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. 2015 Feb 11;89(9):4738–4747. doi: 10.1128/JVI.02296-14

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
a

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

b

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.

c

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.

d

Survival time of mice with no clinical signs and evidence of TSE vacuolation and/or PrP deposition.