scholarly journals Genetic Analysis of Gv1, a Gene Controlling Transcription of Endogenous Murine Polytropic Proviruses

1999 ◽  
Vol 73 (10) ◽  
pp. 8227-8234 ◽  
Author(s):  
Peter L. Oliver ◽  
Jonathan P. Stoye
Keyword(s):  
Genetic Analysis ◽  
Mouse Chromosome ◽  
Murine Leukemia Virus ◽  
Genetic Locus ◽  
Leukemia Virus ◽  
Protection Assay ◽  
Chromosome 13 ◽  
Nuclease Protection Assay ◽  
Genetic Techniques ◽  
Murine Leukemia

ABSTRACT Gv1 is a genetic locus that coordinately regulates the expression of multiple murine leukemia virus-related endogenous proviral sequences. A quantitative nuclease protection assay for typingGv1 inheritance has been developed. Use of this assay demonstrates that Gv1 controls transcription of polytropic but not of modified polytropic endogenous proviruses. A combination of genetic techniques were used to map Gv1; these analyses demonstrate that Gv1 lies approximately 37 centimorgans from the centromeric end of mouse chromosome 13.

scholarly journals Genetic Regulation of Long-Term Nonprogression in E-55+ Murine Leukemia Virus Infection in Mice

1999 ◽  
Vol 73 (11) ◽  
pp. 9232-9236
Author(s):  
Vily Panoutsakopoulou ◽  
Kathryn Hunter ◽  
Thomas G. Sieck ◽  
Elizabeth P. Blankenhorn ◽  
Kenneth J. Blank
Keyword(s):  
Bone Marrow ◽  
Murine Leukemia Virus ◽  
Genetic Locus ◽  
Leukemia Virus ◽  
Inbred Mouse ◽  
Major Histocompatibility Complex Gene ◽  
Mouse Strains ◽  
Term Survival ◽  
Murine Leukemia

ABSTRACT Certain inbred mouse strains display progression to lymphoma development after infection with E-55+ murine leukemia virus (E-55+ MuLV), while others demonstrate long-term nonprogression. This difference in disease progression occurs despite the fact that E-55+ MuLV causes persistent infection in both immunocompetent BALB/c–H-2k (BALB.K) progressor (P) and C57BL/10–H-2k (B10.BR) long-term nonprogressor (LTNP) mice. In contrast to immunocompetent mice, immunosuppressed mice from both P and LTNP strains develop lymphomas about 2 months after infection, indicating that the LTNP phenotype is determined by the immune response of the infected mouse. In this study, we used bone marrow chimeras to demonstrate that the LTNP phenotype is associated with the genotype of donor bone marrow and not the recipient microenvironment. In addition, we have mapped a genetic locus that may be responsible for the LTNP trait. Microsatellite-based linkage analysis demonstrated that a non-major histocompatibility complex gene on chromosome 15 regulates long-term survival and is located in the same region as the Rfv3 gene. Rfv3 is involved in recovery from Friend virus-induced leukemia and has been demonstrated to regulate neutralizing virus antibody titers. In our studies, however, both P and LTNP strains produce similar titers of neutralizing and cytotoxic anti-E-55+ MuLV. Therefore, while it is possible that Rfv3 influences the course of E-55+ MuLV infection, it is more likely that the LTNP phenotype in E-55+ MuLV-infected mice is regulated by a different, closely linked gene.

scholarly journals A MAJOR GENETIC LOCUS AFFECTING RESISTANCE TO INFECTION WITH MURINE LEUKEMIA VIRUSES

1973 ◽  
Vol 137 (3) ◽  
pp. 850-853 ◽  
Author(s):  
Wallace P. Rowe ◽  
James B. Humphrey ◽  
Frank Lilly
Keyword(s):  
Murine Leukemia Virus ◽  
Genetic Locus ◽  
Leukemia Virus ◽  
Chromosome 4 ◽  
Group Viii ◽  
Naturally Occurring ◽  
Mouse Cells ◽  
Resistance To Infection ◽  
Leukemia Viruses ◽  
Murine Leukemia

The Fv-1 gene, which regulates sensitivity of mouse cells to infection by naturally occurring host-range types of murine leukemia virus, was shown to be located on linkage group VIII (chromosome 4), 39 map units from b.

scholarly journals Mml1,a New Common Integration Site in Murine Leukemia Virus-Induced Promonocytic Leukemias Maps to Mouse Chromosome 10

Virology ◽  
1996 ◽  
Vol 224 (1) ◽  
pp. 224-234 ◽  
Author(s):  
Richard Koller ◽  
Marianne Krall ◽  
Beverly Mock ◽  
Juraj Bies ◽  
Viktor Nazarov ◽  
...  
Keyword(s):  
Mouse Chromosome ◽  
Murine Leukemia Virus ◽  
Integration Site ◽  
Leukemia Virus ◽  
Chromosome 10 ◽  
Murine Leukemia ◽  
Common Integration Site

scholarly journals Assignment of the receptor for ecotropic murine leukemia virus to mouse chromosome 5.

