The main hypothesis for prion diseases proposes that the cellular protein (PrPC) can be altered into a misfolded, β-sheet-rich isoform (PrPSc). We describe here that host nucleic acid may catalyze the conversion between PrPC and PrPSc isoforms, by reducing the protein mobility and by making the protein-protein interactions more likely. We summarize the findings, focusing in the biological relevance of the catalytic action of nucleic acid.
Keywords: prion, structural conversion, nucleic acid, catalysis, aggregation