Resistance and susceptibility to challenge infection of polyoma-induced tumor cell clones

Abstract

Resistance to challenge infection with polyoma virus (PV) was studied in 77 clones derived from a PV-induced mouse mammary tumor and in 9 clones derived from a PV-induced mouse parotid tumor clone. There was no spontaneous virus production in cultures of any of these clones. Cloning of 2 uncloned resistant mass populations of the mammary tumor yielded 55% susceptible clones, while cloning of 2 susceptible clones derived from this tumor yielded 7% and 37% resistant clones. The derivation of resistant from susceptible clones was observed through two cycles of recloning. Although the uncloned resistant populations thus gave rise to susceptible clones, and susceptible clones gave rise to resistant clones, resistant clones derived from the mammary and parotid tumor produced only resistant clones. Two susceptible clones and an uncloned susceptible mass population became resistant after a series of transplantations in mice, a result suggesting a selective advantage for resistant cells in vivo. PV inoculation of the grafted mice inhibited in vivo growth after cell grafting, both with a resistant and a susceptible clone. There was no apparent correlation between observed differences in the karyotypes of the tumor cells and their reaction to challenge infection. Clones of PV-induced tumors that were resistant to PV challenge infection supported multiplication of mouse encephalomyocarditis virus. It is concluded that resistance of PV-induced tumor cells to PV challenge infection differs in some respects from the immunity of lysogenic bacteria to superinfection.