Helper-independent mink cell focus-inducing strains of Friend murine type-C virus: potential relationship to the origin of replication-defective spleen focus-forming virus.

Abstract

Recent studies have indicated that both the replication-defective spleen focus-forming virus (SFFV) in the Friend virus complex and the helper-independent mink cell focus-inducing (MCF) viruses derived from AKR-murine leukemia virus (MuLV) are env gene recombinants between ecotropic virus and xenotropic virus. In an attempt to isolate additional env gene recombinants between Friend murine leukemia virus (F-MuLV) and xenotropic virus, we have inoculated cloned ecotropic F-MuLV into newborn NIH Swiss mice and analyzed MuLV released from preleukemic and leukemic spleens of infected mice. Two helper-independent MCF strains of F-MuLV have been isolated. Like the previously described AKR-MCF viruses, the Friend MCF viruses are env gene recombinants between an ecotropic virus (F-MuLV) and a mouse xenotropic virus, as shown by host range, interference pattern, and tryptic peptide analysis of the gp70s of these MuLV. Furthermore, RNA from the Friend MCF viruses hybridizes completely to cDNAsffv, a nucleic acid probe which detects that portion of SFFV which was not derived from P-MuLV. The ability to isolate replicating MCF viruses derived from F-MuLV FURTHER strengthens the parallels between the Friend erythroleukemia system and the AKR thymic leukemia system. Finally, the potential relationship of helper-independent env gene recombinants between F-MuLV and xenotropic virus to be highly leukemogenic SFFV is discussed.

In Vivo Interactions of Ecotropic and Polytropic Murine Leukemia Viruses in Mixed Retrovirus Infections

“…However, two polytropic MuLVs, Fr54 and Fr98, that replicated sufficiently well in the mice were identified and studied. In agreement with other studies of polytropic MuLVs derived by recombination with F-MuLVs (1,26,48), both Fr54 and Fr98 resulted in a proliferative disease characterized by gross splenomegaly and anemia when inoculated into neonatal mice. This was a somewhat unexpected result for Fr98 in that this virus had been reported to induce a neurological disorder rather than a proliferative disease in newborn IRW mice (36).…”

“…1). Similar to other F-MuLV-derived polytropic MuLVs (1,26,48), Fr54 induced splenomegaly accompanied by severe anemia in some NFS/N mice. Surprisingly, Fr98, which induces a severe neurological disease in IRW mice (36), did not induce obvious signs of neurological disease in NFS/N mice.…”

Characterization of a highly oncogenic murine leukemia virus from wild mice

“…The 10A-I virus differs from the spleen focus forming virus (SFFV) component of the Friend MuLV (F-MuLV) system (Troxler et al, 1977) in so far as it is replication competent and incapable of transforming erythroid stem cells in vitro. The IOA-I virus also differs from the F-MuLV helper independent ecotropic xenotropic recombinant derived by in vivo passage through NIH Swiss mouse (Troxler et al, 1978) in that the F-MuLV displays classical host range and interference properties associated with other MCF viruses. Further more, the F-MuLV recombinant produces mainly erythroleukemia (Troxler et al, 1978), a disease not yet seen in feral mice.…”

“…The IOA-I virus also differs from the F-MuLV helper independent ecotropic xenotropic recombinant derived by in vivo passage through NIH Swiss mouse (Troxler et al, 1978) in that the F-MuLV displays classical host range and interference properties associated with other MCF viruses. Further more, the F-MuLV recombinant produces mainly erythroleukemia (Troxler et al, 1978), a disease not yet seen in feral mice. The amphotropic recombinant virus (10A-1) causes null cell splenic lymphomas similar to the Abelson MuLV-lnduced disease (Pratt et al, (1977).…”

Infection of Haematopoietic Stem Cells In Mice With Friend Virus Induced Erythroleukaemia

“…It is important in this context to distinguish between cells that may become infected in the course of the disease and true leukaemic target cells that are obligatory elements in the initiation and/or progression of the disease. Friend viruses do not express highly selective tissue tropisms and are able to infect cells of many lineages, including fibroblasts and lymphoid cells (Eckner, 1975;Troxler et al, 1979), not all of which are likely to be directly involved in the disease, and thus not target cells of the leukaemia.…”