provides an enhanced detection threshold (Murayama et al., 2016; Sohn et al., 2019). Thus, the detection of PrP Sc by western blot analysis was limited, and further in‐depth examination is needed.…”

Polymorphisms of the prion‐related protein gene are strongly associated with cervids’ susceptibility to chronic wasting disease

“…Chronic wasting disease (CWD) is a prion-related transmissible spongiform encephalopathy of cervids such as scrapie in sheep and goats, bovine spongiform encephalopathy (BSE) in cattle and Creutzfeldt-Jakob disease (CJD), fatal familial insomnia and Gerstmann-Sträussler-Scheinker syndrome in humans. [1][2][3][4][5][6][7][8][9][10][11][12] CWD is transmitted horizontally and vertically through abnormal prion protein (PrP Sc ), which originates from normal prion protein (PrP C ). Since CWD was first reported in the USA in 1967, intercontinental propagation has also occurred from America to Asia and Europe.…”