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Table 2 Scrapie infectivity and pathology in wild-type and Prn-p +/0 mice

From: High Prion and PrPSc Levels but Delayed Onset of Disease in Scrapie-Inoculated Mice Heterozygous for a Disrupted PrP Gene

Time (Weeks p.i.) Infectivity (Days to Death)   Pathology (G/S)
Prn-p +/+ a Prn-p +/0 Prn-p +/+ Prn-p +/0
8 166 ± 5 ND ND ND
12 158 ± 12 174 ± 13 + +/- + +/−
16 ND 170 ± 7 ND + +/−
20 149 ± 8 148 ± 7 + + +/+ + + +/+
24 149 ± 7 153 ± 13 + + +/+ + + + +/+
33 Dead 147 ± 5 Dead + + + (f)/+ + (f)
41   151 ± 9   + + +/+ + +
45   157 ± 6   + +/+ +
48   150 ± 9   + +/+ +
50   153 ± 9   + + +/+ +
  1. Four Prn-p0/+ mice were sacrificed at 12, 16, 20, and 24 weeks after inoculation with mouse RML prions. Their brains were excised, pooled, and 1% (w/v) homogenates were titrated by inoculation into 6 Swiss CD-1 mice (incubation time method). Individual Prn-p0/+ brains recovered between 33 and 50 weeks after inoculation were titrated in the same fashion. The 50-week sample was also titrated by endpoint dilution as described in Experimental Procedures. The titers in Prn-p0/+ brain homogenates analyzed by the incubation time method were calculated by using standard curves that describe linear relationships between survival times of Prn-p+/+ mice and infectious titers for RML prions, as described previously (28); (legend to Table 3). Titers given in the table refer to 10% homogenates. −, no gliosis or spongiosis; +, single reactive astrocytes, no spongiosis; + +, clusters of reactive astrocytes and/or mild spongiosis; + + +, confluent foci of gliosis and/or profound spongiosis; ND, not determined; f, focal; G, gliosis; S, spongiosis.
  2. aData from (28) for heated samples.