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首页> 外文期刊>Journal of Virology >Homologous Interference by Incomplete Sendai Virus Particles: Changes in Virus-Specific Ribonucleic Acid Synthesis
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Homologous Interference by Incomplete Sendai Virus Particles: Changes in Virus-Specific Ribonucleic Acid Synthesis

机译：不完全仙台病毒粒子的同源干扰：病毒特异性核糖核酸合成的变化

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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.
机译：不完全仙台病毒颗粒（I颗粒）干扰了几种传染性仙台病毒群（标准病毒）的复制，但不与新城疫病毒，腮腺炎病毒或Sindbis病毒的复制。我颗粒没有诱导干扰素，并且I颗粒的紫外线照射废除了它们干扰的能力。蛋白质合成没有必要建立干扰。干扰程度依赖于细胞暴露于I颗粒和标准病毒攻击之间的间隔，并且这反映在感染细胞中病毒特异性核糖核酸（RNA）合成的抑制程度。最戏剧性的变化降低了感染细胞中50 S 病毒特异性RNA的积累。沉积比50 s 的RNA物种在总量下不显着降低，但杂交实验表明，这些缓慢沉淀的RNA物种的大部分是加股，可能是I中的RNA物种的复制品粒子。当我在标准病毒后8小时后向细胞中添加到细胞中的数量不足的颗粒时，细胞中的病毒特异性RNA物种没有明显的变化;然而，表示I颗粒的后代的大量19和25 RNA物种出现在培养基中。得出结论，干扰是一种影响病毒复制早期步骤的细胞内事件。通过标准病毒所需的细胞位点或粒子的I颗粒的竞争似乎比标准病毒指定的酶的竞争更少的干扰机制。

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