Northrop R L
J Virol. 1969 Aug;4(2):133-40. doi: 10.1128/JVI.4.2.133-140.1969.
Puromycin and actinomycin D were used to treat a line of human conjunctiva cells persistently infected with mumps virus (C-M cells) in order to determine where virus synthesis is inhibited. Although 90% of the cells in C-M cultures are infected, little or no infectious virus is produced by most cells in a growing culture. Adding puromycin to inhibit protein synthesis resulted in the production of infectious virus. Thus, all the viral proteins needed for virus completion were made in the growing cells. When actinomycin D was added to growing cells, infectious virus was again produced. Since mumps virus synthesis is actinomycin D-insensitive, this suggested a host control of the virus. Interferon was not detected. The possible mechanisms of host control are discussed.
使用嘌呤霉素和放线菌素D处理持续感染腮腺炎病毒的人结膜细胞系（C-M细胞），以确定病毒合成受抑制的部位。尽管C-M培养物中90%的细胞被感染，但在生长的培养物中，大多数细胞很少或不产生有感染性的病毒。添加嘌呤霉素抑制蛋白质合成导致产生有感染性的病毒。因此，病毒完成所需的所有病毒蛋白都是在生长的细胞中产生的。当向生长的细胞中添加放线菌素D时，再次产生了有感染性的病毒。由于腮腺炎病毒的合成对放线菌素D不敏感，这表明存在宿主对病毒的控制。未检测到干扰素。讨论了宿主控制的可能机制。
