PATHOGENESIS OF SCRAPIE - STUDY OF THE TEMPORAL DEVELOPMENT OF CLINICAL SYMPTOMS, OF INFECTIVITY TITERS AND SCRAPIE-ASSOCIATED FIBRILS IN BRAINS OF HAMSTERS INFECTED INTRAPERITONEALLY
PATHOGENESIS OF SCRAPIE - STUDY OF THE TEMPORAL DEVELOPMENT OF CLINICAL SYMPTOMS, OF INFECTIVITY TITERS AND SCRAPIE-ASSOCIATED FIBRILS IN BRAINS OF HAMSTERS INFECTED INTRAPERITONEALLY
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DOI：
10.1099/0022-1317-67-9-2005
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发表时间：
1986-09-01
影响因子：
3.8
通讯作者：
DIRINGER, H
中科院分区：
文献类型：
--
作者：
CZUB, M;BRAIG, HR;DIRINGER, H
用羊瘙痒病因子腹膜内感染仓鼠后，在第10至50天之间，早期低而恒定的滴度约为100 LD 50/脑，随后急剧增加至最大水平3 × 104。109 LD 50/脑，约15天内。从第70天到感染后第95天和第123天的首次和最终疾病体征的时间，最大感染性的平台期分别保持不变。即使使用全脑进行分析，在感染后79天之前也无法检测到通过SAF蛋白免疫印迹测量的瘙痒症相关原纤维（SAF）。随后，SAF的浓度逐渐增加约10，000倍，直到临床疾病发生。动力学表明病毒诱导的脑淀粉样变性是疾病的原因。
After an intraperitoneal infection of hamsters with scrapie agent, early low and constant titres of about 100 LD50/brain between days 10 to 50 were followed by a dramatic increase to maximum levels of 3 .times. 109 LD50/brain within about 15 days. The plateau of maximum infectivity remained unchanged from day 70 to the time of the first and final signs of disease at 95 and 123 days post-infection, respectively. Scrapie-associated fibrils (SAF) as measured by immunoblotting of SAF protein could not be detected before 79 days post-infection even when a total brain was used for analysis. Subsequently, the concentration of SAF increased gradually by about 10,000-fold until the time of clinical disease. The kinetics suggest a virus-induced amyloidosis of the brain as the cause of disease.