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1 persistently infected with the mouse-adapted scrapie agent.
2 multiple doses of feed contaminated with the scrapie agent.
3 nucleating the biological replication of the scrapie agent.
4 ty of white-tailed deer (WTD) to the classic scrapie agent.
5 ction by sheep-derived Chandler (Ch) and 22L scrapie agents.
6 ormation upon exposure of cells to different scrapie agents.
7 udied by making 4 serial passages of hamster scrapie agent (263K) in mice.
8 ally and orally infected sheep with clinical scrapie agent and orally infected preclinical and infect
9                              While most anti-scrapie agent compounds inhibit PrP-res formation in vit
10   In addition, sheep with no exposure to the scrapie agent did not contain any measurable prions with
11 nt from sheep or oronasally with the classic scrapie agent from goats (n = 6).
12 nt oral/intranasal exposure with the classic scrapie agent from sheep or oronasally with the classic
13  play a key role in the translocation of the scrapie agent from the gut lumen to the GALT from which
14 ransmitted naturally through exposure to the scrapie agent in wasted placentas of infected ewes.
15 icating that PrP expression was required for scrapie agent induction of other cytokines detected.
16  PrP(sc) was detected in the blood of 55% of scrapie agent-infected animals (n = 80) and 71% of anima
17 nses, primary glial cultures were exposed to scrapie agent-infected brain homogenates.
18 to analyze protein levels of 24 cytokines in scrapie agent-infected C57BL/10 mouse brains, we observe
19 sistant prion protein (PrP-res) formation in scrapie agent-infected cells, we tested other antimalari
20 ve compound tested against RML and 22L mouse scrapie agent-infected cells, with 50% inhibitory concen
21 c, potently inhibits PrP-res accumulation in scrapie agent-infected neuroblastoma cells (50% inhibito
22 e the onset of clinical signs in a subset of scrapie agent-infected sheep, followed from 3 months of
23                                              Scrapie agent-infected wild-type mice and transgenic mic
24 rodegenerative disease by 160 days after RML scrapie agent infection.
25                                              Scrapie agent infectivity was present in the PNS at low
26 and Creutzfeldt-Jakob agents as well as with scrapie agent isolated from sheep or mice.
27 n vivo in GPI(-/-) PrP tg mice infected with scrapie agent may likely involve the GABAergic pathway.
28 stigated the contribution of CD11c(+) DCs in scrapie agent neuroinvasion through use of CD11c-dipther
29                           Using two distinct scrapie agent strains (ME7 and 139A scrapie agents), we
30                            Initial work with scrapie agents suggested that B cells were central vecto
31 ay the onset of intraperitoneally inoculated scrapie agent, the result previously observed with quina
32              After infection with RML murine scrapie agent, transgenic (tg) mice expressing prion pro
33 evels of BSE in the presence of an excess of scrapie agent was also applied to brain and lymphoreticu
34 distinct scrapie agent strains (ME7 and 139A scrapie agents), we show that when CD11c(+) DCs were tra
35 cted with the 263K strain of hamster-adapted scrapie agent were placed in covered quartz-glass crucib
36 oradic CJD and BSE agents and representative scrapie agents were clearly different from kuru in incub