“…However, accumulated evidence has shown that prion infection stimulates pattern recognition receptor (PRR)-related molecules and related signalling pathways, including Toll-like receptors (TLRs), interferon regulatory factors (IRFs), and some cytokines (Prinz et al , 2003; Spinner et al , 2008; Bradford and Mabbott, 2012; Ishibashi et al , 2012 a ; Nuvolone et al , 2015; Kang et al , 2016). We have also reported that IRF3, which upregulates type I interferon (I-IFN) in various cell types, including neurons, plays a role in host defence against prion infection (Ishibashi et al , 2012 a , b ), and that persistent prion infection negatively regulates IRF3 via suppression of the transcription factor Octamer-binding protein-1 (Oct-1) (Homma et al , 2014 a ). Prions also exhibit strain diversity and reciprocal interference between strains, analogous to viral infections (Dickinson et al , 1972, 1975; Manuelidis, 1998).…”