A detailed analysis of F-MuLV- and SFFV-infected cells in Friend virus-infected mice reveals the contribution of both F-MuLV- and SFFV-infected cells to the interleukin-10 host response (original) (raw)
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Proceedings of the …, 1979
We have recently demonstrated that normal hemopoietic cells express RNA sequences that are homologous to sequences specific for the Friend erythroleukemia virus genome [Bernstein, A., Gamble, C., Penrose, D. & Mak, T. W. (1979) Proc. NatL Acad. Sci. USA 76, 4455-4459]. In this communication, we report that the Fv-2 locus, the major genetic determinant controlling host susceptibility to erythroleukemia induction by Friend leukemia virus, also controls the expression of endogenous sequences related to the replication-defective component of Friend leukemia virus, Friend spleen focus-forming virus (SFFV), in normal uninfected mice. Two independent congeneic pairs of mice [C57BL/6 (B6) and B6.S; B6 and
Enhancement of spleen focus formation and virus replication in Friend virus-infected mice
Cancer research, 1969
Spleen focus formation, induced by a member [spleen focus forming virus (SFFV)] of the Friend virus complex, was en hanced in mice that had been infected 2 days previously with Newcastle disease virus or lactic dehydrogenase-elevating virus. Enhancement was also observed in mice treated with erythro poietin or maintained in 10 percent oxygen for 48 hours be fore SFFV infection. Sublethally irradiated mice were able to synthesize 30 times as much SFFV after treatment with S. typhosa endotoxin. Evidence is presented which indicates that these treatments exert their effects, at least in part, by increas ing the number or susceptibility of target cells for SFFV. The data are consistent with the hypothesis that a major portion of the target cells for SFFV are primitive erythroid cells, possibly erythropoietin-sensitive cells.
Journal of Experimental Medicine, 1972
Coinfection of neonatal BALB/c mice with helper-dependent Friend spleen focus-forming virus (SFFV), as contained in the Friend virus (FV) complex, and antigenically distinct Moloney leukemia virus (MolLV) resulted in the recovery of a MolLV pseudotype of SFFV, abbreviated SFFV(MolLV). The antigenic alteration of SFFV was observed by following its neutralization kinetics in vitro by specific Friend or Moloney typing antiserum. Effective pseudotype production was accomplished only when N-tropic LLV-F (the natural helper virus in the FV complex) was inhibited in B-type mice coinfected with an NB-tropic MolLV or other murine leukemia virus (MuLV) preparation. SFFV pseudotypes could not be prepared by using murine viruses other than leukemia viruses. SFFV prepared after two serial passages in the presence of MolLV was effectively neutralized by Moloney antiserum, but not by Friend typing antiserum; therefore, the envelope of the pseudotype virus, SFFV(MolLV), is homogeneous. Pseudotype v...
Journal of virology, 1986
Friend murine leukemia helper viruses (F-MuLV) 57 and B3 were indistinguishable by genomic structural analyses with RNase T1-resistant oligonucleotide fingerprinting and by antigenic reactivity with a panel of 31 monoclonal antibodies directed against murine leukemia viruses. Nevertheless, F-MuLV 57 and B3 had strikingly different virulences. Approximately 2 months after inoculation, IRW and NFS/N mice inoculated as newborns with F-MuLV 57 had gross splenomegaly caused by erythroid proliferation. In contrast, an equivalent dose of F-MuLV B3 induced spleen or lymph node enlargement 4 to 13 months after inoculation. Although most cases of spleen enlargement in F-MuLV B3-inoculated mice were due to erythroid proliferation, lymphoid or myeloid proliferation was also frequently observed. The replication of both F-MuLV 57 and B3 was equally efficient, and both viruses generated recombinant dual-tropic mink cell focus-forming (MCF) viruses with the same kinetics and efficiency. Moreover, M...
