PL EN


Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników
2000 | 56 | 06 |

Tytuł artykułu

Nowa odmiana choroby Creutzfeldta-Jakoba a gabczasta encefalopatia u bydla

Autorzy

Warianty tytułu

Języki publikacji

PL

Abstrakty

EN
In March 1996 the UK government stated that the most likely cause of a new disease defined as being a new variant of Creutzfeldt-Jakob disease (vCJD) was exposure to a causative agent of bovine spongiform encephalopathy (BSE). Since then, further cases and research point to a link between the two diseases. The most convincing evidence has been demonstrated in experiments carried out by two groups of researchers led by Moira Bruce and John Collinge. Both groups reinforce the conclusion that vCJD is quite distinct from other forms of CJD and provide essential data indicating that this new variant of the disease is caused by an agent strain of BSE. These recent results include a large number of transmissions to both transgenic mice expressing human PrP and their non-transgenic counterparts and support the conclusion that vCJD and BSE infective factors are highly similar in their molecular and pathogenic features. The article discusses the data which ,-both confirm and question this conclusion.

Wydawca

-

Rocznik

Tom

56

Numer

06

Opis fizyczny

s.355-362,bibliogr.

Twórcy

autor
  • Akademia Rolnicza, ul. Norwida 31, 50-375 Wroclaw

Bibliografia

  • 1. Aguzzi A., Weissmann C. : Prion research: The next frontiers. Nature 1997, 389, 795-798.
  • 2. Almond J.: Bovine spongiform encephalopathy: does it transit to humans? WPHLS - Microbiol. Dig. 1996, 13, 116-119.
  • 3. Almond J. W., Pattison J.: Human BSE. Nature 1997, 389, 437-438.
  • 4. Born N., Mestre-Frances N., Belli R, Cathala F, Gajdusek D. C., Brown P.: Natural and experimental oral infection 0f non-human primates by bovine spongiform encephalopathy agents. Proc. Ntnl. Acad. Sci. USA 1999, 96, 4046-4052.
  • 5. Brandner S., Isenmann S., Reaber A., Fisher M.: Normal host prion protein necessary for scrapie-induced neurotoxity. Nature 1996, 379, 339-343.
  • 6. Brown K. I., Stewart K., Bruce M. E., Fraser K.: Severely combinet immu- nodeficient SCID mice resist infection with bovine spongiform encephalopathy. J. gen. Virol. 1997, 78, 2707-2712.
  • 7. Bruce M. E., Will R. G., Ironside J. W., Me Connell I., Drummond IX, Suttie A.: Transmissions to mice indicate that new variant CJD is caused by BSE agent. Nature 1997, 388, 498-501.
  • 8. Cohen C. H., CesbronJ. Y, Valleron A. J.: Cost-effectiveness of bovine spongiform encephalopathy screening. Vet. Rec. 1999, 144, 705-707.
  • 9. Collinge J., Sidle K. C. L, Meads J., Ironside I., Hill A. F.: Molecular analysis of prion strain variation and the aetiology of .,new variant” CJD. Nature 1996, 383, 685-690.
  • 10. Collinge J., Palmer M. S., Sidle К. C. L., Hill A. F, GowlandI.: Unaltered susceptibility to BSE in transgenic mice expressing human prion protein. Nature 1997, 389, 526-529.
  • 11. Estibeiro J. P: Multiple roles for PrP in the prion disease. Trends Neurol. Sci. 1996, 19, 257-262.
  • 12. Hill A. F, Desbruslais M., Joiner S., Sidle К. C. L., Gowland I., Collinge J.: The same prion strain causes vCJD and BSE. Nature 1997, 389, 448-450.
  • 13. Hill A. F. Antoniou M., Collinge J.: Protease resistant prion protein produced in vitro lacks detectable infectivity. J. gen. Virol. 1999, 80, 11-17.
  • 14. Kellershohn N., Laurent M.: Species barrier in prion disease: a kinetic interpretation based on the conformational adaptation of the prion protein. Bio­chemical J. (London) 1998, 334, 539-545.
  • 15. Kenward N., London M., Laszlo L., Mayer R. J.: Heat shock proteins, molecular chaperones and prion encephalopaties. Cell Stress Chaperones 1996, 1, 18-24.
  • 16. Klein M. A., FriggR., FlechsigE.: A crucial role for В cells in neuroinvasive scrapie. Nature (London) 1997, 390, 687-690.
