Abstract
The rapid detection of infectivity of several agents that cause Creutzfeldt-Jakob disease has previously been achieved by assaying for deposits of abnormal prion protein (PrPSc) in follicular dendritic cells in the spleens of transgenic mice carrying the human prion protein gene. In this study, transgenic mice expressing the bovine prion protein were inoculated intraperitoneally with classical (C-type) or atypical L-type bovine spongiform encephalopathies (BSE). Proteinase-resistant PrPSc were detected in the spleens of all transgenic mice at 75 days after inoculation with both types of BSE. Infectivity in PrPSc-positive spleens of the transgenic mice revealed that prions of C- and L-type BSE replicated. These results suggest that bioassay system by the transgenic mice could be useful for the rapid detection of BSE infectivity with discriminating between C- and L-type BSEs.
Highlights
Transmissible spongiform encephalopathies (TSEs) are fatal, infectious neurodegenerative diseases; TSEs include bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep and goats, chronic wasting disease mainly in deer and elk, and Creutzfeldt-Jakob disease (CJD) in humans
The follicular dendritic cells (FDCs) assay in the Ki+Tg#40 mice realized that PrPSc was generated in the mouse spleens within 75 days post IP inoculation with bovine spongiform encephalopathies (BSE) cattle brains (Figure 1(a))
In the brain of the Ki+Tg#40 mice, no PrPSc was not detected at 75 days post IP inoculation with C-type or L-type BSE (Figure 1(b)) the PrPSc in the brain was detected when the Ki+Tg#40 mice developed overt clinical signs post IC (Figures 2 and 3) and IP inoculation
Summary
Transmissible spongiform encephalopathies (TSEs) are fatal, infectious neurodegenerative diseases; TSEs include bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep and goats, chronic wasting disease mainly in deer and elk, and Creutzfeldt-Jakob disease (CJD) in humans. Transmissibility of BSE agents to inbred mice has revealed defined incubation period from inoculation to development of clinical signs and distinct histopathological characteristics in the brain, as compared to the other TSE agents [6,7]. In 2006, a Japanese black cow was diagnosed as an atypical BSE [11] Transmission of this agent to cattle or transgenic (Tg) mice over-expressing the bovine PrP gene realized that characteristics of histopathological changes and PrPcore were similar to L-type BSE agents found in Italy, Germany, France and Canada [18,19,20,21]. Incubation period of the Tg mice affected with L-type BSE was approximately 180 days post intracerebral (IC) inoculation and was shorter period than that with C-type BSE which was approximately 230 days [20, 22,23,24]
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