Flanagan J F
J Virol. 1967 Jun;1(3):583-90. doi: 10.1128/JVI.1.3.583-590.1967.
The production of virus-specific ribonucleic acid (RNA) was investigated in KB cells infected with herpes simplex virus. A fraction of RNA annealable to virus deoxyribonucleic acid (DNA) was found in these cells as early as 3 hr after virus inoculation. Production of this species of RNA increased up to 6 or 7 hr after infection, at which time elaboration of virus messenger RNA (mRNA) declined. At 24 hr after infection, the rate of incorporation of uridine into this RNA was approximately one-half of the rate present at 6 hr after inoculation. Nucleotide analysis of the RNA annealable to virus DNA was compatible with that expected for virus mRNA. Centrifugation showed considerable spread in the size of the virus-induced nucleic acid, the bulk of this RNA sedimenting between 12 and 32S. Incorporation of uridine into cell mRNA, ribosomal precursor RNA, and soluble RNA was suppressed rapidly after infection. As is the case with most other cytocidal viruses investigated to date, virus-induced suppression of cell RNA synthesis appears to be a primary mechanism of cell injury.
对感染单纯疱疹病毒的KB细胞中病毒特异性核糖核酸（RNA）的产生进行了研究。早在接种病毒后3小时，就在这些细胞中发现了一部分可与病毒脱氧核糖核酸（DNA）退火的RNA。这种RNA的产生在感染后6至7小时增加，此时病毒信使RNA（mRNA）的合成下降。感染后24小时，尿苷掺入这种RNA的速率约为接种后6小时时速率的一半。可与病毒DNA退火的RNA的核苷酸分析与病毒mRNA预期的结果相符。离心显示病毒诱导的核酸大小有相当大的差异，这种RNA的大部分沉降在12至32S之间。感染后，尿苷掺入细胞mRNA、核糖体前体RNA和可溶性RNA的过程迅速受到抑制。与迄今为止研究的大多数其他杀细胞病毒一样，病毒诱导的细胞RNA合成抑制似乎是细胞损伤的主要机制。
