Human TSE disease - Viral or protein only?

Nature Medicine

Volumn 3, Issue 5, 1997, Pages 491-492

  Chesebro, Bruce ^a  

^a NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BRAIN SPONGIOSIS; CREUTZFELDT JAKOB DISEASE; HUMAN; PRION DISEASE; PRIORITY JOURNAL; SHORT SURVEY; VIRUS INFECTION;

EID: 0030978055     PISSN: 10788956     EISSN: None     Source Type: Journal    
DOI: 10.1038/nm0597-491     Document Type: Short Survey

References (16)

1. Caughey, B. & Chesebro, B. Prion protein and the transmissible spongiform encephalopathies. Trends Biol. Sci. 7, 56-62 (1997).
2. Griffith, J.S. Self-replication and scrapie. Nature 215, 1043-1044 (1967).
3. Prusiner, S.B. Novel proteinaceous infectious particles cause scrapie. Science 216, 136-144 (1982).
4. Gajdusek, D.C. Transmissible and nontransmissible amyloidoses: Autocatalytic post-translational conversion of host precursor proteins to beta-pleated configurations. J. Neuroimmunol. 20, 95-110 (1988).
5. Hsiao, K.K. et al. Spontaneous neurodegeneration in transgenic mice with mutant prion protein. Science 250, 1587-1590 (1990).
6. Westaway, D. et al. Degeneration of skeletal muscle, peripheral nerves, and the central nervous system in transgenic mice overexpressing wild-type prion proteins. Cell 76, 117-129 (1994).
7. Hsiao, K.K. et al. Serial transmission in rodents of neurodegeneration from transgenic mice expressing mutant prion protein. Proc. Natl. Acad. Sci. USA 91, 9126-9130 (1994).
8. Brown, P. et al. Human spongiform encephalopathy: The National Institutes of Health series of 300 cases of experimentally transmitted disease. Ann. Neurol. 35, 513-529 (1994).
9. Silvestrini, M.C. et al. Identification of the prion protein allotypes that accumulate in the brain of sporadic and familial Creutzfeldt-Jakob disease patients. Nature Med. 3, 521-525 (1997).
10. Tagliavini, F. et al. Amyloid fibrils in Cerstmann-Straussler-Scheinker disease (Indiana and Swedish kindreds) express only PrP peptides encoded by the mutant allele. Cell 79, 695-703 (1994).
11. Barbanti, P. et al. Polymorphism at codon 129 or codon 219 of PRNP and clinical heterogeneity in a previously unreported family with Gerstmann-Straussler-Scheinker disease (PrP-P1021. mutation). Neurology 47, 734-741 (1996).
12. Gabizon, R. et al. Insoluble wild-type and protease-resistant mutant protein in brains of patients with inherited prion disease. Nature Med. 2, 59-64 (1996).
13. Kitamoto, T., Yamaguchi, K., Doh-ura, K. & Tateishi, J. A prion protein missense variant is integrated in kuru plaque cores in patients with Gerstmann-Straussler syndrome. Neurology 41, 306-310 (1991).
14. Young, N.S. Parvoviruses. in Fields Virology, (eds. Fields B.N., Knipe, D.M. & Howley P.M.) 2199-2220 (Lippincott-Raven, Philadelphia, 1996).
15. Goldfarb, L.G. et al. Creutzfeldt-Jacob disease associated with the PRNP codon 200Lys mutation: an analysis of 45 families. Eur. J. Epidemiol. 7, 477-486 (1991).
16. Pocchiari, M. et al. A new point mutation of the prion protein gene in Creutzfeldt-Jakob disease. Ann. Neurol. 34, 802-807 (1993).