ライフサイエンスコーパス: BSE

1 BSE prions were found in the sympathetic nervous system

2 BSE was transmitted to the bovine line but did not trans

3 BSE-C causes the fatal prion disease named new variant C

4 Western blotting consistently detected 50% BSE within a mixture, but at higher dilutions it had var

5 of these allegedly resistant species into a BSE-type prion protein.

6 6(+/-) mice challenged with red deer-adapted BSE resulted in 90% to 100% attack rates, and BSE from c

7 Challenge with a mouse-adapted BSE strain results in dramatically shortened incubation

8 propagation of distinct prion strains after BSE prion infection.

9 his sPMCA-based assay specifically amplified BSE PrP(Sc) within brain mixes with 100% specificity and

10 Sporadic CJD and BSE agents and representative scrapie agents were clearl

11 studies revealed the following: (i) CWD and BSE seeded their homologous species' PrP best; (ii) fCWD

12 nces between the species barriers of CWD and BSE.

13 encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2

14 PrP)Prnp(0/0) mice inoculated with nvCJD and BSE brain extracts were indistinguishable and differed d

15 SE resulted in 90% to 100% attack rates, and BSE from cattle failed to transmit, indicating agent ada

16 s associated with both scrapie (PrP[Sc]) and BSE (PrP[BSE]).

17 he potential transmissibility of scrapie and BSE to humans.

18 on protein are fully susceptible to vCJD and BSE prions but not to sporadic CJD prions.

19 zfeldt-Jakob, and in animal diseases such as BSE.

20 Two atypical BSE strains, bovine amyloidotic spongiform encephalopath

21 This was primarily because BSE prions were found to be transmissible to humans.

22 within defined CNS regions, compared between BSE and scrapie cases and also between two experimental

23 ot provide evidence of a causal link between BSE and CJD in Europe as a whole.

24 Both BSE and SFN significantly prevented diabetes-induced car

25 at the same agent strain is involved in both BSE and vCJD.

26 ) with the RT-QuIC assay and found that both BSE forms can be detected and distinguished using partic

27 human deaths considering exposure to bovine BSE alone, with the upper bound increasing to 150,000 on

28 action products indicated that H-, L-, and C-BSE have distinctive prion seeding activities and can be

29 tle are susceptible to both classical BSE (C-BSE) and atypical forms of BSE.

30 ested brain tissue from cattle affected by C-BSE and atypical L-type bovine spongiform encephalopathy

31 lassical bovine spongiform encephalopathy (C-BSE) and the atypical H-type BSE (H-BSE) and L-type BSE

32 lassical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoon

33 c potential of scrapie might be similar to c-BSE.

34 d using multiple rPrPSen substrates, while C-BSE was much more selective.

35 amplified small amounts of ovine and caprine BSE agent which had been mixed into a range of scrapie-p

36 variable with respect to the original cattle BSE prion, suggesting that the naturally low susceptibil

37 have been exposed to BSE early in the cattle BSE epidemic and that serial BSE transmission in sheep m

38 hat allowed us to distinguish prions causing BSE from those causing scrapie.

39 L-BSE agent differs from both ovine classic BSE or CH1641 scrapie maintaining its specific strain pr

40 ropism, clearly differing from ovine classic BSE or from scrapie strain CH1641.

41 hat cattle are susceptible to both classical BSE (C-BSE) and atypical forms of BSE.

42 bit and dog brain homogenates with classical BSE were studied.

43 The incidence of clinical BSE disease after inoculation was high in unweaned lambs

44 ensitive assays that can specifically detect BSE, even within the presence of scrapie prion protein,

45 t assay (ELISA) method consistently detected BSE only when it was present as 99% of the mixture, with

46 both models showed that the risk of disease (BSE) transmission from BGS was negligible and could be a

47 It may be possible to distinguish BSE prions from scrapie strains in sheep by combining co

48 apts to a new species more readily than does BSE and (ii) the barrier preventing transmission of CWD

49 stics of the in vitro-adapted rabbit and dog BSE agent remained invariable with respect to the origin

50 opic resemblance to the bulk silicate Earth (BSE) for many elements, but is considered highly deplete

51 ies suggesting that the bulk silicate Earth (BSE) might have an Sm/Nd ratio 6% higher than chondrites

52 cells, referred to as the bystander effect (BSE), is not well understood in terms of the underlying

53 For all these preventive effects, BSE at high dose provided a similar effect as did SFN.

54 reduced behavioral (HIC) and electrographic (BSE) signs of seizure activity in a dose-related fashion

55 In conjunction with backscattered electron (BSE) and energy-dispersive spectroscopy (EDS) mapping of

56 ample surface, and a backscattered electron (BSE) detector, used to image the milled surfaces, genera

57 on film has very low backscattered electron (BSE) yield compared to that from the particle, so in the

58 roach that detected backscattered electrons (BSEs) and X-rays (from ionization processes) along a lar

59 dents of bovine spongiform encephalopathies (BSE) in humans have underscored this likelihood.

