Friderici K, Priehs C, Fluck M M
J Virol. 1986 Jan;57(1):205-10. doi: 10.1128/JVI.57.1.205-210.1986.
We have characterized the viral sequences integrated in a polyomavirus-transformed mouse cell line, Py-3T3 (clone Py-6), and followed their excision and packaging upon superinfection. The polyomavirus sequences contained in Py-6 cells are present as a single insert of nonidentical tandem copies which includes, in addition to a normal middle T-antigen-coding region, some very rearranged sequences. Infection of Py-6 cells with polyomavirus strains encoding a normal large T antigen leads to the reproducible recovery in the resulting viral stock of specific defective viral genomes. The defective genomes contain a wild-type coding region for middle and small T antigens and intact viral origin and enhancer sequences. The remainder of the viral genome is rearranged or lost, so that there is no capacity to code for large T antigen or viral capsid proteins. The recovered defective sequences are also found integrated in Py-6 genomic DNA. Presumably, in infections of Py-6 cells, large T antigen, provided by the superinfecting virus, amplifies and excises the integrated viral sequences. The superinfecting helper virus must also produce viral capsids for packaging of the defective viral DNA and thus provides a means to shuttle the defective sequences from the mouse cells into other hosts, such as rat cells. In the latter host, the defective sequences are able to induce transformation.
我们已对整合在多瘤病毒转化的小鼠细胞系Py-3T3（克隆Py-6）中的病毒序列进行了特征分析，并追踪了它们在超感染后的切除和包装情况。Py-6细胞中所含的多瘤病毒序列以单个非相同串联拷贝的插入形式存在，除了正常的中间T抗原编码区外，还包括一些非常重排的序列。用编码正常大T抗原的多瘤病毒株感染Py-6细胞，会导致在所得病毒悬液中可重复回收特定的缺陷病毒基因组。这些缺陷基因组包含中间和小T抗原的野生型编码区以及完整的病毒起源和增强子序列。病毒基因组的其余部分发生了重排或丢失，因此没有能力编码大T抗原或病毒衣壳蛋白。回收的缺陷序列也被发现整合在Py-6基因组DNA中。据推测，在Py-6细胞感染中，由超感染病毒提供的大T抗原会扩增并切除整合的病毒序列。超感染的辅助病毒还必须产生病毒衣壳来包装缺陷病毒DNA，从而提供了一种将缺陷序列从小鼠细胞转运到其他宿主（如大鼠细胞）的方法。在后者宿主中，缺陷序列能够诱导转化。
