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1 us 1, hepatitis C virus, enterovirus 70, and variant Creutzfeldt-Jakob disease.
2 d from human beings affected by sporadic and variant Creutzfeldt-Jakob disease.
3 case of bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease.
4 this could lead to a more virulent strain of variant Creutzfeldt-Jakob disease.
5 of prion disease in humans were diagnosed as variant Creutzfeldt-Jakob disease.
6 s a source of human-to-human transmission of variant Creutzfeldt-Jakob disease.
7 m those observed in sporadic, iatrogenic and variant Creutzfeldt-Jakob disease.
8 e methionine homozygote to both sporadic and variant Creutzfeldt-Jakob disease.
9 ease) or can be acquired, as is the case for variant Creutzfeldt-Jakob disease.
10 tissues in a unique series of nine cases of variant Creutzfeldt-Jakob disease.
11 laria, severe acute respiratory syndrome, or variant Creutzfeldt-Jakob disease.
12 iform encephalopathy (BSE) prions causes new variant Creutzfeldt-Jakob disease.
13 al targets for therapy, for example, in 'new variant' Creutzfeldt-Jakob disease.
14 RNP MV genotype individual can propagate the variant Creutzfeldt-Jakob disease agent and that the inf
15 d the possibility that the properties of the variant Creutzfeldt-Jakob disease agent could change aft
17 the PrP(Sc) that accumulates in the brain in variant Creutzfeldt-Jakob disease also contains a minori
18 ined from human post-mortem samples, of both variant Creutzfeldt-Jakob disease and Alzheimer's diseas
19 e chronic human neurodegenerative conditions variant Creutzfeldt-Jakob disease and Alzheimer's diseas
20 sions from donors who subsequently developed variant Creutzfeldt-Jakob disease and an asymptomatic re
21 etectable only in the urine of patients with variant Creutzfeldt-Jakob disease and had the typical el
22 14 urine samples obtained from patients with variant Creutzfeldt-Jakob disease and in none of the 224
23 nce that either Creutzfeldt-Jakob disease or variant Creutzfeldt-Jakob disease are transmitted by tra
24 issible spongiform encephalopathies, such as variant Creutzfeldt-Jakob disease, are believed to resul
25 ly 10(5)-fold dilution of 10% (wt/vol) human variant Creutzfeldt-Jakob disease brain homogenate, with
26 phoreticular system is a defining feature of variant Creutzfeldt-Jakob disease, but that the biochemi
27 eview focuses on transfusion-transmission of variant Creutzfeldt-Jakob disease by red cell preparatio
28 covered by this review, the transmission of variant Creutzfeldt-Jakob disease by transfusion has bee
29 tion as a precaution against transmission of variant Creutzfeldt-Jakob disease by transfusion of dome
31 iod makes it difficult to predict future new variant Creutzfeldt-Jakob disease case numbers; further
32 terest, and findings were followed-up in six variant Creutzfeldt-Jakob disease cases with 9.4 T high-
35 spongiform encephalopathy (BSE) to humans as variant Creutzfeldt-Jakob disease (CJD) has affected ove
37 ine spongiform encephalopathy to people as a variant Creutzfeldt-Jakob disease (CJD), it becomes crit
40 to be susceptible to prions from humans with variant Creutzfeldt-Jakob disease (CJD); on second passa
42 Urine samples obtained from patients with variant Creutzfeldt-Jakob disease contained minute quant
44 ablish whether the strain characteristics of variant Creutzfeldt-Jakob disease had been modified by t
47 ll transfusion recipient, who did not die of variant Creutzfeldt-Jakob disease, has been identified w
49 all previous definite and probable cases of variant Creutzfeldt-Jakob disease have been methionine h
50 form encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns
53 fection for three individuals diagnosed with variant Creutzfeldt-Jakob disease in the USA and Canada.
54 compared with other transmission studies in variant Creutzfeldt-Jakob disease, including those on th
55 ntial for significant numbers of subclinical variant Creutzfeldt-Jakob disease individuals in at leas
56 n strain modification, the identification of variant Creutzfeldt-Jakob disease infection in a PRNP 12
58 analysis of prion strains suggests that new variant Creutzfeldt-Jakob disease is caused by BSE expos
59 ditions of humans and animals, one of which (variant Creutzfeldt-Jakob disease) is known to be a zoon
61 tudy of PrP(Sc) from autopsy-proved cases of variant Creutzfeldt-Jakob disease (n = 59) and compare t
63 , 1998, 35 deaths had been attributed to new variant Creutzfeldt-Jakob disease (nvCJD) in the United
67 kdown of Hsp110 or DnaJ-1 gene expression in variant Creutzfeldt-Jakob disease prion-exposed human Pr
70 polymorphic codon in humans associated with variant Creutzfeldt-Jakob disease, pulls the N terminus
71 s) in lymphoid tissues of patients with 'new variant' Creutzfeldt-Jakob disease, sheep with natural s
74 indicates a single PrP(Sc) molecular type in variant Creutzfeldt-Jakob disease (termed type 2B), pres
75 type 1 PrP(Sc) was found in all 21 cases of variant Creutzfeldt-Jakob disease tested, irrespective o
79 s our current understanding of the risks of (variant) Creutzfeldt-Jakob disease transmission via dent
80 vidual were totally consistent with those of variant Creutzfeldt-Jakob disease transmitted to 129 met
84 causes the fatal neurodegenerative condition variant Creutzfeldt-Jakob disease (vCJD) and, based on r
85 Our study indicates a prototype blood-based variant Creutzfeldt-Jakob disease (vCJD) assay has suffi
86 ical instruments from, a deceased carrier of variant Creutzfeldt-Jakob disease (vCJD) can be followed
95 rion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and h
96 ings are relevant to the current outbreak of variant Creutzfeldt-Jakob disease (vCJD) in the United K
104 sceptibility to, and clinical expression of, variant Creutzfeldt-Jakob disease (vCJD) is essential fo
106 eographical variation in the distribution of variant Creutzfeldt-Jakob disease (vCJD) might indicate
107 ortex samples, from prion-affected patients (variant Creutzfeldt-Jakob disease (vCJD) n = 20, iatroge
108 f bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) prions are fait
110 appear to be a reservoir for transmission of variant Creutzfeldt-Jakob disease (vCJD) to humans.
112 e an increasing concern since the reports of variant Creutzfeldt-Jakob disease (vCJD) transmission th
114 Identification of possible transmission of variant Creutzfeldt-Jakob disease (vCJD) via blood trans
118 on (PMCA) in urine of patients affected with variant Creutzfeldt-Jakob disease (vCJD), a prion diseas
120 cephalopathy (BSE) and its human equivalent, variant Creutzfeldt-Jakob disease (vCJD), are caused by
121 sfusion has been described in cases of human variant Creutzfeldt-Jakob disease (vCJD), experimental o
122 is C, bovine spongiform encephalopathy (BSE)/variant Creutzfeldt-Jakob disease (vCJD), Nipah virus, s
123 centers in lymphoid tissues of patients with variant Creutzfeldt-Jakob disease (vCJD), sheep with nat
130 ce between PrP(Sc) types was maintained when variant Creutzfeldt-Jakob disease was transmitted to wil
131 an be detected in the urine of patients with variant Creutzfeldt-Jakob disease, we used the protein m