Summers W C, Klein G
J Virol. 1976 Apr;18(1):151-5. doi: 10.1128/JVI.18.1.151-155.1976.
Growth of lymphoblastoid cells (B95-8, Raji) is not inhibited by the presence of 0.4 mM phosphonoacetic acid. The synthesis of Epstein-Barr virus (EBV) in the producer line B95-8 is completely inhibited, as shown by the total inhibition of viral capsid antigen synthesis. Early viral antigens are made normally in the presence of phosphonoacetic acid, but EBV DNA synthesis is blocked in cells entering the productive cycle. Nonproducer cells in the population replicate the resident EBV DNA by a mechanism that is resistant to phosphonoacetic acid. These results are consistant with the hypotheses that EBV DNA is replicated by two mechanisms, one in the noninduced cell and a different mechanism in the producer cell, and that prior replication of EBV DNA, probably by the second mode, is a prerequisite for late gene expression.
0.4 mM膦酰乙酸的存在不会抑制淋巴母细胞样细胞（B95 - 8、Raji）的生长。如病毒衣壳抗原合成被完全抑制所示，在产生细胞系B95 - 8中，爱泼斯坦 - 巴尔病毒（EBV）的合成被完全抑制。早期病毒抗原在膦酰乙酸存在的情况下正常产生，但EBV DNA合成在进入生产周期的细胞中被阻断。群体中的非产生细胞通过一种对膦酰乙酸有抗性的机制复制常驻EBV DNA。这些结果与以下假设一致：EBV DNA通过两种机制复制，一种在未诱导的细胞中，另一种在产生细胞中不同，并且EBV DNA的先前复制，可能通过第二种模式，是晚期基因表达的先决条件。
