仙台病毒（副流感病毒I型）对多瘤病毒合成的短暂抑制作用。I. 灭活病毒抑制作用的证明及其性质
Transient inhibition of polyoma virus synthesis by Sendai virus (parainfluenza I). I. Demonstration and nature of the inhibition by inactivated virus.
作者信息
Smith G L, Consigli R A
出版信息
J Virol. 1972 Dec;10(6):1091-7. doi: 10.1128/JVI.10.6.1091-1097.1972.
Abstract
Superinfection of polyoma virus-infected mouse embryo cells by beta-propiolactone-inactivated Sendai virus resulted in a 90% inhibition of the synthesis of infectious polyoma progeny. The interference is dependent upon the time of superinfection and the concentration of the inactivated virus. The inhibition of polyoma virus synthesis is transient in nature since normal synthesis of polyoma progeny virus is seen upon prolonged incubation. Interferon does not appear to be implicated in the interference. Various aspects of the biological and synthetic capabilities of beta-propiolactone-inactivated Sendai virus are also described.
摘要
用β-丙内酯灭活的仙台病毒对多瘤病毒感染的小鼠胚胎细胞进行超感染，导致感染性多瘤子代病毒的合成受到90%的抑制。这种干扰取决于超感染的时间和灭活病毒的浓度。多瘤病毒合成的抑制本质上是短暂的，因为长时间培养后可观察到多瘤子代病毒的正常合成。干扰现象似乎与干扰素无关。文中还描述了β-丙内酯灭活的仙台病毒的生物学和合成能力的各个方面。
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