These experiments clearly show that this BSE-derived strain does not require diglycosylated host PrP (the predominant characteristic of the glycoform used to identify BSE strains) to be pathogenic; however, the presence of sugars at N196 of host PrP would appear to allow more efficient progression of TSE disease, because the time taken to reach terminal disease is dramatically shorter in wild-type mice having normal PrPC glycosylation. The gene discussed is PRNP; the disease is human prion disease.