Chemical and biophysical insights into the propagation of prion strains
Author(s) -
Jeppe Falsig,
K. Peter R. Nilsson,
Tuomas P. J. Knowles,
Adriano Aguzzi
Publication year - 2008
Publication title -
hfsp journal
Language(s) - English
Resource type - Journals
eISSN - 1955-2068
pISSN - 1955-205X
DOI - 10.2976/1.2990786
Subject(s) - biology , nucleic acid , tropism , prion protein , virology , context (archaeology) , transmissible spongiform encephalopathy , in vitro , strain (injury) , disease , infectious agent , in vivo , scrapie , genetics , virus , medicine , pathology , paleontology , anatomy
Transmissible spongiform encephalopathies (TSEs) are lethal infectious neurodegenerative diseases. TSEs are caused by prions, infectious agents lacking informational nucleic acids, and possibly identical with higher-order aggregates of the cellular glycolipoprotein PrP(C). Prion strains are derived from TSE isolates that, even after inoculation into genetically identical hosts, cause disease with distinct patterns of protein aggregate deposition, incubation times, morphology of the characteristic brain damage, and cellular tropism. Most of these traits are relatively stable across serial passages. Here we review current techniques for studying prion strain differences in vivo and in cells, and discuss the strain phenomena in the general context of the knowledge gained from modeling prion fibril growth in vitro and in simple organisms.
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