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  • The inconsistences noted at primary passage in attack rate and lack of TSE vacuolation, could have been a consequence of the interaction between human and mouse genetic backgrounds i.e. PRNP codon 129 genotype and Prnp or Prnp or could be due to a lower titre of infectivity in the spleen isolates causing longer incubation periods and decreased numbers of mice exhibiting signs of prion disease within their lifespan (Bruce et al., 2001; Bruce, 2003; Ritchie et al., 2009).
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