Numerous curable prion strains/variants appear when anti-prion systems are disabled

We have identified genes that block prion generation, cure most nascent prions as they are formed, and limit the pathogenicity of those prions that form in spite of the two other anti-prion activities. Defects in the prion-curing proteins result in much higher frequency of spontaneous prion generation, and the prions that arise are usually cured by replacement of the normal level of the anti-prion protein. These systems constitute an "innate immunity" to prions. It is hoped that analogous or homologous systems in humans will be sought based on our work that will be useful in treatment of human amyloid diseases.