NR AHUZ
AU Manuelidis,L.; Fritch,W.; Xi,Y.G.
TI Evolution of a strain of CJD that induces BSE-like plaques
QU Science 1997 Jul 4; 277(5322): 94-8
PT journal article
AB Bovine spongiform encephalopathy (BSE) has become a public health issue because a recently evolved BSE agent has infected people, yielding an unusual form of Creutzfeldt-Jakob disease (CJD). A new CJD agent that provokes similar amyloid plaques and cerebellar pathology was serially propagated. First-passage rats showed obvious clinical signs and activated microglia but had negligible PrPres (the more protease-resistant form of host PrP) or cerebellar lesions. Microglia and astrocytes may participate in strain selection because the agent evolved, stabilized, and reproducibly provoked BSE-like disease in subsequent passages. Early vacuolar change involving activated microglia and astrocytes preceded significant PrPres accumulation by more than 50 days. These studies reveal several inflammatory host reactions to an exogenous agent.
MH Amyloid beta-Protein Precursor/analysis; Animal; Astrocytes/chemistry/*ultrastructure; Brain/*pathology; Brain Chemistry; Cerebellum/chemistry/pathology; Creutzfeldt-Jakob Syndrome/metabolism/*pathology; Cricetulus; Encephalopathy, Bovine Spongiform/metabolism/*pathology; Glial Fibrillary Acidic Protein/genetics/metabolism; Glycoproteins/analysis; Hamsters; Inflammation; Macrophages/chemistry/ultrastructure; Mice; Mice, Inbred Strains; Microglia/chemistry/*ultrastructure; Microscopy, Electron; PrPsc Proteins/*analysis/pathogenicity; RNA/metabolism; Rats; Rats, Sprague-Dawley; Support, U.S. Gov't, P.H.S.; Time Factors; Ubiquitins/analysis; Vacuoles/ultrastructure; Virulence
AD Section of Neuropathology, Yale Medical School, 310 Cedar Street, New Haven, CT 06510, USA. laura.manuelidis@yale.edu
SP englisch
PO USA