Coggin J H
J Virol. 1969 May;3(5):458-62. doi: 10.1128/JVI.3.5.458-462.1969.
Since transformation of hamster cells in vitro by simian virus 40 (SV40) is a rare event in a homogeneously infected cell population, physiochemical studies of the events of virus transformation are difficult. Similarly, other deoxyribonucleic acid-containing oncogenic viruses produce transformed-cell foci in vitro with low efficiency. Sublethal doses of X-ray irradiation, as well as preincubation of hamster embryo cells with the radiomimetic analogue, 5-iododeoxyuridine, markedly sensitized hamster embryo cells to SV40 in vitro. Agents were used at dosages which neither produced lethality nor caused neoplastic transformation in the absence of virus. Embryo cells maintained in vitro for long periods of time became increasingly more sensitive to SV40 transformation. Radiation also stimulated transformation by adenovirus 31. Delay in the addition of virus to preirradiated cells reduced the susceptibility to transformation by SV40 which was observed for cells infected immediately after irradiation, suggesting that radiation repair mechanisms or, possibly, release from radiation-induced "mitotic delay" may interfere with the process of neoplastic conversion by SV40.
由于在均匀感染的细胞群体中,猿猴病毒40(SV40)在体外转化仓鼠细胞是一个罕见事件,因此对病毒转化事件进行物理化学研究很困难。同样,其他含脱氧核糖核酸的致癌病毒在体外产生转化细胞集落的效率也很低。亚致死剂量的X射线照射,以及用放射模拟类似物5-碘脱氧尿苷对仓鼠胚胎细胞进行预孵育,可使仓鼠胚胎细胞在体外对SV40明显敏感。所用试剂的剂量在无病毒时既不产生致死性也不引起肿瘤转化。长时间在体外培养的胚胎细胞对SV40转化变得越来越敏感。辐射也刺激了腺病毒31的转化。延迟向预照射细胞中添加病毒会降低其对SV40转化的敏感性,而这种敏感性在照射后立即感染的细胞中可以观察到,这表明辐射修复机制或者可能是从辐射诱导的“有丝分裂延迟”中释放出来的过程可能会干扰SV40的肿瘤转化过程。