TABLE 3.
263K inoculation into glycosylation-deficient mice at first and second passagesa
Mouse line | Inoculum | Incubation timeb (days) ± SEM (range) | Clinical disease (no. positive/total no.) | TSE vac and/or PrP depositionc | Survival time (days) of mice with TSE vac and/or PrPd |
---|---|---|---|---|---|
G1 | 263K | 0/14 | 4/14 | 579 ± 35 (507–674) | |
G2 | 263K | 0/18 | 11/18 | 552 ± 18 (461–629) | |
G3 | 263K | 0/16 | 0/16 | ||
Wt | 263K | 0/18 | 11/18 | 612 ± 18 (503–698) | |
G2 | G2–263Ka | 284 ± 7 | 12/12 | 12/12 | |
Wt | G2–263Ka | 437 ± 32 | 10/12 | 9/12 | |
G2 | G2–263Kb | 320 ± 7 | 11/11 | 11/11 | |
Wt | G2/263Kb | 536 ± 6 | 4/10 | 6/10 | 343 ± 61 (282–408) |
G2 | Wt263K | 365 ± 0 | 11/12 | 12/12 | |
Wt | Wt263K | 172 ± 5 | 9/10 | 10/10 |
Brain material from two 263K-inoculated G2 mice and one 263K-inoculated wild-type mouse with pathological evidence of disease were further passaged into G2 and wild type mice
Incubation time for mice with clinical signs and evidence of TSE vacuolation. Studies were maintained to ∼700 dpi for mice with no clinical signs of TSE disease.
TSE vacuolation and/or PrP deposition were used as evidence of transmission for primary passage due to low numbers of mice with clinical signs and vacuolation present. Limited confirmatory immunohistochemistry for PrP deposition was carried out in the second passage due to high numbers of mice with clinical signs and vacuolation present.
Survival time of mice with no clinical signs and evidence of TSE vacuolation and/or PrP deposition.