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. 2004 Feb;78(4):2088–2099. doi: 10.1128/JVI.78.4.2088-2099.2004

TABLE 3.

Propagation of GSS(P101L) prions in transgenic mice

Inoculuma Treatment Time to disease (days ± SEM) n/n0b Time elapsed (days)
Tg196c None 478 ± 37 6/7 >500
PTA 432 1/8 >550
PK/PTA 468 ± 22 2/9 >500
PTA/PK 483 1/9 >500
Tg2866d None 305 ± 17 10/10
PTA 278 ± 16 10/10
PK/PTA 262 ± 12 8/8
PTA/PK 226 ± 8 10/10
Tg196(2866)e None 351 ± 13 8/8
PTA 294 ± 4 9/9
PK/PTA 286 ± 3 10/10
PTA/PK 279 ± 7 9/9
Tg196(196(301V))f None 144 ± 4 6/7 >550
PTA 148 ± 6 7/7
PK/PTA 126 ± 3 5/5
PTA/PK 131 ± 3 8/8
a

All transmissions were carried out using Tg(MoPrP,P101L)196/Prnp0/0 mice as recipients. For each inoculum series, a pool of at least three brain homogenates was split among the following treatments: none, untreated; PTA, sodium phosphotungstate precipitation; PK/PTA, PK digestion followed by PTA precipitation; PTA/PK, PTA precipitation followed by PK digestion.

b

Number of ill animals (n) over number of animals under observation (n0).

c

Samples from clinically normal Tg(MoPrP,P101L)196/Prnp0/0 mice age-matched with ill Tg196(2866) mice at ∼300 days of age.

d

Tg2866 corresponds to spontaneously ill Tg(MoPrP,P101L)2866/Prnp0/0 mice at ∼130 days of age.

e

Tg196(2866) corresponds to ill Tg(MoPrP,P101L)196/Prnp0/0 mice (∼300 days of age) following inoculation with brain homogenates from spontaneously ill Tg2866 mice.

f

Tg196(196(301V)) inoculum was obtained from the secondary transmission of 301V prions into Tg(MoPrP,P101L)196/Prnp0/0 mice (see Table 1).