实验性麻疹脑炎：一项遗传学分析。
Experimental measles encephalitis: a genetic analysis.
作者信息
Haspel M V, Duff R, Rapp F
出版信息
Infect Immun. 1975 Oct;12(4):785-90. doi: 10.1128/iai.12.4.785-790.1975.
Abstract
The encephalitogenic potential of nine temperature-sensitive mutants of measles virus was determined in newborn golden Syrian hamsters. The parental virus produced acute encephalitis without any prior adaptation. Six of the mutants were attenuated, two were virulent, and one was associated with hydrocephalus with acute onset. The attenuated mutants, blocked before measles virus antigen and ribonucleic acid synthesis at 39 C, were all members of one complementation group. The virulent temperature-sensitive mutants, defective in hemolysin antigen synthesis at 39 C, were members of a second complementation group. The hydrocephalus-inducing mutant was genetically distinct from the other mutants. The mechanism of attenuation most probably does not involve a temperature-induced inhibition of virus replication, but rather appears to be related to the partial defectiveness of the mutants under permissive conditions.
摘要
在新生叙利亚金黄仓鼠中测定了麻疹病毒的九个温度敏感突变体的致脑炎潜力。亲本病毒无需任何预先适应即可引发急性脑炎。其中六个突变体减毒，两个具有毒性，还有一个与急性发作的脑积水有关。在39℃时，减毒突变体在麻疹病毒抗原和核糖核酸合成之前受阻，它们均属于一个互补群。在39℃时溶血素抗原合成有缺陷的毒性温度敏感突变体属于第二个互补群。诱导脑积水的突变体在基因上与其他突变体不同。减毒机制很可能不涉及温度诱导的病毒复制抑制，而是似乎与突变体在允许条件下的部分缺陷有关。
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