Condensation of PrPC into insoluble aggregates is, as with other AMPs, overtly a host response to entrap and inactivate the target pathogen (in this case, specific nucleic acids), but PrPSc formation only takes place late in infection (reviewed in reference [5]) – and sometimes not at all if there is mismatching between donor and recipient (e.g., first passages of BSE in mice [56–58, 60]), despite high titers of infectivity – raising the question of the molecular form of the infectious TSE agent before it is sequestered into PrPSc aggregates. This evidence concerns the gene PRNP and infection.