TSE agent strains and PrP: reconciling structure and function.
The molecular structures of the infectious agents that cause transmissible spongiform encephalopathy (TSE) diseases are still not known despite the current wide acceptance of the prion hypothesis as the basis for their resolution. Here, data supporting and challenging the prion hypothesis in relation to both the biochemical and biological properties of TSE infectious agents are discussed. The need for the independent transmission of TSE agent-specific genetic information is described and the requirements for the molecule to carry this information are proposed. Such a molecule is likely to be a small nucleic acid encoding information to determine the diversity of the pathogenesis of TSE agents.
Somerville
Robert A
RA
Neuropathogenesis Unit, Institute for Animal Health, West Mains Road, Edinburgh, Scotland, UK, EH9 3JF. robert.somerville@bbsrc.ac.uk
D000818:Animals; D018620:PrPSc Proteins / Q000737:chemistry / Q000235:genetics / Q000472:pathogenicity; D017096:Prion Diseases / Q000209:etiology* / Q000235:genetics; D011328:Prions / Q000737:chemistry / Q000145:classification* / Q000235:genetics / Q000472:pathogenicity*; D013329:Structure-Activity Relationship
D018620:PrPSc Proteins; D011328:Prions