Nonetheless, it’s still possible that either VV2 prions were the source of infection or that passage through humans altered the properties of the original infectious prions leading to an iCJD MV2K prion strain or strains that do not recapitulate the sCJD MV2K phenotype when inoculated into transgenic mice over-expressing human PrPC-M129. Here, PRNP is linked to infection.