  • 17. Korth C., Stierli B., Streit P, Moser M.: Prion PrP90 - specific epitope defined by mononucleal antibody. Nature (London) 1997, 390, 74-79.
  • 18. Larski Z.: Gąbczasta encefalopatia bydła (BSE), nowe fakty i hipotezy. Medycyna Wet. 1997, 52, 479-483.
  • 19. Lasmezas C. I., Deslys J. P, Demamay R., Adiou K. I., Lamoury F: BSE transmission to macaques. Nature 1996, 381, 743-744.
  • 2D.Lasmezas С. I., Deslys J. P, Robain O., Jaegly A.: Transmission of the BSE agent to mice in the absence of detectable prion protein. Science 1997, 275, 402-405.
  • 21 .Lee K. H., Harrington M. G.: 14-3-3 protein and BSE. Vet. Rec. 1997, 140, 206-209.
  • 22. Liberski P: Nagroda Nobla 1997: Priony - za i przeciw kontrowersyjnej hipotezie. Postępy Mikrobiol. 1999, 37, 9-32.
  • 23. Manuelidis L., Fritch W., Xi You Gen.: Evolution of a strain of CJD that induces BSE like plaques. Science 1997, 277, 94-98.
  • 24. Moore R. C., Malton D. W.:Transgenic analysis of prion diseases. Mol. Human Reproduct. 1997, 3, 529-537.
  • 25. Nathanson N., Wilesmith J., Griot C: Bovine spongiphorm encephalopathy (BSE): Causes and consequences of a common source epidemic. Am. J. Epidemiol. 1997, 145, 959-967.
  • 26. PrusinerS. B.: Molecular biology and pathogenesis of prion diseases., Trends Biochim. Sci. 1996, 21, 482-490.
  • 27. Prusiner S. B., Scott M. R.:Genetics of prions., Ann. Rev. Gen. 1997, 31, 139.
  • 28. Rabber A. J., Klein M. A., Frigg R., Flechsig E., Aguzzi A., Weissmann C.: PrP-dependent association of prions with splenic but not circulating lymphocytes of scrapie-infected mice. EMBO J. 1999, 18, 2702-2734.
  • 29. Raymond G. R., Hope J., Kocisko D. A., Priola S. A., RaymondL. D., Res- sers A.: Molecular assessment of the potential transmissibilities of BSE and scrapie to humans. Nature (London) 1997, 388, 285-288.
  • 30. Rick R., Hornemann S., Wilder G., Billeter M., Glockshuber R., Wuthrich K.: NMR structure of the mouse prion protein domain PrP (121-231). Nature 1996, 382, 180-183.
  • 31. Robey W. G., Jackson R., Walters R. L.:Use of cerebrospinal fluid levels of 14-3-3 in predicting neurodegeneration in confirmed BSE symptomatic cattle. Vet. Rec. 1998, 143, 50-53.
  • 32.Schreuder В. E. C., Wilesmith J. W., Ryan J. В. M., Straub О. C.: Risk of BSE from the import of cattle from the United Kingdom into countries of the European Union. Vet. Rec. 1997, 141, 187-190.
  • 33.Scott M. R., SafarJ., Telling J., Nguyen D.: Identification of a prion protein epitope modulating transmission of bovine spongiphorm encephalopathy prions to transgenic mice. Proc. Natl. Acad. Sci. USA 1997,94, 14279-14292.
  • 34. Somerville R. A., Chong A., Mulqueen O. U., Birkett C. R., Collinge J. : Biochemical typing of scrapie strains. Nature 1997, 386, 564-567.
  • 35. Telling G. C., Parchi P, De Armond G. J., Cortelli P: Evidence for the conformation of the pathologic isoform of the prion protein enciphering and propagating prion diversity. Science 1996, 274, 2079-2082.
  • 36. Van Keulen L. J. M, Schreider В. E. C., Vromans M. E. W, Langeveld J. P. M., Smith M. A.: Scrapie-associated prion proteinin the gastro-intestinal tract of sheep with natural scrapie. J. comp. Path. 1999, 121, 55-64.
  • 37. Will R. G.: A new variant of Creutzfeldt-Jakob disease in UK., Proc. Univ. Coll. Chester UK 1997, s. 85-88.
  • 38. Young G. R., Fletcher N. A., Zeidler M., Estibeiro K. L., Ironside J. W.: Creutzfeldt-Jakob disease in a beef farmer. Lancet 1996, 348, 610-615.
  • 39. Bovine spongiform encephalopathy (BSE). New release 16 June 1999. UK Institute of Food Science and Technology. Report, London 1999, Internet:/ http:/www.bse.org.uk.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

bwmeta1.element.agro-article-86696528-a3ff-460c-a28b-3029f56fbe41
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.