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不完全仙台病毒颗粒的同源干扰:病毒特异性核糖核酸合成的变化

Homologous interference by incomplete Sendai virus particles: changes in virus-specific ribonucleic acid synthesis.

作者信息

Portner A, Kingsbury D W

出版信息

J Virol. 1971 Oct;8(4):388-94. doi: 10.1128/JVI.8.4.388-394.1971.

Abstract

Incomplete Sendai virus particles (I particles) interfered with the replication of several strains of infectious Sendai virions (standard virus) but not with the replication of Newcastle disease virus, mumps virus, or Sindbis virus. I particles did not induce interferon, and ultraviolet irradiation of I particles abolished their ability to interfere. Protein synthesis was not necessary to establish interference. The degree of interference depended on the interval between exposure of cells to the I particles and challenge by standard virus, and this was reflected in the degree of inhibition of virus-specific ribonucleic acid (RNA) synthesis in infected cells. The most dramatic change was decreased accumulation of 50S virus-specific RNA in infected cells. RNA species sedimenting slower than 50S were not as markedly reduced in total amount, but hybridization experiments showed that a substantial portion of these slowly sedimenting RNA species were plus strands, presumably representing replicas of the RNA species in I particles. When I particles in insufficient numbers to interfere were added to cells as late as 8 hr after standard virus, there were no obvious changes in virus-specific RNA species in the cells; however, significant amounts of 19 and 25S RNA species, representing progeny of the I particles, appeared in the culture medium. It was concluded that interference was an intracellular event affecting an early step in virus replication. Competition by I particles for cell sites or substrates needed by standard virus seemed a less likely mechanism of interference than competition for enzymes specified by standard virus.

摘要

不完全仙台病毒颗粒(I颗粒)可干扰多种传染性仙台病毒株(标准病毒)的复制,但不干扰新城疫病毒、腮腺炎病毒或辛德毕斯病毒的复制。I颗粒不诱导干扰素,对I颗粒进行紫外线照射可消除其干扰能力。建立干扰不需要蛋白质合成。干扰程度取决于细胞接触I颗粒与受到标准病毒攻击之间的间隔时间,这反映在受感染细胞中病毒特异性核糖核酸(RNA)合成的抑制程度上。最显著的变化是受感染细胞中50S病毒特异性RNA的积累减少。沉降速度比50S慢的RNA种类总量减少不那么明显,但杂交实验表明,这些沉降较慢的RNA种类中有很大一部分是正链,推测代表I颗粒中RNA种类的复制产物。当数量不足以产生干扰的I颗粒在标准病毒感染8小时后才加入细胞时,细胞中病毒特异性RNA种类没有明显变化;然而,培养基中出现了大量代表I颗粒子代的19S和25S RNA种类。得出的结论是,干扰是一种细胞内事件,影响病毒复制的早期步骤。与竞争标准病毒指定的酶相比,I颗粒竞争标准病毒所需的细胞位点或底物似乎不太可能是干扰机制。

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Effect of interferon on the replication of Sendai virus.干扰素对仙台病毒复制的影响。
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