Friend Erythroleukemia Virus Complex: Role of Viral Components in Modifying Erythroid Differentiation in Mice<xref ref-type="fn" rid="fn2">2</xref><xref ref-type="fn" rid="fn3">3</xref>

Abstract

The present study was carried out to determine which component of the polycythemic strain of Friend erythroleukemia virus (FV-P)--Friend helper virus [Friend murine leukemia virus (F-MuLV)] of the replication-defective spleen focus-forming virus (SFFV)--is responsible for inducing erythropoietin-independent erythropoiesis and expansion of the erythroid compartment in infected mice. F-MuLV and SFFV were cloned in SC1 cells to give a cell line 643/22N, which released only F-MuLV and SC204, a nonproducer cell line carrying SFFV. On superinfection with specific helper viruses, SC204 yielded further cell lines, which released SFFV in conjunction with 1) Friend, 2) Moloney, or 3) Gross helper viruses. With the use of an in vitro colony formation assay to monitor erythropoiesis in the bone marrow of inbred DBA/2J mice infected with any of the virus preparations containing SFFV plus helper virus, the erythroid precursor cell population was found to become erythropoietin-independent and amplified; adult mice infected with any of the helper viruses alone did not develop any symptoms of Friend disease. Thus the biologic activity of the FV-P complex was unaffected by replacement of the F-MuLV with an unrelated helper virus (Moloney or Gross). These results indicated that the SFFV component of FV-P is responsible for modifying erythroid differentiation in adult mice.