Nucleic acid-free mutation of prion strains.
While prions share the ability to propagate strain information with nucleic acid-based pathogens, it is unclear how they mutate and acquire fitness in the absence of this informational component. Because prion diseases occur as epidemics, understanding this mechanism is of paramount importance for implementing control strategies to limit their spread and for evaluating their zoonotic potential. Here we review emerging evidence indicating how prion protein primary structures, in concert with PrP(Sc) conformational compatibility, determine prion strain mutation.
Telling
Glenn C
GC
Department of Microbiology, Immunology and Molecular Genetics, Sanders Brown Center on Aging, Department of Neurology, University of Kentucky Medical Center, Lexington, KY, USA. gtell2@uky.edu
D000818:Animals; D006801:Humans; D009154:Mutation / Q000235:genetics*; D009696:Nucleic Acids / Q000378:metabolism*; D017096:Prion Diseases / Q000235:genetics / Q000635:transmission; D011328:Prions / Q000737:chemistry / Q000235:genetics*; D013045:Species Specificity
D009696:Nucleic Acids; D011328:Prions