Rao D D, Huang A S
J Virol. 1980 Dec;36(3):756-65. doi: 10.1128/JVI.36.3.756-765.1980.
In cells coinfected by standard vesicular stomatitis virus (VSV) and defective interfering (DI) T particles, small RNA consisting of 46 nucleotides was synthesized in molar excess over other VSV-specific RNAs. Although its rate of synthesis increased over time, small RNA accumulated linearly, suggesting that the molecule is unstable. In contrast, replication of the genome RNA of DI T particles was relatively constant after 3 h of infection, resulting in the intracellular accumulation of stable genomic and antigenomic RNA of DI T particles. Coinfection of cells with DI T particles and selected temperature-sensitive mutants from all five complementation groups of VSV indicated that the replication of DI genomes was controlled separately from the synthesis of small RNA. Also, when viral RNA replication was inhibited by cycloheximide, small RNA continued to be synthesized as long as there were enough templates present. These results indicate that small RNA is synthesized by the enzyme(s) involved in VSV transcription and that its dependence on RNA replication is due to the requirement for template amplification.
在被标准水疱性口炎病毒（VSV）和缺陷干扰（DI）T颗粒共同感染的细胞中，由46个核苷酸组成的小RNA以摩尔过量的形式合成，其合成量超过其他VSV特异性RNA。尽管其合成速率随时间增加，但小RNA呈线性积累，这表明该分子不稳定。相比之下，DI T颗粒的基因组RNA在感染3小时后复制相对恒定，导致DI T颗粒的稳定基因组和反基因组RNA在细胞内积累。用DI T颗粒和从VSV的所有五个互补组中选择的温度敏感突变体共同感染细胞表明，DI基因组的复制与小RNA的合成是分开控制的。此外，当病毒RNA复制被环己酰亚胺抑制时，只要有足够的模板存在，小RNA就会继续合成。这些结果表明，小RNA是由参与VSV转录的酶合成的，其对RNA复制的依赖性是由于对模板扩增的需求。
