Beekes M, McBride P A, Baldauf E
Robert Koch-Institut, Bundesinstitut für Infektionskrankheiten und nicht übertragbare Krankheiten, Berlin, Germany.
J Gen Virol. 1998 Mar;79 ( Pt 3):601-7. doi: 10.1099/0022-1317-79-3-601.
The pathogenesis of scrapie and other transmissible spongiform encephalopathies (TSEs) following oral uptake of agent is still poorly understood and can best be studied in mice and hamsters. The experiments described here further extend the understanding of the pathways along which infection spreads from the periphery to the brain after an oral challenge with scrapie. Using TSE-specific amyloid protein (TSE-AP, also called PrP) as a marker for infectivity, immunohistochemical evidence suggested that the first target area in the brain of hamsters orally infected with scrapie is the dorsal motor nucleus of the vagus nerve (DMNV), rapidly followed by the commissural solitary tract nucleus (SN). The cervical spinal cord was affected only after TSE-AP had been deposited in the DMNV, SN and other medullary target areas. For the first time, these results demonstrate conclusively that, in our animal model, initial infection of the brain after oral ingestion of scrapie agent occurs via the vagus nerve, rather than by spread along the spinal cord.
经口摄入病原体后，羊瘙痒症及其他传染性海绵状脑病（TSEs）的发病机制仍了解甚少，而在小鼠和仓鼠身上进行研究是最佳途径。本文所述实验进一步拓展了我们对羊瘙痒症经口攻击后感染从外周扩散至大脑的途径的理解。使用TSE特异性淀粉样蛋白（TSE-AP，也称为PrP）作为感染性标志物，免疫组化证据表明，经口感染羊瘙痒症的仓鼠大脑中首个靶区是迷走神经背运动核（DMNV），随后很快是连合孤束核（SN）。仅在TSE-AP沉积于DMNV、SN及其他延髓靶区后，颈脊髓才会受到影响。这些结果首次确凿证明，在我们的动物模型中，经口摄入羊瘙痒症病原体后，大脑的初始感染是通过迷走神经发生的，而非沿脊髓扩散。
