Peebles P T, Bassin R H, Haapala D K, Phillips L A, Nomura S, Fischinger P J
J Virol. 1971 Nov;8(5):690-4. doi: 10.1128/JVI.8.5.690-694.1971.
The nature of murine sarcoma virus (MSV) "defectiveness" was investigated by employing an MSV-transformed mouse 3T3 cell line which releases noninfectious virus-like particles. Rescue kinetics of MSV, observed after murine leukemia virus (MuLV) superinfection of these "sarcoma-positive leukemia-negative (S + L -)" mouse 3T3 cells, consisted of a 9- to 12-hr eclipse period followed by simultaneous release of both MSV and MuLV with no evidence for release of infectious MSV prior to the production of progeny MuLV. Addition of thymidine to the growth medium of MuLV-superinfected S + L - cells at a concentration suppressing deoxyribonucleic acid synthesis inhibited the replication of MuLV and the rescue of MSV. MSV production closely paralleled MuLV replication under a variety of experimental conditions. These results suggest that replication of MuLV is required for the rescue of infectious MSV from S + L - cells and that one (or more) factor, produced late in the MuLV replicative cycle, is utilized by both viruses during virion assembly. During the course of these experiments, virus stocks were recovered which contained infectious MSV in apparent excess over MuLV. These stocks were used for generating new S + L - cell lines by simple end point dilution procedures.
通过使用一种能释放无感染性病毒样颗粒的MSV转化的小鼠3T3细胞系，对鼠肉瘤病毒（MSV）“缺陷性”的本质进行了研究。在用鼠白血病病毒（MuLV）对这些“肉瘤阳性白血病阴性（S + L -）”小鼠3T3细胞进行超感染后观察到的MSV拯救动力学，包括9至12小时的隐蔽期，随后同时释放MSV和MuLV，在子代MuLV产生之前没有传染性MSV释放的证据。在MuLV超感染的S + L -细胞的生长培养基中添加胸苷，其浓度可抑制脱氧核糖核酸合成，这抑制了MuLV的复制和MSV的拯救。在各种实验条件下，MSV的产生与MuLV的复制密切平行。这些结果表明，从S + L -细胞中拯救传染性MSV需要MuLV的复制，并且在MuLV复制周期后期产生的一种（或多种）因子在病毒体组装过程中被两种病毒利用。在这些实验过程中，回收了病毒株，其中所含的传染性MSV明显超过MuLV。这些病毒株通过简单的终点稀释程序用于产生新的S + L -细胞系。
