Rex Risser

In 1970 Abelson and Rabstein (1) isolated a variant of Moloney leukemia virus from a nonthymic l y m p h o m a of a BALB/c mouse. Subsequent studies indicated that this virus, now termed Abelson murine leukemia virus (MuLV-A), 1 induces a malignant disease of primitive bone marrow-derived lymphocytes (2-5). Under certain conditions, M u L V A also induces tumors of highly differentiated B cells, i.e. plasmacytomas (6). Thus, it is apparent that M u L V A differs from other murine leukemia viruses in its target cell specificity. Virologic studies indicate that M u L V A is a complex of defective virus and nondefective Moloney leukemia virus. The defective virus, which can be assayed in vitro by focus formation on certain etablished cell lines, is responsible for the induction of nonthymic l ymphoma (7). Recent evidence indicates that M u L V A can exert its oncogenic effect on lymphoid cells in tissue culture (5, 8-10). The studies reported here examined the age and virus dose dependence of M u L V A lymphomagenesis, and the pat tern of susceptibility of various mouse strains to MuLV-A. Results from studies of BALB/c × C57BL/6 recombinant inbred strains indicate that susceptibility to M u L V A lymphomagenesis is controlled by two loci, designated Av-I and Av-2, at which sensitivity alleles are dominant . Furthermore, the genes involved in this disease are not identical to genes controlling other pathologic forms of murine leukemia.