Disease relevance of Friend murine leukemia virus

• Erythroleukemia induction by Friend murine leukemia virus: insertional activation of a new member of the ets gene family, Fli-1, closely linked to c-ets-1 [1].
• Leukemic cells from all human chronic granulocytic leukemia (CGL) and some acute myelomonocytic leukemia (AMML) donors are lysed by rabbit antisera to a purified glycoprotein of Friend murine leukemia virus (FLV gp71) in a microcytotoxicity assay [2].
• Two new amino acid derivatives with the fluorene substituent, when administered ip to female inbred ICR-CD1 mice inoculated with Friend murine leukemia virus, significantly inhibited virus-induced splenomegaly, reduced viable virus titers in spleen and plasma, and significantly prolonged survival time [3].
• Identification of a non-H-2 gene (Rfv-3) influencing recovery from viremia and leukemia induced by Friend virus complex [4].
• Among these are the Friend virus susceptibility factor 1/lentivirus susceptibility factor 1/restriction factor 1 (Ref1) class of restriction factors, which block infection by targeting the capsids of diverse retroviruses [5].

High impact information on Friend murine leukemia virus

• By sequencing the envelope gene of a biologically active MPLV clone, we found that this region comprises a novel oncogene named v-mpl in phase with two parts of the Friend murine leukemia virus envelope gene [6].
• Rearrangements of the cellular p53 gene in erythroleukaemic cells transformed by Friend virus [7].
• The structure of the receptor-binding domain of the envelope glycoprotein from Friend murine leukemia virus was determined to 2.0 angstrom resolution by x-ray crystallography [8].
• This influence of the H-2I region on T cell recognition of the envelope glycoprotein appeared to control in vivo induction of protective immunity against Friend virus complex after immunization with the vaccinia-F-MuLV env vaccine [9].
• H-2D control of recovery from Friend virus leukemia: H-2D region influences the kinetics of the T lymphocyte response to Friend virus [10].

Chemical compound and disease context of Friend murine leukemia virus

• Studies on the role of the host immune response in recovery from Friend virus leukemia. I. Antiviral and antileukemia cell antibodies [11].
• The Friend erythroleukemia cell line T3-C12, which produces Friend murine leukemia virus (F-MuLV) and can be induced to synthesize hemoglobin by dimethyl sulfoxide (DMSO), was monitored for viral RNA-dependent DNA polymerase reverse transcriptase (RT) activity [12].
• Target cell of the polycythemia-inducing Friend virus: studies with myleran [13].
• Stimulation with bacterial lipopolysaccharide (LPS) of splenic B-lymphocytes infected in vitro with Friend virus complex increased the number of cells with replicating murine leukemia virus (MuLV) [i.e., infectious centers (IC)] up to 100-fold [14].
• Chromatin proteins from erythroleukemia cells transformed by Friend virus were analyzed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis [15].

Biological context of Friend murine leukemia virus

• Fv-4: gene controlling resistance to NB-tropic Friend murine leukemia virus. Distribution in wild mice, introduction into genetic background of BALB/c mice, and mapping of chromosomes [16].
• We investigated the ability of the U3 region of the long terminal repeats (LTR) of the Friend murine leukemia virus (Fr-MuLV) and Moloney murine leukemia virus (Mo-MuLV) to promote transcription in a variety of human cell lines [17].
• Induction of erythroid differentiation by dimethylsulfoxide in cells infected with Friend virus: relationship to the cell cycle [18].
• The block to reverse transcription was overridden at multiplicity of infection >1 or by preincubation of the nonhuman primate cells with virus, a feature reminiscent of the Friend virus resistance gene-1 (FV-1), restriction to murine leukemia virus replication in mouse cells [19].
• We have reported that the insertion of an expressed selectable marker gene (driven by the Friend virus enhancer/promoter) into the LCR disrupts the LCR-mediated regulation of globin transcription [20].

Anatomical context of Friend murine leukemia virus

• H-2D (Rfv-1) gene influence on recovery from Friend virus leukemia is mediated by nonleukemic cells of the spleen and bone marrow [21].
• The function of Cip/Kip proteins p21(Cip1) and p27(Kip1) during erythropoietin-induced terminal differentiation of primary erythroblasts isolated from the spleens of mice infected with the anemia-inducing strain of Friend virus was investigated [22].
• The anemic Friend virus gp55 envelope protein induces erythroid differentiation in fetal liver colony-forming units-erythroid [23].
• The structure of the erythropoietin receptor has been identified in this laboratory as two proteins of 100 and 85 kDa by cross-linking 125I-erythropoietin (125I-EP) to the surface of erythroid cells purified from the spleens of mice infected with the anemia strain of Friend virus [24].
• Identification of a protective CD4+ T-cell epitope in p15gag of Friend murine leukemia virus and role of the MA protein targeting the plasma membrane in immunogenicity [25].

Gene context of Friend murine leukemia virus

• These results suggest that Friend virus activates both sf-STK and the EPOR to cause deregulated erythroid proliferation and differentiation [26].
• This observation, coupled with earlier work, suggested that Sf-Stk drives the expansion of infected cells by forming a complex with the Friend virus envelope glycoprotein, gp55, and the erythropoietin receptor [27].
• Abnormal erythropoietin (EPO)-independent cell growth is induced after infection of erythroid progenitor cells with a polycythemic strain of Friend virus (FVp) [28].
• Introduction of a mutation that results in failure to bind Grb2 abrogates the ability of Sf-Stk to induce colonies in response to Friend virus, while the Grb2 binding site from EGFR restores this response [29].
• Taken together, these data indicate that a Sf-Stk/Grb2/Gab2 complex mediates the growth of primary erythroid progenitor cells in response to Friend virus [30].

Analytical, diagnostic and therapeutic context of Friend murine leukemia virus

• The specificity of a single rabbit antiserum pool raised against the purified major glycoprotein, gp71, of Friend murine leukemia virus was determined for a variety of virus-producing mouse, feline, and gibbon ape cell lines by viable cell membrane immunofluorescence absorption [31].
• The oligomeric structure of the Friend murine leukemia virus envelope glycoprotein has been investigated using crosslinking reagents and sucrose density gradient centrifugation [32].
• CBA/J mice receiving multiple injections of sodium caseinate (CAS) or bovine serum albumin (BSA) were assayed for marrow dependent functions by measuring their ability (i) to reject bone marrow allografts and (ii) to resist Friend virus (FV)-induced suppression of lymphocyte mitogenesis [33].
• The sugar composition of the surface glycoprotein from Friend murine leukemia virus was determined by gas-liquid chromatography of the alditol acetates and by the thiobarbituric acid method, respectively [34].

References