Skip to main content

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.