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在猴细胞混合感染期间,腺病毒2型对猿猴病毒40 DNA复制的干扰。

Interference with simian virus 40 DNA replication by adenovirus type 2 during mixed infection of monkey cells.

作者信息

van Roy F, Fiers W

出版信息

J Virol. 1978 Aug;27(2):275-87. doi: 10.1128/JVI.27.2.275-287.1978.

Abstract

Infection of monkey cells with human adenovirus (Ad) is abortive, but the infection can be enhanced by coinfecting with simian virus 40 (SV40). However, in the coinfected monkey cells, Ad interferes strongly with SV40 DNA biosynthesis. This interference was found to be a reproducible, delicately controlled phenomenon that was proportional to the multiplicity of infection of Ad and dependent on the active expression of the Ad genome. Newly synthesized SV40 DNA was not broken down in cells after delayed superinfection with Ad, and several early events of SV40 infection such as adsorption, penetration, uncoating, induction of cellular DNA synthesis, and enhancement of Ad infection were not markedly influenced by Ad-mediated interference. It is unlikely that interference is simply due to competition between SV40 and Ad for metabolites, enzymes, or replication sites. The interference effect could be partially neutralized by an increase in the multiplicity of coinfecting SV40 or by an increase in the time interval between SV40 infection and Ad coinfection. Interference was shown to be due to the activity of an Ad early gene product. However, the detailed mechanism of this Ad interference is still unclear.

摘要

用人腺病毒(Ad)感染猴细胞是流产性的,但通过与猿猴病毒40(SV40)共同感染可增强这种感染。然而,在共同感染的猴细胞中,Ad强烈干扰SV40 DNA的生物合成。发现这种干扰是一种可重复的、精细控制的现象,它与Ad的感染复数成正比,并依赖于Ad基因组的活性表达。在Ad延迟超感染后,新合成的SV40 DNA在细胞中未被分解,并且SV40感染的几个早期事件,如吸附、穿透、脱壳、诱导细胞DNA合成以及增强Ad感染,并未受到Ad介导的干扰的显著影响。干扰不太可能仅仅是由于SV40和Ad在代谢物、酶或复制位点上的竞争。通过增加共同感染的SV40的复数或增加SV40感染与Ad共同感染之间的时间间隔,干扰效应可以部分被中和。已表明干扰是由于Ad早期基因产物的活性。然而,这种Ad干扰的详细机制仍不清楚。

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