Adoptive Transfer of Antiviral Resistance by Lymphoid Cells from Mice Protected against Friend Leukemia Virus-induced Disease by Passive Serum Therapy¹

Spleen and bone marrow cells from DBA/2 mice protected against infection with a leukemogenic dose of Friend leukemia virus (FLV) by passive therapy with chimpanzee anti-FLV serum were shown to be able to adoptively transfer antiviral resistance to unimmunized irradiated syngeneic recipients. Similar to the results obtained with donor mice immunized against a syngeneic FLV erythroleukemia cell line, spleen cells from serumprotected donor mice were more effective in transferring antiviral resistance than were the corresponding bone marrow cells. In contrast to the previously demonstrated close correlation between passive serum therapy protection and the development of a host antiviral humoral response, adoptive cell transfer-mediated resistance to FLV challenge was not accompanied by the presence of detectable antiviral antibodies. While the cell type(s) responsible for transfer of antiviral resistance have not been conclusively identified, studies presented in this report indicate that elimination of T-cells by treatment with anti-Thy 1.2 antibodies plus complement does not affect the ability of spleen cells from serum-protected mice to adoptively transfer antiviral resistance. Furthermore, the idea that mature T-cells do not play a critical role in the FLV serum protection mechanism is further supported by the fact that the serum therapy protocol operates effectively in nude athymic mice. In the course of the adoptive transfer studies, it was observed that sublethal irradiation of DBA/2 mice prevented the development of FLV-induced splenomegaly (which reflects the activity of the defective spleen focus-forming virus component) without affecting the replication of the helper nondefective lymphatic leukemia virus. This irradiation effect could be reversed by reconstituting the mice with spleen or bone marrow cells from normal or FLV-infected syngeneic mice, suggesting that the irradiation effect is due to the inactivation of a spleen focus-forming virus target cell, presumably of an erythroid stem cell nature, which can be replaced by normal or leukemic spleen or bone marrow cells.