RD-114 virus rapidly induces fusion of the KC cell line, a human malignant glioma cell transformed by Rous sarcoma virus. Treatment of the virus with trypsin, heat, ultrasonic vibration, or ether, completely eliminated fusion activity, while deoxyribonuclease (DNase), ribonuclease (RNase), or neuraminidase treatment had no effect. β-Propiolactone inactivation of the virus resulted in no decrease of fusion activity, though infectivity was completely lost. The KC cell line was productively infected with RD-114 virus, and in this condition was completely refractory to fusion by RD-114, either in response to endogenous virus or to large amounts of exogenous virus. Treatment of the normal KC cells with actinomycin C, cytosine β--arabinofuranoside, or cycloheximide did not prevent fusion in response to RD-114 virus. These data suggest that intact, but not necessarily infectious, virus is required for fusion, and that the process is very similar to the fusion of XC cells by murine leukaemia viruses.


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