Evolution of a strain of CJD that induces BSE-like plaques
Evolution of a strain of CJD that induces BSE-like plaques
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DOI：
10.1126/science.277.5322.94
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发表时间：
1997-07-04
期刊：
影响因子：
56.9
通讯作者：
Xi, YG
中科院分区：
文献类型：
--
作者：
Manuelidis, L;Fritch, W;Xi, YG
牛海绵状脑病 (BSE) 已成为一个公共卫生问题，因为最近进化的 BSE 病原体感染了人类，产生了一种不寻常的克雅氏病 (CJD)。一种引起类似淀粉样斑块和小脑病理学的新克雅氏病药物被连续传播。首代大鼠表现出明显的临床症状和激活的小胶质细胞，但 PrP-res（宿主 PrP 的蛋白酶抵抗力更强的形式）或小脑病变可忽略不计。小胶质细胞和星形胶质细胞可能参与菌株选择，因为该物质在随后的传代中进化、稳定并可重复地引发类似 BSE 的疾病。涉及激活的小胶质细胞和星形胶质细胞的早期液泡变化先于显着的 PrP-res 积累 50 多天。这些研究揭示了宿主对外源性物质的几种炎症反应。
Bovine spongiform encephalopathy (BSE) has become a public health issue because a recently evolved BSE agent has infected people, yielding an unusual form of Creutzfeld-Jakob disease (CJD). A new CJD agent that provokes similar amyloid plaques and cerebellar pathology was serially propagated. First-passage rats showed obvious clinical signs and activated microglia but had negligible PrP-res (the more protease-resistant form of host PrP) or cerebellar lesions. Microglia and astrocytes may participate in strain selection because the agent evolved, stabilized, and reproducibly provoked BSE-like disease in subsequent passages. Early vacuolar change involving activated microglia and astrocytes preceded significant PrP-res accumulation by more than 50 days. These studies reveal several inflammatory host reactions to an exogenous agent.