Frenkel G D
J Virol. 1977 Jan;21(1):423-6. doi: 10.1128/JVI.21.1.423-426.1977.
During infection of BS-C-1 cells (a permissive line of monkey kidney cells) with simian virus 40, there was a loss of infecting viral supercoiled (component I) DNA molecules which was partially inhibited by cycloheximide. The kinetics of loss of component I in the presence of cycloheximide suggested that the loss was the result of at least two activities acting on the DNA, one cycloheximide sensitive and the second cycloheximide insensitive. Nucleotides from degraded infecting viral DNA were reincorporated into cell DNA that was synthesized during the infection.
在用猴病毒40感染BS - C - 1细胞(一种允许性猴肾细胞系)的过程中,感染性病毒超螺旋(组分I)DNA分子会丢失,环己酰亚胺可部分抑制这种丢失。在存在环己酰亚胺的情况下组分I丢失的动力学表明,这种丢失是至少两种作用于DNA的活性的结果,一种对环己酰亚胺敏感,另一种对环己酰亚胺不敏感。来自降解的感染性病毒DNA的核苷酸会重新掺入感染期间合成的细胞DNA中。