60 f vCJD and bovine spongiform encephalopathy (BSE) and an assessment of the effect of the codon-129 po

61 on between bovine spongiform encephalopathy (BSE) and bovine PRNP exon 3 has not been detected.

62 ackwash of bovine spongiform encephalopathy (BSE) and foot-and-mouth disease (FMD), and the advent of

63 Bovine spongiform encephalopathy (BSE) and human Creutzfeldt-Jakob disease (CJD) are among

64 Bovine spongiform encephalopathy (BSE) and its human equivalent, variant Creutzfeldt-Jakob

65 at include bovine spongiform encephalopathy (BSE) and scrapie in animals and Creutzfeldt-Jakob diseas

66 humans and bovine spongiform encephalopathy (BSE) and scrapie in animals.

67 perties of bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) prions

68 ected with bovine spongiform encephalopathy (BSE) appear to be a reservoir for transmission of varian

69 d epidemic bovine spongiform encephalopathy (BSE) are caused by a related group of infectious agents.

70 sheep and bovine spongiform encephalopathy (BSE) are manifest as ataxic illnesses.

71 utbreak of bovine spongiform encephalopathy (BSE) arose in the United Kingdom as a result of prions e

72 exposed to bovine spongiform encephalopathy (BSE) by consumption of BSE-infected beef.

73 ental oral bovine spongiform encephalopathy (BSE) challenge study was performed to elucidate the rout

74 since the bovine spongiform encephalopathy (BSE) crisis, their use has been strictly regulated.

75 The recent bovine spongiform encephalopathy (BSE) epidemic in the UK and the incidence of prion-relat

76 n from the bovine spongiform encephalopathy (BSE) epidemic, led to concerns about the potential risk

77 after the bovine spongiform encephalopathy (BSE) epidemic, when >200 cases of prion disease in human

78 ntal sheep bovine spongiform encephalopathy (BSE) from classical scrapie.

79 Bovine spongiform encephalopathy (BSE) has become a public health issue because a recently

80 rP(BSE) in bovine spongiform encephalopathy (BSE) in cattle and PrP(CJD) in Creutzfeldt-Jakob disease

81 ervids and bovine spongiform encephalopathy (BSE) in cattle are prion diseases that are caused by the

82 in causing bovine spongiform encephalopathy (BSE) in cattle has infected human beings, manifesting it

83 in sheep, bovine spongiform encephalopathy (BSE) in cattle, chronic wasting disease in deer and elk,

84 illance of bovine spongiform encephalopathy (BSE) indicates that cattle are susceptible to both class

85 In bovine spongiform encephalopathy (BSE) infection, the polymorphism effect is quite differe

86 Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE)

87 attle with bovine spongiform encephalopathy (BSE) may have been passed to humans (Hu), resulting in a

88 ected with bovine spongiform encephalopathy (BSE) may have entered the human food chain.

89 ncern that bovine spongiform encephalopathy (BSE) may have passed from cattle to humans.

90 fy them as bovine spongiform encephalopathy (BSE) or non-BSE.

91 ith either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropatholo

92 (vCJD) and bovine spongiform encephalopathy (BSE) prions are two of the prion strains most relevant t

93 ected with bovine spongiform encephalopathy (BSE) prions causes new variant Creutzfeldt-Jakob disease

94 t to which bovine spongiform encephalopathy (BSE) prions have been transmitted to humans, as a result

95 xposure to bovine spongiform encephalopathy (BSE) prions in the UK, has led to renewed interest in ku

96 Bovine spongiform encephalopathy (BSE) prions were responsible for an unforeseen epizootic

97 propagate bovine spongiform encephalopathy (BSE) prions without posing a transmission barrier.

