Diamond L
J Virol. 1967 Dec;1(6):1109-16. doi: 10.1128/JVI.1.6.1109-1116.1967.
When the hamster cell lines BHK21 and Nil-2 were infected at a multiplicity of 100 with the adenovirus 7-simian virus 40 (SV40) hybrid (strain LLE46), SV40 T antigen was induced in 0.1 to 6% of the cells during the first 96 hr postinfection, morphological changes occurred 3 to 7 weeks later, and eventually all the cells contained SV40 T antigen, but no adeno 7 T antigen. Results were similar when primary and secondary monolayer cultures of hamster embryo (HE) cells were infected with the adeno 7-SV40 hybrid, and when primary HE cells were infected with SV40. However, infection of BHK21, Nil-2, and secondary HE cells with the same multiplicity of SV40 did not induce SV40 T antigen or morphological transformation. This suggests that the target cells required for infection with SV40 virions, but not those required for infection with the hybrid, are lost or altered in secondary HE cultures and in the two cell lines. In most of the virus-host cell systems in which SV40 T antigen and transformation were induced, there was a decrease in the number of T antigen-positive cells after the initial infection. This was followed by a lag period of up to 2 months before the onset of a progressive increase in the number of positive cells. The beginning of the rise in T antigen production coincided with the first morphological changes.
当仓鼠细胞系BHK21和Nil-2以感染复数100被腺病毒7-猴病毒40（SV40）杂种（LLE46株）感染时，在感染后的最初96小时内，0.1%至6%的细胞中诱导出SV40 T抗原，3至7周后出现形态学变化，最终所有细胞都含有SV40 T抗原，但没有腺病毒7 T抗原。当仓鼠胚胎（HE）细胞的原代和传代单层培养物被腺病毒7-SV40杂种感染，以及原代HE细胞被SV40感染时，结果相似。然而，用相同感染复数的SV40感染BHK21、Nil-2和传代HE细胞，并未诱导出SV40 T抗原或形态转化。这表明，在传代HE培养物和这两种细胞系中，被SV40病毒体感染所需的靶细胞丢失或发生了改变，但被杂种感染所需的靶细胞没有。在大多数诱导出SV40 T抗原和转化的病毒-宿主细胞系统中，初次感染后T抗原阳性细胞的数量会减少。随后会有长达2个月的滞后期，之后阳性细胞数量才开始逐渐增加。T抗原产生增加的开始与首次形态学变化同时发生。
