Indexed on: 01 Dec '70Published on: 01 Dec '70Published in: Archiv fur die gesamte Virusforschung
The increased resistance to poliovirus of SV40 transformed human amnion cells compared with primary cells has been shown to involve reduced cytopathic effect (CPE), delayed and reduced production of virus, inefficiency of infectious center formation, and the failure of transformed cell monolayers to support poliovirus plaque formation. At multiplicities of exposure (plaque-forming units/ cell) less than 10, CPE was negligible in the poliovirus infected transformed cell cultures which could be maintained as living cultures yielding poliovirus up to three months. Infectious center formation at different multiplicities showed that both cell types could be infected with single infectious units, but in cultures of transformed cells, the probability of initiating infection was reduced about 25-fold. Resistance was not observed in primary amnion cultures infected with SV40 in the absence of transformation. However, cellular resistance developed as morphologic transformed cells appeared in SV40 infected cultures. Transformed cells maintained resistance when SV40 multiplication in transformed cultures was suppressed with metabolic inhibitors or eliminated by isolating virus-free clones of transformed cells in the presence of SV40 antiserum.The mechanism of the increased resistance of SV40 transformed human amnion cells to poliovirus infection involves an inefficiency in the initiation of infection. When compared to the highly susceptible untransformed primary cells, no significant differences in the adsorption, penetration or eclipse of poliovirus were demonstrated. There was no detectable interferon production in the transformed cultures either before or after poliovirus infection. Since infection with infectious poliovirus RNA bypassed resistance, it is concluded that the resistance of the SV40 transformed cells results from an inefficiency in the uncoating of poliovirus to infectious RNA.