1978 ◽  
Vol 148 (2) ◽  
pp. 451-465 ◽  
Author(s):  
N H Ruddle ◽  
B S Conta ◽  
L Leinwand ◽  
C Kozak ◽  
F Ruddle ◽  
...  
Keyword(s):  
Mouse Chromosome ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Chinese Hamster ◽  
Receptor Expression ◽  
Chromosome 5 ◽  
Chinese Hamster Lung Fibroblast ◽  
Vesicular Stomatitis ◽  
Hypoxanthine Guanine Phosphoribosyltransferase ◽  
Murine Leukemia

The gene for the receptor for ecotropic murine leukemia virus (Rev) has been assigned to mouse chromosome 5. This determination was made possible by an analysis of somatic cell hybrids between mouse and Chinese hamster cells. The parents of these hybrids were A/HeJ or Mus poschiavinus peritoneal exudate cells or BALB/c primary embryo fibroblasts and E36, a Chinese hamster lung fibroblast deficient in hypoxanthine guanine phosphoribosyltransferase. Segregation of mouse chromosomes in these hybrids was analyzed by chromosome banding and isozyme expression. Cells were tested for their ability to absorb and replicate vesicular stomatitis virus (murine leukemia virus [MuLV]) pseudotype particles and ecotropic MuLV as measured by the XC test. The presence of chromosome 5 was essential for receptor expression as determined by three statistical procedures. Segregation of the receptor for ecotropic murine leukemia virus was also followed in two series of subclones. In both, receptor expression was syntenic with phosphoglucomutase-1, an isozyme which has been mapped to mouse chromosome 5.

Recent Studies on a Murine Leukemia Virus Grown in Tissue Culture

1967 ◽  
Vol 25 ◽  
pp. 106-107
Author(s):  
L. Z. de Tkaczevski ◽  
E. de Harven ◽  
C. Friend
Keyword(s):  
Tissue Culture ◽  
Solid Tumors ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Supernatant Fluid ◽  
Virus Particles ◽  
Friend Leukemia ◽  
Type C ◽  
Leukemia Viruses ◽  
Murine Leukemia

Despite extensive studies, the correlation between the morphology and pathogenicity of murine leukemia viruses (MLV) has not yet been clarified. The virus particles found in the plasma of leukemic mice belong to 2 distinct groups, 1 or 2% of them being enveloped A particles and the vast majority being of type C. It is generally believed that these 2 types of particles represent different phases in the development of the same virus. Particles of type A have been thought to be an earlier form of type C particles. One of the tissue culture lines established from Friend leukemia solid tumors has provided the material for the present study. The supernatant fluid of the line designated C-1A contains an almost pure population of A particles as illustrated in Figure 1. The ratio is, therefore, the reverse of what is unvariably observed in the plasma of leukemic mice where C particles predominate.

Immunoferritin Labelling of Murine Leukemia Virus Antigens in thin Sections

1980 ◽  
Vol 38 ◽  
pp. 508-509
Author(s):  
Ray A. Weigand ◽  
Gregory C. Varjabedian
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Intracellular Localization ◽  
Uranyl Acetate ◽  
Antibody Technique ◽  
Thin Sections ◽  
Tumor Virus ◽  
Labelling Procedure ◽  
Unlabelled Antibody ◽  
Murine Leukemia

We previously described the intracellular localization of murine mammary tumor virus (MuMTV) p28 protein in thin sections (1). In that study, MuMTV containing cells fixed in 3% paraformaldehyde plus 0.05% glutaraldehyde were labelled after thin sectioning using ferritin-antiferritin in an unlabelled antibody technique. We now describe the labelling of murine leukemia virus (MuLV) particles using the unlabelled antibody technique coupled to ferritin-Fab antiferritin. Cultures of R-MuLV in NIH/3T3 cells were grown to 90% confluence (2), fixed with 2% paraformaldehyde plus 0.5% glutaraldehyde in 0.1 M cacodylate at pH 7.2, postfixed with buffered 17 OsO4, dehydrated with a series of etha-nols, and embedded in Epon. Thin sections were collected on nickel grids, incubated in 107 H2O2, rinsed in HEPES buffered saline, and subjected to the immunoferritin labelling procedure. The procedure included preincubation in 27 egg albumin, a four hour incubation in goat antisera against purified gp69/71 of MuLV (3) (primary antibody), incubation in F(ab’)2 fragments of rabbit antisera to goat IgG (secondary antibody), incubation in apoferritin, incubation in ferritin-Fab ferritin, and a brief fixation with 2% glutaraldehyde. The sections were stained with uranyl acetate and examined in a Siemens IA electron microscope at an accelerating voltage of 60 KV.

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