Journal of Virology, 1984
The pathogenic Friend virus complex is of considerable interest in that, although members of this group are genetically related, they differ markedly in biochemical and biological properties. Heteroduplex mapping of molecular clones of the Friend virus complex, which includes the replication-competent ecotropic Friend murine leukemia virus (F-MuLV) and mink cell focus-forming virus (F-MCF) and replication-defective polycythemia- and anemia-inducing strains of spleen focus-forming virus (SFFVp and SFFVa, respectively), was employed to provide insight into the molecular basis of their relationships. In heteroduplexes of F-MuLV X F-MCF, a major substitution of 0.89 kilobases in the env gene of F-MCF was discerned. Heteroduplexes of SFFVp X F-MuLV or F-MCF and SFFVa X F-MuLV or F-MCF showed several major deletions in the pol gene region and a single major deletion in the 3' half of the env gene region of SFFVp and SFFVa. A major substitution of 0.89 kilobases was mapped to the 5'...
Journal of Experimental Medicine, 1970
Proliferation and erythroid differentiation of transplanted DBA/2 marrow cells and Friend virus-induced leukemic cells were assessed in syngeneic, allogeneic (H-2 compatible), and (BALB/c x DBA/2)F1 hybrid mice (CDF1). Measurements were made 5 days after transplantation of donor cells into nonirradiated or X-irradiated mice by the spleen colony or the 125IUdR-59Fe uptake methods. Growth of DBA/2J (Jackson subline) marrow grafts was poor in irradiated CDF1J hybrids as compared with growth in syngeneic and allogeneic hosts. The DBA/2J transplants proliferated, however, without impairment in irradiated CDF1 hybrids which were the progeny of DBA/2 male parents of other sublines, e.g. DBA/2Ha, DBA/2Cr, and DBA/2Cum. In contrast, tissue-cultured Friend leukemic cells of DBA/2J origin grew deficiently in all CDF1 hybrids tested, regardless of irradiation and of the DBA/2 parent's subline. The growth pattern of transplanted DBA/2J cells was a manifestation of hybrid resistance. The resu...
Loss of pathogenicity of spleen focus-forming virus after pseudotyping with Akv
Journal of Virology, 1988
Friend virus complex (FV), which comprises replication-competent Friend murine leukemia virus (FMuLV) plus replication-defective spleen focus-forming virus (SFFV), induces a multistage erythroleukemia. We have examined the role of replication-competent helper virus in the early and late stages of FV disease by replacing FMuLV, the native helper, with Akv, the endogenous ecotropic MuLV of AKR mice. SFFVP/FRE, an established fibroblast line nonproductively infected with the polycythemic strain of SFFV, was superinfected with FMuLV or with Akv. Although supernatants from these cells showed similar titers in the XC plaque assay, supernatants from Akv-infected SFFVP/FRE cells showed 100- to 5,000-fold less activity than did those from FMuLV-infected cells with respect to spleen focus induction in vivo. Since virions isolated from these two supernatants contained similar ratios of SFFV to helper virus genomic RNA, it did not appear that the difference was due to a relative inability of Ak...
Journal of Experimental Medicine, 1980
Two distinct clones of Friend spleen focus-forming virus (SFFV), differing in their erythroleukemic potential, are described. These isolates have been cloned free of their associated helper viruses and shown to be replication-defective. Both SFFV isolates have been rescued from rat fibroblast nonproducer cell clones with cloned replication-competent viruses, F-MuLVA and F-MuLVP, obtained from the anemia- or polycythemia-inducing isolates of Friend virus complex, respectively. These rescued viruses induce a rapid proliferative disease associated with the appearance of macroscopic spleen foci and splenomegaly. In addition, each is subject to regulation by the W, Steel (Sl), and Fv-2 host gene loci. These two isolates of SFFV can, however, be distinguished by both biological and molecular criteria. Friend SFFVP induces a rapid polycythemia associated with the appearance of large numbers of erythropoietin (EPO)-independent erythroid colony-forming cells in the marrow and spleen. In cont...