胍在脊髓灰质炎病毒抑制脱氧核糖核酸合成编程中的特殊作用。
Specific effect of guanidine in the programming of poliovirus inhibition of deoxyribonucleic acid synthesis.
作者信息
Powers C D, Miller B A, Kurtz H, Ackermann W W
出版信息
J Virol. 1969 Mar;3(3):337-42. doi: 10.1128/JVI.3.3.337-342.1969.
Inhibition of HeLa cell deoxyribonucleic acid (DNA) synthesis, which occurred by the 4th to 5th hr after infection with poliovirus, could be blocked completely by guanidine only when it was present before the 2nd hr. At the 2nd hr, there was no significant ribonucleic acid (RNA)-replicase activity, and addition of guanidine inhibited all production of virus but allowed 57% of maximal DNA inhibition to develop. Maximum DNA inhibition developed in cells infected for 4 hr in the presence of guanidine when the guanidine was removed for a 10-min interval. RNA-replicase activity was not enzymatically detectable and viral multiplication did not develop in these cells unless the interval without guanidine was extended to 60 min. The interpretation of the data was that the effect of guanidine on viral-induced inhibition of DNA synthesis was distinct and not a consequence of the inhibition of RNA-replicase.
脊髓灰质炎病毒感染后第4至5小时出现的HeLa细胞脱氧核糖核酸（DNA）合成抑制，只有在第2小时之前存在胍时，才能被胍完全阻断。在第2小时，没有明显的核糖核酸（RNA）复制酶活性，添加胍可抑制所有病毒产生，但允许最大DNA抑制的57%发展。当胍在10分钟间隔内被去除时，在存在胍的情况下感染4小时的细胞中出现最大DNA抑制。除非无胍间隔延长至60分钟，否则在这些细胞中无法通过酶法检测到RNA复制酶活性，且病毒增殖也不会发生。对数据的解释是，胍对病毒诱导的DNA合成抑制的作用是独特的，并非RNA复制酶抑制的结果。
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