Grant J A, Sabina L R
Antimicrob Agents Chemother. 1972 Sep;2(3):201-5. doi: 10.1128/AAC.2.3.201.
9-beta-d-Arabinofuranosyladenine (Ara-A) effectively inhibited the production of infectious vesicular stomatitis virus (VSV) in MDBK cells. Furthermore, inhibition was shown to begin as early as the first 3 hr of infection. Studies employing (3)H-l-leucine indicated that Ara-A did not affect protein synthesis in uninfected cells, although it did cause a marked stimulation of protein synthesis in VSV-infected cells during the log phase of the growth cycle. Puromycin, an inhibitor of protein synthesis, was a more effective viral inhibitor than Ara-A. However, the combination of Ara-A and puromycin was less effective than puromycin alone except when present for long time periods. Short-term labeling experiments with (3)H-uridine demonstrated that Ara-A depressed ribonucleic acid (RNA) synthesis in uninfected cells, whereas periods of stimulation and depression of radioisotope incorporation occurred in infected cells. The results support the notion that Ara-A is incorporated into RNA early during viral replication.
9-β-D-阿拉伯呋喃糖基腺嘌呤(Ara-A)可有效抑制水泡性口炎病毒(VSV)在MDBK细胞中的产生。此外,研究表明抑制作用最早在感染后的前3小时就开始了。使用³H-L-亮氨酸的研究表明,Ara-A对未感染细胞的蛋白质合成没有影响,尽管它在生长周期的对数期确实会显著刺激VSV感染细胞中的蛋白质合成。蛋白质合成抑制剂嘌呤霉素是比Ara-A更有效的病毒抑制剂。然而,Ara-A和嘌呤霉素的组合比单独使用嘌呤霉素效果更差,除非长时间存在。用³H-尿苷进行的短期标记实验表明,Ara-A可抑制未感染细胞中的核糖核酸(RNA)合成,而在感染细胞中则会出现放射性同位素掺入的刺激和抑制期。这些结果支持了Ara-A在病毒复制早期被掺入RNA的观点。