98 ibility to bovine spongiform encephalopathy (BSE) prions, the causal agent of variant Creutzfeldt-Jak

99 6(+/-), to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species

100 xposure to bovine spongiform encephalopathy (BSE) prions.

101 r cases of bovine spongiform encephalopathy (BSE) remains an enigma.

102 mission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt-Jakob disease (CJD

103 effect on bovine spongiform encephalopathy (BSE) transmission to goats is not clear.

104 in whether bovine spongiform encephalopathy (BSE) was transmitted to sheep in the past via feed suppl

105 , scrapie, bovine spongiform encephalopathy (BSE), and Creutzfeldt-Jakob disease (CJD).

106 ntal ovine bovine spongiform encephalopathy (BSE), and natural sheep scrapie, demonstrating that bloo

107 Bovine spongiform encephalopathy (BSE), scrapie of sheep, and Creutzfeldt-Jakob disease (C

108 Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed t

109 urrence of bovine spongiform encephalopathy (BSE), there has been concern that transmission of BSE to

110 ected with bovine spongiform encephalopathy (BSE), we examined the extent of a putative epidemic.

111 Bovine spongiform encephalopathy (BSE)-associated prions were preferentially transported f

112 d the same bovine spongiform encephalopathy (BSE)-contaminated meat and bone meal that was fed to cat

113 umption of bovine spongiform encephalopathy (BSE)-contaminated meat.

114 ction with bovine spongiform encephalopathy (BSE)-like prions.

115 le disease bovine spongiform encephalopathy (BSE).

116 e agent of bovine spongiform encephalopathy (BSE).

117 e agent of bovine spongiform encephalopathy (BSE).

118 patitis C, bovine spongiform encephalopathy (BSE)/variant Creutzfeldt-Jakob disease (vCJD), Nipah vir

119 eases like bovine spongiform encephalopathy (BSE; "mad cow" disease) and Creutzfeldt-Jakob's disease,

120 om cattle (bovine spongiform encephalopathy [BSE]), both PrP variants occur in equal ratios.

121 ch actin filament has a basal strain energy (BSE) when the cell adheres to the substrate without stre

122 01 treatment conditions resulted in enhanced BSE activity during the entire fourth (untreated) withdr

123 EEG (high-voltage "brief spindle episodes" (BSE)) activity.

124 blic health issue because a recently evolved BSE agent has infected people, yielding an unusual form

125 Bundle sheath extensions (BSEs) are key features of leaf structure with currently

126 its natural source, broccoli sprout extract (BSE) by gavage every other day for 3 months, with four g

127 bovine than feline rPrP; (iv) and CWD, fCWD, BSE, and FSE all converted human rPrP, although not as e

128 ies, we studied feline CWD (fCWD) and feline BSE (i.e., feline spongiform encephalopathy [FSE]).

129 w; however, a simple model of flock-to-flock BSE transmission shows that horizontal transmission, if

130 Unlike in rodents and ruminants, foodborne BSE-associated prions entered the simian CNS via afferen

131 transmission rates by transfusion of 36% for BSE and 43% for scrapie.

132 osmium tetroxide/potassium ferricyanide, for BSE imaging, for the preparation and platinum deposition

133 smission rate higher than those reported for BSE-C.

134 In asymptomatic animals, we found BSE in 50% and 12% of gut- and tonsil-derived samples, r

135 sporadic CJD may have a disease arising from BSE exposure.

136 type PrP fractions in PrP(res) material from BSE-infected ARR/VRQ sheep.

137 as able to discriminate between PrP(Sc) from BSE-infected cattle and Tg(BoPrP) mice as well as from c

138 High-definition LF images from BSEs and X-rays were essentially generated by assembling

139 hs, with four groups: vehicle (0.1 ml/10 g), BSE-low dose (estimated SFN availability at 0.5 mg/kg),

140 esults demonstrate that transmission of goat BSE is genotype dependent, and they highlight the pivota

141 genotypes were orally inoculated with a goat-BSE isolate to assess their relative susceptibility to B

142 d on the GW plus Bethe-Salpeter equation (GW-BSE) approach of many-body perturbation theory (MBPT) is

143 sed on a GW plus Bethe-Salpeter equation (GW-BSE) approach, which employed many-body Green's-function

144 red with ab initio calculations using the GW-BSE approach.

145 ly used Tamm-Dancoff approximation to the GW-BSE approach.

