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 Properties of the Naturally Occurring Soluble Surface Glycoprotein of Ecotropic Murine Leukemia Virus: Binding Specificity and Possible Conformational Change after Binding to Receptor

2000 ◽  
Vol 74 (4) ◽  
pp. 1815-1826 ◽  
Author(s):  
Hidetoshi Ikeda ◽  
Kanako Kato ◽  
Takako Suzuki ◽  
Hiroshi Kitani ◽  
Yutaka Matsubara ◽  
...  
Keyword(s):  
Conformational Changes ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Surface Glycoprotein ◽  
Cell Surface Receptor ◽  
Dependent Manner ◽  
Temperature Dependent ◽  
Naturally Occurring ◽  
Mouse Cells ◽  
Murine Leukemia

ABSTRACT Ecotropic murine leukemia virus (MuLV) infection is initiated by the interaction between the surface glycoprotein (SU) of the virus and its cell-surface receptor mCAT-1. We investigated the SU-receptor interaction by using a naturally occurring soluble SU which was encoded by the envelope (env) gene of a defective endogenous MuLV, Fv-4r . Binding of the SU to mCAT-1-positive mouse cells was completed by 1 min at 37°C. The SU could not bind to mouse cells that were persistently infected by ecotropic MuLVs (but not amphotropic or dualtropic MuLVs) or transfected with wild-type ecotropic env genes or a mutantenv gene which can express only precursor Env protein that is restricted to retention in the endoplasmic reticulum. These cells were also resistant to superinfection by ecotropic MuLVs. Thus, superinfection resistance correlated with the lack of SU-binding capacity. After binding to the cells, the SU appeared to undergo some conformational changes within 1 min in a temperature-dependent manner. This was suggested by the different properties of two monoclonal antibodies (MAbs) reactive with the same C-terminal half of theFv-4r SU domain, including a proline-rich motif which was shown to be important for conformation of the SU and interaction between the SU and the transmembrane protein. One MAb reacting with the soluble SU bound to cells was dissociated by a temperature shift from 4 to 37°C. Such dissociation was not observed in cells synthesizing the SU or when another MAb was used, indicating that the dissociation was not due to a temperature-dependent release of the MAb but to possible conformational changes in the SU.

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.

scholarly journals Specificity studies on cytolytic T lymphocytes directed against murine leukemia virus-induced tumors. Analysis of monoclonal cytolytic T lymphocytes.

1982 ◽  
Vol 155 (4) ◽  
pp. 1050-1062 ◽  
Author(s):  
F Plata
Keyword(s):  
T Lymphocytes ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Target Cells ◽  
Cytolytic T Lymphocytes ◽  
Tumor Target ◽  
Induced Tumors ◽  
Definition Of ◽  
Leukemia Viruses ◽  
Murine Leukemia

The specificities of cloned cytolytic T lymphocytes (CTL) were studied for the analysis of CTL populations generated against murine leukemia viruses (MuLV) in H-2 congenic BALB/c (H-2d) and BALB.B (H-2b) mice. In particular, CTL generated in response to tumors induced by Gross MuLV and Friend MuLV were studied; these tumors expressed virus-induced antigens that do not cross-react and that can be distinguished from each other. The systematic study of 92 CTL clones clearly indicated that MuLV-immune CTL were highly heterogeneous with respect to both the intensities of target cell lysis that they mediated and to their specificity of recognition of MuLV-induced tumor target cells. Various categories of CTL clones were identified, ranging from CTL clones tht were tightly H-2 restricted and specific for the immunizing tumor to CTL clones that displayed no discernible patterns of specificity and that attacked a large number of different target cells. In addition, the surface markers of these cloned CTL were defined, and the best conditions for their prolonged maintenance in culture were determined. The present data indicate that future efforts in the definition of target antigens recognized by tumor-specific CTL should be performed with monoclonal lymphocytes.

scholarly journals Replacement of Murine Leukemia Virus Readthrough Mechanism by Human Immunodeficiency Virus Frameshift Allows Synthesis of Viral Proteins and Virus Replication

2003 ◽  
Vol 77 (5) ◽  
pp. 3345-3350 ◽  
Author(s):  
Marie-Noëlle Brunelle ◽  
Léa Brakier-Gingras ◽  
Guy Lemay
Keyword(s):  
Human Immunodeficiency Virus ◽  
Murine Leukemia Virus ◽  
Stop Codon ◽  
Leukemia Virus ◽  
Viral Proteins ◽  
Immunodeficiency Virus ◽  
Virus Model ◽  
Polyprotein Precursor ◽  
Leukemia Viruses ◽  
Murine Leukemia

ABSTRACT Retroviruses use unusual recoding strategies to synthesize the Gag-Pol polyprotein precursor of viral enzymes. In human immunodeficiency virus, ribosomes translating full-length viral RNA can shift back by 1 nucleotide at a specific site defined by the presence of both a slippery sequence and a downstream stimulatory element made of an extensive secondary structure. This so-called frameshift mechanism could become a target for the development of novel antiviral strategies. A different recoding strategy is used by other retroviruses, such as murine leukemia viruses, to synthesize the Gag-Pol precursor; in this case, a stop codon is suppressed in a readthrough process, again due to the presence of a specific structure adopted by the mRNA. Development of antiframeshift agents will greatly benefit from the availability of a simple animal and virus model. For this purpose, the murine leukemia virus readthrough region was rendered inactive by mutagenesis and the frameshift region of human immunodeficiency virus was inserted to generate a chimeric provirus. This substitution of readthrough by frameshift allows the synthesis of viral proteins, and the chimeric provirus sequence was found to generate infectious viruses. This system could be a most interesting alternative to study ribosomal frameshift in the context of a virus amenable to the use of a simple animal model.

scholarly journals Molecular cloning of infectious integrated murine leukemia virus DNA from infected mouse cells.

1980 ◽  
Vol 77 (1) ◽  
pp. 614-618 ◽  
Author(s):  
D. R. Lowy ◽  
E. Rands ◽  
S. K. Chattopadhyay ◽  
C. F. Garon ◽  
G. L. Hager
Keyword(s):  
Molecular Cloning ◽  
Infected Mouse ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Mouse Cells ◽  
Murine Leukemia

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 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.

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