O'Hare P, Honess R W
J Virol. 1983 Apr;46(1):279-83. doi: 10.1128/JVI.46.1.279-283.1983.
The effects of phosphonoacetic acid on the synthesis of herpesvirus saimiri-specific polypeptides in productively infected cells were examined. At concentrations that inhibited virus DNA synthesis (greater than or equal to 150 micrograms/ml), phosphonoacetic acid prevented the synthesis of the majority of virus-specific polypeptides while allowing the synthesis of a subset of virus proteins (i.e., 110,000 [110K], 76K, 72K, 51K, 48K, 29K, 24K, and 20K or 21K) and the protracted synthesis of host-specified polypeptides. Other inhibitors of DNA synthesis (e.g., cytosine arabinoside) showed the same selective inhibition of late virus protein synthesis and identified the same resistant subset of early virus-specific polypeptides. This DNA synthesis-independent subset included the 51K phosphoprotein, which, together with the 110K, 48K, and 31K polypeptides, accumulated in the nuclear fraction of infected cells.
研究了膦甲酸对产生性感染细胞中赛米利疱疹病毒特异性多肽合成的影响。在抑制病毒DNA合成的浓度(大于或等于150微克/毫升)下,膦甲酸可阻止大多数病毒特异性多肽的合成,同时允许一部分病毒蛋白(即110000[110K]、76K、72K、51K、48K、29K、24K和20K或21K)的合成以及宿主特异性多肽的持续合成。其他DNA合成抑制剂(如阿糖胞苷)也显示出对晚期病毒蛋白合成的相同选择性抑制,并鉴定出相同的早期病毒特异性多肽抗性亚群。这个不依赖DNA合成的亚群包括51K磷蛋白,它与110K、48K和31K多肽一起积聚在感染细胞的核部分。