Schlesinger S, Weiss B, Dohner D
Med Biol. 1975 Oct;53(5):372-9.
This article summarizes our studies with defective-interfering particles of Sindbis virus obtained by high multiplicity passaging of the virus in BHK cells. Cells infected with these defective passages accumulate a species of RNA (20S) at the expense of 26S RNA--the mRNA coding for the viral structural proteins. Although the structure of the RNA in defective particles remains undefined, our studies of replicative forms and replicative intermediates suggest that it is larger than the intracellular 20S RNA. The defective particles are unable to synthesize detectable amounts of viral structural proteins when they infect a cell in the absence of standard virus and they do not contribute to the stimulation of intracellular viral RNA synthesis. We have proposed a model for the mechanism of interference by these defective particles in which standard and defective RNAs compete for a limited amount of viral-specific replicase.
本文总结了我们对通过辛德毕斯病毒在BHK细胞中高倍传代获得的缺陷干扰颗粒的研究。感染这些缺陷传代病毒的细胞以26S RNA(编码病毒结构蛋白的mRNA)为代价积累了一种RNA(20S)。尽管缺陷颗粒中RNA的结构仍未明确,但我们对复制形式和复制中间体的研究表明,它比细胞内的20S RNA更大。当缺陷颗粒在没有标准病毒的情况下感染细胞时,它们无法合成可检测量的病毒结构蛋白,也不会促进细胞内病毒RNA的合成。我们提出了一个关于这些缺陷颗粒干扰机制的模型,其中标准RNA和缺陷RNA竞争有限量的病毒特异性复制酶。