Farber M S, Baum S G
J Virol. 1978 Jul;27(1):136-48. doi: 10.1128/JVI.27.1.136-148.1978.
The mechanism of blocked replication of human adenoviruses in monkey cells was examined. Previous experiments have placed the replicative block at the level of transcription of translation of adenovirus mRNA. Coinfection of the monkey cells with simian virus 40 enhances adenovirus replication in these cells. We compared the adenovirus mRNA transcribed during infection of permissive human cells and enhanced and unenhanced monkey cells. Adenovirus mRNA from enhanced monkey cells appeared to be identical to adenovirus mRNA from human cells. This indicated that simian virus 40 coinfection did not overcome the blocked replication by substituting for a missing adenovirus transcript. Comparison of adenovirus mRNA from enhanced and unenhanced monkey cell infection revealed two types of transcriptional discrepancies. There was a decrease in both the complexity and the relative abundance of several regions of the enhanced adenovirus mRNA. However, neigher of these transcriptional defects was sufficient to totally explain the difference in yield of infectious virus and viral protein seen in these two types of infection.
对人腺病毒在猴细胞中复制受阻的机制进行了研究。先前的实验已将复制阻断置于腺病毒mRNA转录或翻译水平。用猿猴病毒40对猴细胞进行共感染可增强腺病毒在这些细胞中的复制。我们比较了在允许性人细胞以及增强和未增强的猴细胞感染过程中转录的腺病毒mRNA。来自增强型猴细胞的腺病毒mRNA似乎与人细胞的腺病毒mRNA相同。这表明猿猴病毒40共感染并未通过替代缺失的腺病毒转录本来克服复制阻断。对增强和未增强的猴细胞感染的腺病毒mRNA进行比较,发现了两种转录差异。增强型腺病毒mRNA几个区域的复杂性和相对丰度均有所降低。然而,这些转录缺陷均不足以完全解释在这两种感染中所见的感染性病毒和病毒蛋白产量的差异。