Inheritance of Susceptibility to Friend Mouse Leukemia Virus: VI. Reciprocal Alteration of Innate Resistance or Susceptibility by Bone Marrow Transplantation Between Congenic Strains

Abstract

Two newly established mouse strains which are congenic with standard inbred strains were used for the study of the locus Fv which controls the susceptibility to Friend leukemia virus in mice. A strain in each congenic pair shares the major histocompatibility gene with the corresponding partner strain but differs from the latter in the Fv locus. Mice with Fv(r)/Fv(r) genotype (DDD-Fv(r), C57BL/6) do not develop marked spleen enlargement upon virus challenge, whereas spleens of mice with Fv(s)/Fv(s) genotype (DDD, C57BL/6-Fv(s)) become large even with a virus inoculum 1/10(3) to 1/10(5) times that used for the resistant strains. Mice of each strain were heavily irradiated, inoculated with bone marrow cells taken from either syngenic or corresponding congenic mice, and challenged later with the leukemia virus. When Fv(s)/Fv(s) mice had been restored with bone marrow cells taken from Fv(r)/Fv(r) mice, the spleens remained small after the virus inoculation. In contrast, Fv(r)/Fv(r) mice receiving Fv(s)/Fv(s) cells responded to the virus with marked spleen enlargement. In the enlarged spleens of the C57BL/6 mice which do not otherwise allow the virus multiplication, a considerable amount of infectious virus was found. The altered response seems to be due to repopulation of destroyed tissues by the transplanted bone marrow cells. It is concluded that the locus Fv is expressed on hemopoietic cells, and cells derived from bone marrow play a predominant role in the development of splenomegaly by Friend leukemia virus.