Baric R S, Carlin L J, Johnston R E
J Virol. 1983 Jan;45(1):200-5. doi: 10.1128/JVI.45.1.200-205.1983.
Host cell involvement in Sindbis virus (SB) replication was examined in cells which had been treated with either actinomycin D (AMD) or alpha-amanitin (alpha-A). Treatment with these inhibitors of host transcription before infection reduced the ability of cells to support SB growth by 1 to 2 orders of magnitude, while having little or no effect on the replication of vesicular stomatitis virus. SB replication was sensitive to alpha-A in wild-type Chinese hamster ovary (CHO) cells but was resistant to alpha-A in CHOama-1 cells, a line which contains an alpha-A-resistant RNA polymerase II. A mutant of SB, SBamr, was isolated by mutagenesis followed by selection in cells which had been treated with AMD. SBamr grew normally not only in cells treated with AMD but also in alpha-A-treated cells. Our results suggest (i) that the synthesis of cellular mRNA (and presumably protein) is required for replication of SB, (ii) that prior treatment with either drug affects the same aspect of SB replication, and (iii) that mutations in the SB genome allow the virus to overcome the effect of inhibitors of host transcription.
在已用放线菌素D（AMD）或α-鹅膏蕈碱（α-A）处理过的细胞中，研究了宿主细胞在辛德毕斯病毒（SB）复制过程中的作用。在感染前用这些宿主转录抑制剂进行处理，会使细胞支持SB生长的能力降低1至2个数量级，而对水疱性口炎病毒的复制几乎没有影响。在野生型中国仓鼠卵巢（CHO）细胞中，SB复制对α-A敏感，但在CHOama-1细胞中对α-A具有抗性，CHOama-1细胞系含有一种对α-A抗性的RNA聚合酶II。通过诱变然后在经AMD处理的细胞中进行筛选，分离出了SB的一个突变体SBamr。SBamr不仅在经AMD处理的细胞中能正常生长，在经α-A处理的细胞中也能正常生长。我们的结果表明：（i）细胞mRNA（可能还有蛋白质）的合成是SB复制所必需的；（ii）用这两种药物中的任何一种预先处理都会影响SB复制的同一个方面；（iii）SB基因组中的突变使病毒能够克服宿主转录抑制剂的作用。
