SPECIFIC MEMBRANOUS STRUCTURES ASSOCIATED WITH REPLICATION OF GROUP A ARBOVIRUSES
SPECIFIC MEMBRANOUS STRUCTURES ASSOCIATED WITH REPLICATION OF GROUP A ARBOVIRUSES
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DOI：
10.1128/jvi.10.3.492-503.1972
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发表时间：
1972-01-01
影响因子：
5.4
通讯作者：
LEVIN, JG
中科院分区：
文献类型：
--
作者：
GRIMLEY, PM;FRIEDMAN, RM;LEVIN, JG
一种独特类型的胞质膜内结构与三种A组虫媒病毒的复制有关：塞姆利基森林病毒（SFV）、辛德毕斯病毒或西方马脑脊髓炎病毒。这些结构被称为1型细胞病变空泡（CPV-1），具有膜限制性，特征是由直径为50 nm的规则膜性小球排列。典型的膜状小球中心密度很小，但既不是病毒核心也不是病毒粒子。在感染后3 ~ 6小时用电子显微镜检测CPV-1，与病毒快速生长的时间相吻合，并先于病毒核衣壳的积累。当病毒在鸡胚、幼仓鼠肾或小鼠L细胞中生长时，在感染后6至9小时，每100个传代细胞切片计数20至100个CPV-1谱。即使感染复数变化超过100倍，最大计数也保持在相同范围内。在SFV感染期间，放线菌素D对细胞核糖核酸（RNA）和蛋白质合成的抑制并没有降低CPV-1的计数;然而，当病毒RNA合成（胍）或病毒蛋白质合成（放线菌酮）抑制剂限制病毒复制时，CPV-1的生物合成减少。根据目前和以前的研究结果，我们得出结论，CPV-1的形成必须由病毒特异性修饰预先存在的宿主细胞大分子引起。
Intracytoplasmic membranous structures of a unique type were associated with the replication of three group A arboviruses: Semliki Forest virus (SFV), Sindbis virus, or Western equine encephalomyelitis virus. The structures, referred to as type 1 cytopathic vacuoles (CPV-1), were membrane-limited and characteristically lined by regular membranous spherules measuring 50 nm in diameter. The membranous spherules typically contained a fine central density, but were neither virus cores nor virions. Detection of CPV-1 by electron microscopy at 3 to 6 hr postinfection coincided with the time of rapid virus growth and preceded the accumulation of virus nucleocapsids. A range of 20 to 100 CPV-1 profiles were counted per 100 ultrathin cell sections at 6 to 9 hr postinfection when viruses were grown in chick embryo, baby hamster kidney, or mouse L cells. Maximum counts remained in the same range even when the multiplicity of infection was varied over 100-fold. Inhibition of cellular ribonucleic acid (RNA) and protein synthesis by actinomycin D during SFV infection did not decrease the counts of CPV-1; however, biogenesis of CPV-1 was decreased when viral replication was limited by inhibitors of viral RNA synthesis (guanidine) or of viral protein synthesis (cycloheximide). On the basis of present and earlier findings, we concluded that formation of CPV-1 must result from a virus-specified modification of pre-existing host cell macromolecules.