I. Hellström

Further studies on superinfection of polyoma-induced mouse tumors with polyoma virus in vitro.

Abstract Explants of six serially transplanted polyoma tumor lines, five of which have been induced in vivo and one in vitro , were superinfected with polyoma virus in tissue culture in doses of 10–68 HA units per 0.2 ml medium. Chromosomal analysis was used to identify the cultured cells as tumor cells. Four of the five in vivo -induced tumors were sensitive: they reacted with cytopathic changes and released virus. One in vivo -induced tumor, an osteogenic sarcoma, was resistant to the cytopathic effect. The in vitro -induced tumor, carried by serial in vivo passage, showed a relative resistance to superinfection: it was not affected by 13 HA units of virus per 0.2 ml, but 26–68 HA units per 0.2 ml produced a clear-cut cytopathic effect. Two sensitive tumors that showed recovery from polyoma infection in vitro were resistant to superinfection with the virus. This resistance was maintained during a number of serial transfers in vivo . After 5 and 9 in vivo passages, respectively, the resistance was lost, however, and the tumors became sensitive again. All tumors studied, some of which have been carried up to 24 serial passages in vivo , released hemagglutinating virus in vitro , at least occasionally.

Abrogation of Allogeneic Inhibition by Cortisone

Tumor cells from homozygous mice grow better upon transplanation to syngeneic mice than to F1 hybrids between the tumor strain and a foreign strain. The inhibition of cell growth in the hybrids (called allogeneic inhibition), which is detected by tumor transplantation into mice, cotuld be abrogated by treatment of the recipient mice with cortisone acetate. Cortisone also abolished allogeneic inhibition in vitro; abolition was detected by treating tumor cultures with cell extracts containing foreign isoantigens of the H-2 type.