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SV40-腺病毒“杂交”群体中缺陷病毒在猴细胞中的复制。

Replication in simian cells of defective viruses in an SV40-adenovirus "hybrid" population.

作者信息

Butel J S, Rapp F

出版信息

J Bacteriol. 1966 Jan;91(1):278-84. doi: 10.1128/jb.91.1.278-284.1966.

Abstract

Butel, Janet S. (Baylor University College of Medicine, Houston, Tex.), and Fred Rapp. Replication in simian cells of defective viruses in an SV40-adenovirus "hybrid" population. J. Bacteriol. 91:278-284. 1966.-An SV40-adenovirus type 7 "hybrid" virus population, previously shown to contain two viruses capable of complementation in green monkey kidney (GMK) cells, has a growth cycle in GMK cells similar to that of adenovirus type 7 in the presence of SV40. Extending previous preliminary results, the addition of adenovirus types 2, 7, or 12 to monolayers of GMK cells enhanced plaque formation by the SV40-adenovirus hybrid by as much as 200-fold. The terminal enhanced plaques, initiated by the hybrid in the presence of helper adenovirus, were found to contain progeny which could induce the synthesis of SV40 tumor antigen but which were coated with the protein of the helper adenovirus, type 2, 7, or 12, respectively. The particle carrying the SV40 tumor antigen determinant, named PARA, is defective in that it cannot direct the synthesis of capsid protein; information for the coat for PARA is supplied by the adenovirus. One-step growth curves of the hybrid virus population in monkey cells revealed that synthesis of both types of particles, adenovirus and PARA, proceeds at a similar rate, with a latent period of 16 to 20 hr being followed by an exponential increase in titer during the following 20 hr. Maximal titers for both particles were obtained 48 hr after inoculation of the cultures. Neither the PARA nor the adenovirus component replicated in GMK cells in the absence of the other.

摘要

布特尔,珍妮特·S.(得克萨斯州休斯敦贝勒医学院),以及弗雷德·拉普。SV40 - 腺病毒“杂交”群体中缺陷病毒在猴细胞中的复制。《细菌学杂志》91:278 - 284。1966年。——一个SV40 - 7型腺病毒“杂交”病毒群体,先前已证明在绿猴肾(GMK)细胞中包含两种能够互补的病毒,在SV40存在的情况下,其在GMK细胞中的生长周期与7型腺病毒相似。扩展先前的初步结果,将2型、7型或12型腺病毒添加到GMK细胞单层中,可使SV40 - 腺病毒杂交体的噬斑形成增强多达200倍。发现由杂交体在辅助腺病毒存在下引发的终末增强噬斑含有子代,这些子代能够诱导SV40肿瘤抗原的合成,但分别被2型、7型或12型辅助腺病毒的蛋白质所包裹。携带SV40肿瘤抗原决定簇的颗粒,命名为PARA,有缺陷,因为它不能指导衣壳蛋白的合成;PARA衣壳的信息由腺病毒提供。杂交病毒群体在猴细胞中的一步生长曲线显示,腺病毒和PARA这两种颗粒的合成以相似的速率进行,潜伏期为16至20小时,随后在接下来的20小时内滴度呈指数增加。接种培养物48小时后获得两种颗粒的最大滴度。在没有另一种成分的情况下,PARA和腺病毒成分都不能在GMK细胞中复制。

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