Abstract
Different mouse cell strains exposed in vitro to the polyoma virus showed wide reactions ranging from high sensitivity of MB III lymphoblasts or malignant N1 T fibroblasts to a state of nonsensitivity of the Z1 strain. The low-cancer N2 line, when associated with the polyoma virus (N2 Pma), produced regularly latent infection characterized by unlimited increase of cell population parallel to virus multiplication. Treatment with specific antipolyoma serum for 9 months did not suppress the infection. A high proportion of cells containing virus was disclosed in antiserum-treated or untreated N2 Pma cultures. These cultures displayed an increased resistance to herpes virus infection or to reinfection with polyoma virus. In the virus-free supernatant of ultracentrifuged N2 Pma cultures, a self-inhibitory factor interfering with polyoma-virus multiplication and its cytopathogenic effect was disclosed. The mechanism of virus transmission in the carrier N2 Pma cultures and the possible role of inhibiting factor in virus latency are discussed.