May E, May P, Weil R
Proc Natl Acad Sci U S A. 1973 Jun;70(6):1654-8. doi: 10.1073/pnas.70.6.1654.
Simian Virus 40 (SV40) induces in "contact-inhibited" tissue culture cells of mouse kidney an abortive infection that leads to the appearance of intra-nuclear SV40-specific tumor (T-) antigen, followed by replication of the mouse-cell chromatin and mitosis, while no viral progeny DNA or capsid protein is produced. Synthesis of "early" SV40-specific RNA ("19S RNA") begins a few hours before the appearance of T-antigen and appears to be switched off after the onset of chromatin replication. As the most simple working hypothesis that can account for the experimental results available, we assume that early SV40 RNA contains information necessary for production of T-antigen and that this antigen (or an unknown early virus-specific function that would simply parallel the appearance of T-antigen) activates or de-inhibits a cellular regulatory element that governs chromosome replication and mitosis. The experimental results agree with the idea that SV40 acts primarily as a mitogen.
猿猴病毒40（SV40）在小鼠肾脏的“接触抑制”组织培养细胞中引发一种流产感染，导致细胞核内出现SV40特异性肿瘤（T-）抗原，随后小鼠细胞染色质复制并进行有丝分裂，而不产生病毒子代DNA或衣壳蛋白。“早期”SV40特异性RNA（“19S RNA”）的合成在T抗原出现前数小时开始，并且在染色质复制开始后似乎被关闭。作为能够解释现有实验结果的最简单可行假设，我们假定早期SV40 RNA包含产生T抗原所需的信息，并且这种抗原（或与T抗原出现简单平行的未知早期病毒特异性功能）激活或解除抑制一个控制染色体复制和有丝分裂的细胞调节元件。实验结果与SV40主要作为一种促细胞分裂剂的观点相符。
