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Abelson murine leukemia virus: effect of helper virus from regressing Friend virus on leukemia development
Abstract:
Replication defective Abelson murine leukemia virus (A-MuLV) induces a non-thymic lymphoma in vivo and transforms both hematopoietic and fibroblastic cells in vitro. In vivo leukemogenicity and the efficiency of in vitro transformation of hematopoietic cells by A-MuLV are known to be affected by the replication competent helper virus present in A-MuLV stocks. The helper virus isolated from the regressing strain of Friend virus (RF-MuLV) is responsible for the spontaneous regression of erythroleukemia induced by replication defective spleen-focus forming virus and itself induces a lymphocytic leukemia which spontaneously regresses. The diseases produced by A-MuLV stocks containing either RF-MuLV or Moloney leukemia virus, the helper virus associated with the original isolate of A-MuLV, were compared to determine if RF-MuLV can influence the disease produced by a replication defective virus with a discrete transforming gene. Both virus stocks induced leukemias with similar efficiency and gross pathology. Spontaneous regression was not observed when RF-MuLV was used as the helper virus. Examination of the leukemic cells and cell lines derived from leukemic tissues indicated that the target cell for A-MuLV transformation was not affected by the helper virus. Both transformed lymphoid and monocytic cells were cultured from leukemic tissues and established as cell lines. The lymphoid cells were phenotypically similar to pre-B cells or null cells, while the monocytic cell lines resemble promonocytes. The frequency with which promonocytic cell lines were isolated from leukemic mice suggests that A-MuLV leukemogenesis may often involve transformation of monocytic series cells as well as lymphoid cells. Thus, RF-MuLV can serve as an efficient helper virus for A-MuLV and does not appear to alter the in vivo target cell for transformation. It is unable, however, to alter the progressive course of Abelson virus induced disease.