146 In combination with GW-BSE theory, we prove that the excitons are of Wannier ty

147 pathy (C-BSE) and the atypical H-type BSE (H-BSE) and L-type BSE (L-BSE) strains.

148 Here, we demonstrate an RT-QuIC assay for H-BSE that can detect as little as 10(-9) dilutions of bra

149 as yet been described for the detection of H-BSE or the discrimination of each of the major bovine pr

150 cted in sheep, and in only two instances has BSE been discovered in goats.

151 review the likelihood that any UK sheep have BSE, how they might have got it, how a case could be ide

152 samples were tested with the IDEXX HerdChek BSE-Scrapie Ag Kit to detect the abnormal prion protein,

153 Surprisingly, however, BSE transmission to these transgenic mice, in addition t

154 hods as listed in the regulation to identify BSE in a blinded series of brain samples, in which ovine

155 However, identifying BSE in a sheep is not straightforward, because of its si

156 If BSE is present within the small ruminant populations, it

157 the UK has been threatened with slaughter if BSE is found in farmed sheep, largely on the grounds tha

158 However, the results also suggest that if BSE in sheep were to come to resemble scrapie it would l

159 rapolation from our results suggests that if BSE were to infect sheep in the field it may, with time

160 Here we show that, if BSE entered the sheep population and a degree of transmi

161 on-ruminant PAPs for avoiding an increase in BSE incidents, these methods are fit for monitoring non-

162 st reliable surrogate marker of infection in BSE-contaminated food, crosses the human intestinal epit

163 PrP(res) in BSE contained equimolar amounts of VRQ- and ARR-PrP, whi

164 signature able to distinguish intracranially BSE-infected macaques from healthy ones, with SERPINA3 s

165 The new U.K. BSE agent spread to many species, including humans, and

166 e (estimated SFN availability at 0.5 mg/kg), BSE-high dose (estimated SFN availability at 1.0 mg/kg),

167 Although the C- and L-BSE strains can be detected and discriminated by ultrase

168 typical H-type BSE (H-BSE) and L-type BSE (L-BSE) strains.

169 SE transmitted similarly to cattle-derived L-BSE, with respect to survival periods, histopathology, a

170 g L-type bovine spongiform encephalopathy (L-BSE), although RQ171 sheep specifically propagated a dis

171 t PrP fragment (HMM PrPres), distinct from L-BSE in QQ171 sheep.

172 e spongiform encephalopathy (L-type BSE or L-BSE) with the RT-QuIC assay and found that both BSE form

173 ogical properties of QQ171 and RQ171 ovine L-BSE prions were investigated in transgenic mice expressi

174 In both mouse lines, ovine L-BSE transmitted similarly to cattle-derived L-BSE, with

175 Specifically, L-BSE was detected using multiple rPrPSen substrates, whil

176 The L-BSE agent differs from both ovine classic BSE or CH1641

177 of ovine PrP transgenic mice infected with L-BSE from RQ171 sheep at first passage, reminiscent, in l

178 hy techniques) were unveiled in detail by LF BSE images and in calcium and phosphorus elemental maps

179 Mechanistically, BSE, like SFN, significantly up-regulated Nrf2 transcrip

180 spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countr

181 ovine spongiform encephalopathy (BSE) or non-BSE.

182 iple human and animal prion diseases but not BSE.

183 Since 2005, naturally occurring BSE has been identified in two goats.

184 lely to determine the presence or absence of BSE.

185 strong evidence that the causative agent of BSE in cattle and vCJD in humans share a common origin.

186 herent ability of these infectious agents of BSE and scrapie to affect humans following equivalent ex

187 assay based on the specific amplification of BSE PrP(Sc) using the serial protein misfolding cyclic a

188 terature on the status of risk assessment of BSE transmission was conducted, and two risk assessment

189 Relatively few cases of BSE have occurred in cattle born after 1993, and it is p

190 redicts that fewer than 20 clinical cases of BSE in sheep would be expected in 2001 if maternal trans

191 itative estimate is that about 6950 cases of BSE will occur in cattle in the UK during 1997-2001 if n

192 Despite intensive surveillance for cases of BSE within the small ruminant populations of the United

193 pidemic peak in 1990, the number of cases of BSE-infected sheep would have ranged from fewer than 10

194 iform encephalopathy (BSE) by consumption of BSE-infected beef.

195 exposed to the infectivity by consumption of BSE-infected beef.

