It is thus possible that virus infections might increase the conversion rate of PrPC into PrPSc, by increasing the accessibility of PrPC to PrPSc through enhancing the cell surface binding of PrPSc molecules and stimulating their internalization to lysosomal compartments, where PrPSc is supposed to convert PrPC into PrPSc, and/or increasing the release of PrPSc from prion-infected cells to prion-uninfected neighboring cells (Figure 1). The gene discussed is PRNP; the disease is viral infectious disease.