Gentil A, Daya-Grosjean L, Margot A, Sarasin A
Biochimie. 1985 Mar-Apr;67(3-4):393-8. doi: 10.1016/s0300-9084(85)80087-0.
Survival and mutagenesis of UV-irradiated, temperature-sensitive simian virus 40 mutants (SV40) have been studied after infection of human fibroblasts. Survival of the viral progeny obtained after 6,8 or 10 days at permissive temperature decrease as a function of the UV-dose delivered to the virus. In cels which have been pretreated with 10 Jm-2 of UV 24 hours before infection, progeny survival was increased as compared to survival in control cells. The reactivation factor varies from one to ten, depending on the number of lytic cycles carried out at permissive temperature. The level of mutation frequency, as measured by the reversion from a temperature sensitive growth phenotype towards a wild type phenotype, increases with the dose of UV-irradiation given to the virus. Moreover, the mutation frequency is increased in the viral progeny produced in UV-irradiated human cells. Similar experiments carried out with SV40-transformed human fibroblasts, which constitutively express SV40 T antigen, gave comparable results. These experiments show that, as in monkey cells, a new error-prone recovery pathway can be induced by pretreating human cells with UV-light before infection.
在感染人成纤维细胞后,对紫外线照射的、温度敏感的猴病毒40突变体(SV40)的存活和诱变情况进行了研究。在允许温度下培养6、8或10天后获得的病毒后代的存活率随给予病毒的紫外线剂量而降低。在感染前24小时用10 Jm-2紫外线预处理的细胞中,与对照细胞中的存活率相比,后代存活率有所提高。再激活因子从1到10不等,这取决于在允许温度下进行的裂解周期数。通过从温度敏感生长表型向野生型表型的回复来衡量的突变频率水平,随着给予病毒的紫外线照射剂量而增加。此外,在紫外线照射的人细胞中产生的病毒后代中的突变频率增加。用组成型表达SV40 T抗原的SV40转化的人成纤维细胞进行的类似实验得到了可比的结果。这些实验表明,与在猴细胞中一样,在感染前用紫外线预处理人细胞可以诱导一种新的易出错的恢复途径。