Zur Hausen H
J Virol. 1968 Sep;2(9):915-7. doi: 10.1128/JVI.2.9.915-917.1968.
The fate of hamster cells, abortively infected with adenovirus type 12, has been studied by correlation of chromosomal aberrations with induction of T antigens and cloning efficiency. The incidence of chromosomal changes paralleled to some extent the T antigen formation, but was inversely related to the cloning efficiency of the cells. At an input multiplicity of 100, within 24 hr after infection, nearly all of the cells or metaphases revealed the presence of T antigens and chromosomal lesions, respectively, but no clones of cells were obtained. Inhibition of cellular deoxyribonucleic acid synthesis was not noted during this period. Increasing doses of ultraviolet irradiation reduced, successively, the capacity of the virus to induce chromosomal aberrations and correspondingly improved cloning efficiency of the exposed cells. It is concluded that most, if not all, cells revealing chromosomal lesions 24 hr after infection fail to enter further mitoses.
通过将染色体畸变与T抗原诱导及克隆效率相关联,研究了感染12型腺病毒后未成功感染的仓鼠细胞的命运。染色体变化的发生率在一定程度上与T抗原形成平行,但与细胞的克隆效率呈负相关。在感染复数为100时,感染后24小时内,几乎所有细胞或中期细胞分别显示出T抗原和染色体损伤的存在,但未获得细胞克隆。在此期间未观察到细胞脱氧核糖核酸合成受到抑制。增加紫外线照射剂量会依次降低病毒诱导染色体畸变的能力,并相应提高受照射细胞的克隆效率。得出的结论是,感染后24小时显示出染色体损伤的大多数(如果不是全部)细胞无法进入进一步的有丝分裂。