196 In the present study, low doses of BSE were fed to lambs of a range of ages (~24 h, 2 to 3

197 , largely on the grounds that an epidemic of BSE in sheep could be harder to contain than was the cas

198 istics of CJD as a result of the epidemic of BSE.

199 Atypical forms of BSE appear to be sporadic and thus may never be eradicat

200 classical BSE (C-BSE) and atypical forms of BSE.

201 Kingdom and European Union, no instances of BSE have been detected in sheep, and in only two instanc

202 of exposure to infected feed, and number of BSE-susceptible sheep in the United Kingdom showed that

203 To determine if the incubation periods of BSE and vCJD prions could be shortened, we generated tra

204 A also consistently detected the presence of BSE in mixtures at 0.1%.

205 in Tg mice supports the rapid propagation of BSE and vCJD prions and suggest that Tg(GPPrP) mice may

206 chemical and neuropathological properties of BSE and vCJD prions, including the presence of type 2 pr

207 A proportion of BSE-infected transfusion recipients (3 of 8) survived fo

208 hat the present-day (143)Nd/(144)Nd ratio of BSE is similar to that of some deep mantle plumes rather

209 d bovine tissues prior to the recognition of BSE.

210 isk analysis, it is evident that the risk of BSE infection from BGS is several orders of magnitude le

211 ited Kingdom would have been at high risk of BSE infection only if neonatal animals had inadvertently

212 d the implications of different scenarios of BSE spread in sheep for relative human exposure levels a

213 increase the danger of additional spread of BSE or vCJD infection by contaminated blood, surgical in

214 r results decipher the centripetal spread of BSE prions along the autonomic nervous system to the cen

215 pie-infected sheep was compared with that of BSE-infected sheep with a similar genotype.

216 efficiencies and known transmissibilities of BSE, sheep scrapie and CJD.

217 inary data demonstrating the transmission of BSE and natural scrapie by blood transfusion in sheep.

218 Transmission of BSE to human beings is probably restricted by the presen

219 that it might represent the transmission of BSE to humans.

220 there has been concern that transmission of BSE to the human population might result in a change in

221 persistence of a barrier to transmission of BSE-derived prions on subpassage.

222 ever, primary and secondary transmissions of BSE and vCJD in guinea pigs result in long incubation pe

223 esized that low r(be) due to the presence of BSEs would increase the rate of stomatal opening (V) dur

224 As this second of the two-part article on BSE shows, there has been slippage in some of our contro

225 These data suggest that more than one BSE-derived prion strain might infect humans; it is ther

226 e include exposure from the worst-case ovine BSE scenario examined.

227 then ongoing public health risks from ovine BSE are likely to be greater than those from cattle, but

228 n become infectious at early stages of ovine BSE infection and that the PrP(d) immunohistochemical ph

229 nded series of brain samples, in which ovine BSE and distinct isolates of scrapie are mixed at variou

230 ies of bovine-derived and Tg(BoPrP)-passaged BSE prions were similar, the stability of sheep scrapie

231 (Bo) prion protein (PrP) serially propagate BSE prions and that there is no species barrier for tran

232 ovine or human prion protein for propagating BSE and vCJD prions.

233 olved, stabilized, and reproducibly provoked BSE-like disease in subsequent passages.

234 indicated that PrP(263K), PrP(CWD), and PrP(BSE) were reduced by at least 2 log10, 1-2 log10, and 1

235 l cellular prion protein PrP(C), such as PrP(BSE) in bovine spongiform encephalopathy (BSE) in cattle

236 ), and bovine spongiform encephalopathy (PrP(BSE)) in lab-scale composters and PrP(263K) in field-sca

237 ted with both scrapie (PrP[Sc]) and BSE (PrP[BSE]).

238 strain like the one described here; rather, BSE prions may have arisen spontaneously in a cow or by

239 Bioassay and sPMCA reported BSE in all samples where it was present, down to 1%.

240 ly practical and sensitive tests for routine BSE detection and strain discrimination.

241 kedly influences infection by sheep scrapie, BSE, mouse-adapted scrapie, deer chronic wasting disease

242 y in the cattle BSE epidemic and that serial BSE transmission in sheep might have resulted in adaptat

243 etection and discrimination of at least some BSE forms.

244 ly believed to be caused by only one strain, BSE-C.

245 fe expectancy, although fourfold longer than BSE.

