Evolution of a strain of CJD that induces BSE-like plaques

被引:118
作者
Manuelidis, L
Fritch, W
Xi, YG
机构
[1] Section of Neuropathology, Yale Medical School, New Haven, CT 06510
关键词
D O I
10.1126/science.277.5322.94
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:94 / 98
页数:5
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共 66 条
[51]  
Carp R.I., Et al., Trends Neurosci., 17, (1994)
[52]  
Race R.E., Et al., Neuron, 15, (1995)
[53]  
Tagliavini F., Et al., Transmisssible Subacute Spongiform Encephalopathies: Prion Diseases, pp. 323-327, (1996)
[54]  
Brown D.R., Schmidt B., Kretzschmar H.A., Nature, 380, (1996)
[55]  
Bueler H., Et al., Cell, 73, (1993)
[56]  
Sakaguchi S., Et al., J. Virol., 69, (1995)
[57]  
Diringer H., Ehlers B., J. Gen. Virol., 72, (1991)
[58]  
Manuelidis E.E., Gorgacz E.J., Manuelidis L., Science, 200, (1978)
[59]  
Manuelidis E.E., Kim J.H., Mericangas J.R., Manuelidis L., Lancet, 2, (1985)
[60]  
Tateishi J., Lancet