Kang C Y, Allen R
J Virol. 1978 Jan;25(1):202-6. doi: 10.1128/JVI.25.1.202-206.1978.
Suppression of host cell function by treatment with actinomycin D prior to infection prevented the induction of defective interfering particles of vesicular stomatitis virus, which had been cloned and propagated in cell pretreated with actinomycin D. Replication of defective interfering particles already present in an infecting virus stock, however, was not affected by pretreatment of cells with actinomycin D. Thus, the induction, but not the replication, of defective interfering particles appears to be a host cell function-dependent phenomenon. The implications of this phenomenon for host defense mechanisms against virus infections are discussed.
在感染前用放线菌素D处理宿主细胞,抑制其功能,可阻止水泡性口炎病毒缺陷干扰颗粒的诱导,该病毒已在经放线菌素D预处理的细胞中克隆并繁殖。然而,感染病毒悬液中已存在的缺陷干扰颗粒的复制不受放线菌素D预处理细胞的影响。因此,缺陷干扰颗粒的诱导而非复制似乎是一种依赖宿主细胞功能的现象。本文讨论了这一现象对宿主抗病毒感染防御机制的影响。