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    Presence of subclinical infection in gene-targeted human prion protein transgenic mice exposed to atypical bovine spongiform encephalopathy

    Date
    2013-12-01
    Author
    Wilson, Rona
    Dobie, Karen
    Hunter, Nora
    Casalone, Cristina
    Baron, Thierry
    Barron, Rona
    Metadata
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    Citation
    Wilson, R., Dobie, K., Hunter, N., Casalone, C., Baron, T. and Barron, R.M. (2013) ‘Presence of subclinical infection in gene-targeted human prion protein transgenic mice exposed to atypical bovine spongiform encephalopathy’, Journal of General Virology, 94(12), pp. 2819–2827. Available at: https://doi.org/10.1099/vir.0.052738-0.
    Abstract
    The transmission of bovine spongiform encephalopathy (BSE) to humans, leading to variant Creutzfeldt–Jakob disease has demonstrated that cattle transmissible spongiform encephalopathies (TSEs) can pose a risk to human health. Until recently, TSE disease in cattle was thought to be caused by a single agent strain, BSE, also known as classical BSE, or BSE-C. However, due to the initiation of a large-scale surveillance programme throughout Europe, two atypical BSE strains, bovine amyloidotic spongiform encephalopathy (BASE, also named BSE-L) and BSE-H have since been discovered. To model the risk to human health, we previously inoculated these two forms of atypical BSE (BASE and BSE-H) into gene-targeted transgenic (Tg) mice expressing the human prion protein (PrP) (HuTg) but were unable to detect any signs of TSE pathology in these mice. However, despite the absence of TSE pathology, upon subpassage of some BASE-challenged HuTg mice, a TSE was observed in recipient gene-targeted bovine PrP Tg (Bov6) mice but not in HuTg mice. Disease transmission from apparently healthy individuals indicates the presence of subclinical BASE infection in mice expressing human PrP that cannot be identified by current diagnostic methods. However, due to the lack of transmission to HuTg mice on subpassage, the efficiency of mouse-to-mouse transmission of BASE appears to be low when mice express human rather than bovine PrP.
    URI
    https://eresearch.qmu.ac.uk/handle/20.500.12289/12705
    Official URL
    https://doi.org/10.1099/vir.0.052738-0
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    • Dietetics, Nutrition and Biological Sciences

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