Bovine spongiform infectivity

If the source of the infechon persists, after onset, then the incidence of new cases is maintained at a level which is commensurate with the infechvity of the pathogen and the ffequeney of exposure of individuals. In this manner, if cases of the variant Creutzfeldt-Jacob disease (vCJD), first recognized in the mid-1990s, relates to human exposure to bovine spongiform encephalopathy-infected beef in the early 1980s, then... 

However, the emergence of variant Creutzfeldt-Jakob disease (vCJD) in the UK and France has raised concern about a new theoretical risk of infection in patients treated with blood and blood products (198). Animal experiments in which blood from sheep infected with bovine spongiform encephalopathy and natural scrapie-infected sheep into scrapie-free recipient animals have suggested disease transmission by the blood transfusion route in 2 of 24 sheep with bovine spongiform encephalopathy and in 4 of 21 sheep with scrapie (199). Many European countries have incorporated leukodepletion of all blood products, as leukocytes are believed to play a key role in the pathogenesis of variant Creutzfeldt-Jakob disease (198). In some countries, people who have lived in the UK for a period longer than 6 months between 1980 and 1996 are excluded from blood donation (13). Furthermore, it has been shown that various steps used in the manufacture of plasma-derived products also contribute to reduced infectivity by bovine spongiform encephalopathy (198). 

Pattison, J. (1998) The emergence of bovine spongiform encephalopathy. Emerg Infect Dis, 4,390-394. 

Prions (small proteinaceous infectious particles) are a unique class of infectious agent causing spongiform encephalopathies such as bovine spongiform encephalopathy (BSE) in cattle and Creutzfeldt-Jakob disease (CJD) in humans. There is considerable concern about the transmission of these agents from infected animals or patients. Risk of infec-tivity is highest in brain, spinal cord and eye tissues. There are still many unknown factors regarding de-... 

Buschmann A, Groschup MH (2005) Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J Infect Dis 192 934-942... 

Robinson MM, Hadlow WJ, Huff TP, Wells GAH, Dawson M, Marsh RF, Gorham JR (1994) Experimental infection of mink with bovine spongiform encephalopathy. J Gen Virol 75 2151-2155... 

Plinston C, Hart P, Chong A, Hunter N, Foster J, PiccardoP, Manson JC, Barron RM (2011) Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy infection following passage in sheep. J Virol 85 1174—1181... 

Rodriguez A, Martin M, Albasanz JL, Barrachina M, Espinosa JC, Torres JM, Ferrer 1 (2006) Adenosine A1 receptor protein levels and activity is increased in the cerebral cortex in Creutzfeldt-Jakob disease and in bovine spongiform encephalopathy-infected bovine-PrP mice. J Neuropathol Exp Neurol 65 964-975... 

Bons, N., Mestie-Frances, N., Belh, P, Cathala, F., Gajdusek, D. C., and Brown, P. 1999. Natural and experimental oral infection of nonhuman primates by bovine spongiform encephalopathy agents. Proc. Natl. Acad. Sci. 96 4046-4051... 

Brown, D. R., Qin, K., Herms, J. W., Madlung, A., Manson, J., Strome, R., Fraser, P. E., Kruck, T., von Bohlen, A., Schulz-Schaeffer, W., Giese, A., Westaway, D., and Kretzschmar, H. 1997. The cellular prion protein binds copper in vivo. Nature 390 684-687 Brown, R, WiU, R. G., Bradley, R., Asher, D. M., and DetwUer, L. 2001. Bovine spongiform encephalopathy and variant Creutzfeldt— Jacob disease background, evolution, and current concerns. Emerging Infect. Dis. 7 6-16... 

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