TSE pathogenesis in cattle and sheepLucien J.M. van Keulen, Alex Bossers and Fred van Zijderveld
Department of Bacteriology and TSE's, Central Institute for animal Disease Control (CIDC), Wageningen University and Research Centre, PO Box 2004, 8203 AA Lelystad, the Netherlands
Received 27 April 2007; accepted 9 November 2007 ; published online 8 February 2008
Abstract - Many studies have been undertaken in rodents to study the pathogenesis of transmissible spongiform encephalopathies (TSE). Only a few studies have focused on the pathogenesis of bovine spongiform encephalopathy (BSE) and scrapie in their natural hosts. In this review, we summarize the most recent insights into the pathogenesis of BSE and scrapie starting from the initial uptake of TSE agents and crossing of the gut epithelium. Following replication in the gut-associated lymphoid tissues (GALT), TSE agents spread to the enteric nervous system (ENS) of the gut. Infection is then carried through the efferent fibers of the post-ganglionic neurons of the parasympathetic and sympathetic nervous system to the pre-ganglionic neurons in the medulla oblongata of the brain and the thoracic segments of the spinal cord. The differences between the pathogenesis of BSE in cattle and scrapie in sheep are discussed as well as the possible existence of additional pathogenetic routes.
Key words: prion / PrP / scrapie / bovine spongiform encephalopathy (BSE) / pathogenesis
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© INRA, EDP Sciences 2008