246 ory, with three related hypotheses: (1) that BSE was acquired from a human TSE (prion disease); (2) t

247 This has raised serious concerns that BSE may have spread to humans, putatively by dietary exp

248 Fears that BSE might transmit to man were raised when atypical case

249 These results indicated that BSE at high dose prevents DCM in a manner congruent with

250 The theoretical possibility that BSE prions might have transferred to other species and c

251 Our findings suggest that BSE prions did not arise from a sheep scrapie strain lik

252 Therefore, it suggests that BSE could potentially be used as a natural and safe trea

253 It is thought that BSE is a result of cannibalism in which faulty industria

254 tus and their ecological correlates and that BSEs play several key roles in the functional ecology of

255 These results support the hypothesis that BSEs reduce r(be).

256 To test the hypothesis that BSEs reduce the hydraulic resistance from the bundle she

257 onnections between DNA damage repair and the BSE.

258 We detected the BSE prion protein within a large excess of classical, at

259 d ratio 6% higher than chondrites (i.e., the BSE is superchondritic).

260 ie prions was higher than that found for the BSE prions but lower if the scrapie prions were passaged

261 ompared to that from the particle, so in the BSE mode the particle image is seen with very high contr

262 exposed during the preclinical phase of the BSE epidemic.

263 meat and bone meal, the main vehicle of the BSE epidemic.

264 xchange (SCE) frequencies as a marker of the BSE, we performed cell transfer strategies that enabled

265 that was fed to cattle and precipitated the BSE epidemic in the United Kingdom that peaked more than

266 tle and the continental crust shows that the BSE, reconstructed using the depleted mantle and contine

267 riant CJD have resulted from exposure to the BSE agent via rendering plants involved in the productio

268 ave been due to past dietary exposure to the BSE agent.

269 bystander signal, helping to explain why the BSE is a low-dose phenomenon.

270 ecreased to zero or increased to twice their BSEs.

271 ents are formed in the direction where their BSEs are minimally altered.

272 arise after exposure of humans or animals to BSE, this could markedly increase the danger of addition

273 pleted in many volatile elements compared to BSE due to high-temperature volatile loss from Moon-form

274 Kingdom sheep flock may have been exposed to BSE early in the cattle BSE epidemic and that serial BSE

275 ably millions of others have been exposed to BSE-contaminated food substances.

276 al evidence that it is caused by exposure to BSE has highlighted the need to understand the molecular

277 riant in the oral susceptibility of goats to BSE.

278 imeric Bo/Mo PrP transgene were resistant to BSE prions whereas mice expressing Hu or Hu/Mo PrP trans

279 s and leporids, were apparently resistant to BSE.

280 erable interest in the responses of sheep to BSE inoculation.

281 attle, dose responses of cattle and sheep to BSE, levels of exposure to infected feed, and number of

282 in GPPrP might mediate its susceptibility to BSE and vCJD prions.

283 e to assess their relative susceptibility to BSE infection.

284 Other species were also susceptible to BSE either by natural infection (e.g., felids, caprids)

285 cephalopathy (C-BSE) and the atypical H-type BSE (H-BSE) and L-type BSE (L-BSE) strains.

286 d the atypical H-type BSE (H-BSE) and L-type BSE (L-BSE) strains.

287 ype bovine spongiform encephalopathy (L-type BSE or L-BSE) with the RT-QuIC assay and found that both

288 n humans, the BASE strain is a more virulent BSE strain and likely lymphotropic.

289 th 100% specificity and 97% sensitivity when BSE agent was diluted into scrapie-infected brain homoge

290 To determine whether BSE is potentially circulating at low levels within the

291 vidence to date that prions from cattle with BSE have infected humans and caused fatal neurodegenerat

292 Like most cattle with BSE, vacuolation and astrocytic gliosis were confined in

293 as been consistently observed in cattle with BSE.

294 United Kingdom could have been infected with BSE by being fed contaminated meat and bone meal supplem

295 ential if these animals became infected with BSE.

296 ion from donors experimentally infected with BSE; these were either clinically or subclinically affec

297 In human infection with BSE prions, species-barrier effects, which are character

298 , primary and secondary human infection with BSE-derived prions may result in sporadic CJD-like or no

299 Mice were inoculated with BSE or vCJD and assessed for clinical and pathological s

300 Inoculation of Tg(GPPrP) mice with BSE and vCJD prions resulted in mean incubation periods