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pubmed:abstractText |
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.
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