Sturman L S, Takemoto K K
Infect Immun. 1972 Oct;6(4):501-7. doi: 10.1128/iai.6.4.501-507.1972.
Plaque formation by A59 virus, a murine coronavirus, was facilitated in AL/N and Balb mouse cells transformed by polyoma virus, simian virus 40, murine sarcoma virus, or mammary tumor virus. In these virus-transformed cells, A59 virus plaques were larger, they appeared earlier, and plaquing efficiencies were higher than in normal, untransformed cells. "Spontaneously" transformed AL/N cells behaved similarly to untransformed cells, whereas "spontaneously" transformed Balb cells resembled virus-transformed cell hosts. Both untransformed and transformed AL/N and Balb cells were permissive hosts for A59 virus. However, multiplication of A59 virus was enhanced at least fivefold in the virus-transformed AL/N cell hosts. Larger differences (100-fold or greater) in A59 virus production were obtained during the first cycle of infection in Balb cells at low multiplicities and in AL/N cells after multiple cycles of virus growth. In virus-transformed and "spontaneously" transformed Balb cells, A59 virus induced extensive syncytia formation.
多瘤病毒、猿猴病毒40、鼠肉瘤病毒或乳腺肿瘤病毒转化的AL/N和Balb小鼠细胞有助于鼠冠状病毒A59病毒形成噬斑。在这些病毒转化的细胞中，A59病毒噬斑更大，出现更早，且噬斑形成效率高于正常未转化细胞。“自发”转化的AL/N细胞表现与未转化细胞相似，而“自发”转化的Balb细胞类似于病毒转化的细胞宿主。未转化和转化的AL/N及Balb细胞都是A59病毒的允许性宿主。然而，在病毒转化的AL/N细胞宿主中，A59病毒的增殖至少增强了五倍。在低感染复数时Balb细胞的第一轮感染以及病毒多次生长循环后的AL/N细胞中，A59病毒产量存在更大差异（100倍或更大）。在病毒转化和“自发”转化的Balb细胞中，A59病毒诱导广泛的合胞体形成。
