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首页> 外文期刊>Journal of Virology >Evolution of virus and defective-interfering RNAs in BHK cells persistently infected with Sindbis virus.
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Evolution of virus and defective-interfering RNAs in BHK cells persistently infected with Sindbis virus.

机译：病毒的演变与干扰腹腔细胞中的干扰RNA持续感染SINDBIS病毒。

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We analyzed a BHK cell line persistently infected with Sindbis virus for 16 months and a virus (Sin-16) cloned from these cells. Sin-16 virus was resistant to the defective interfering particles present in the original infection. We found that (i) cells infected with Sin-16 were impaired in the processing of a viral precursor glycoprotein, (ii) high-multiplicity passaging of Sin-16 gave rise to a variant that was able to generate and be inhibited by defective-interfering particles to which the original Sin-16 virus was resistant, and (iii) the persistently infected culture contained a heterogeneous mixture of defective Sindbis virus RNAs which were not packaged into extracellular particles. To determine whether these intracellular RNAs could interfere with the replication of Sin-16, we analyzed cells that were cloned from the persistently infected culture. One clone (A3) synthesized a single defective viral RNA which was lost with continued passaging in culture. Infection of A3 cells with Sin-16 showed that the presence of the defective RNA greatly enhanced cell survival and led to enrichment of this RNA. In contrast, cured cells were highly susceptible to killing by Sin-16, and survivors did not synthesize this RNA. Thus, A3 cells were not genetically altered in their response to Sin-16, but were protected from the cytopathic effects of infection by an RNA with the characteristics of a defective-interfering RNA.
机译：我们分析了一种持久地感染的BHK细胞系，持续感染Sindbis病毒16个月，病毒（SIN-16）克定这些细胞。 Sin-16病毒对原始感染中存在的缺陷干扰颗粒具有抗性。我们发现（i）用SIN-16感染的细胞在处理病毒前体糖蛋白的加工中受到损害，（ii）SIN-16的高分性传代引起能够产生和缺陷抑制的变体 - 干扰原始Sin-16病毒是抗性的干扰颗粒，并且（iii）持续受感染的培养物含有缺陷的SINDBIS病毒RNA的异质混合物，其未包装成细胞外颗粒。为了确定这些细胞内RNA是否可能干扰SIN-16的复制，我们分析了从持续受感染的培养物中克定的细胞。一种克隆（A3）合成了一种缺陷的病毒RNA，培养缺失失去。用SIN-16感染A3细胞表明，存在缺陷的RNA大大提高了细胞存活率，并导致富集该RNA。相比之下，通过SIN-16杀死固化的细胞，并且幸存者没有合成该RNA。因此，A3细胞在对SIN-16的反应中没有遗传改变，但是免受RNA感染的细胞病变效应，其特征具有缺陷干扰的RNA。

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