scholarly journals Mus cervicolor Murine Leukemia Virus Isolate M813 Belongs to a Unique Receptor Interference Group

2001 ◽  
Vol 75 (10) ◽  
pp. 4490-4498 ◽  
Author(s):  
Vladimir Prassolov ◽  
Sibyll Hein ◽  
Marion Ziegler ◽  
Dmitry Ivanov ◽  
Carsten Münk ◽  
...  
Keyword(s):  
Host Range ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Cell Entry ◽  
Chromosome 2 ◽  
Coding Region ◽  
Common Receptor ◽  
Type C ◽  
Murine Leukemia ◽  
Receptor Interference

ABSTRACT Murine leukemia virus (MuLV) M813 was originally isolated from the Southeast Asian rodent Mus cervicolor. As with the ecotropic MuLVs derived from Mus musculus, its host range is limited to rodent cells. Earlier studies have mapped its receptor to chromosome 2, but it has not been established whether M813 shares a common receptor with any other MuLVs. In this study, we have performed interference assays with M813 and viruses from four interference groups of MuLV. The infection efficiency of M813 was not compromised in cells expressing any one of the other MuLVs, demonstrating that M813 must use a distinct receptor for cell entry. The entire M813 env coding region was molecularly cloned. Sequence analysis revealed high similarity with other MuLVs but with a unique receptor-binding domain. Substitution of M813env sequences in Moloney MuLV resulted in a replication-competent virus with a host range and interference profile similar to those of the biological clone M813. M813 thus defines a novel receptor interference group of type C MuLVs.

scholarly journals Sodium-Dependent myo-Inositol Transporter 1 Is a Cellular Receptor for Mus cervicolor M813 Murine Leukemia Virus

2003 ◽  
Vol 77 (10) ◽  
pp. 5926-5932 ◽  
Author(s):  
Sibyll Hein ◽  
Vladimir Prassolov ◽  
Yuanming Zhang ◽  
Dmitry Ivanov ◽  
Jürgen Löhler ◽  
...  
Keyword(s):  
Host Range ◽  
Conformational Changes ◽  
Murine Leukemia Virus ◽  
Molecular Mechanisms ◽  
Leukemia Virus ◽  
Receptor Gene ◽  
Viral Envelope ◽  
Cell Entry ◽  
Sodium Dependent ◽  
Murine Leukemia

ABSTRACT Retrovirus infection is initiated by binding of the surface (SU) portion of the viral envelope glycoprotein (Env) to specific receptors on cells. This binding triggers conformational changes in the transmembrane portion of Env, leading to membrane fusion and cell entry, and is thus a major determinant of retrovirus tissue and species tropism. The M813 murine leukemia virus (MuLV) is a highly fusogenic gammaretrovirus, isolated from Mus cervicolor, whose host range is limited to mouse cells. To delineate the molecular mechanisms of its restricted host range and its high fusogenic potential, we initiated studies to characterize the cell surface protein that mediates M813 infection. Screening of the T31 mouse-hamster radiation hybrid panel for M813 infectivity localized the receptor gene to the distal end of mouse chromosome 16. Expression of one of the likely candidate genes (slc5a3) within this region in human cells conferred susceptibility to both M813 infection and M813-induced fusogenicity. slc5a3 encodes sodium myo-inositol transporter 1 (SMIT1), thus adding another sodium-dependent transporter to the growing list of proteins used by MuLVs for cell entry. Characterization of SMIT1 orthologues in different species identified several amino acid variations within two extracellular loops that may restrict susceptibility to M813 infection.

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 Pseudotype Formation of Moloney Murine Leukemia Virus with Sendai Virus Glycoprotein F

1998 ◽  
Vol 72 (6) ◽  
pp. 5296-5302 ◽  
Author(s):  
Martin Spiegel ◽  
Michael Bitzer ◽  
Andrea Schenk ◽  
Heidi Rossmann ◽  
Wolfgang J. Neubert ◽  
...  
Keyword(s):  
Host Range ◽  
Murine Leukemia Virus ◽  
Sendai Virus ◽  
Mdck Cells ◽  
Leukemia Virus ◽  
Direct Proof ◽  
Hepatoma Cells ◽  
The Other ◽  
Moloney Murine Leukemia Virus ◽  
Murine Leukemia

ABSTRACT Mixed infection of cells with both Moloney murine leukemia virus (MoMLV) and related or heterologous viruses produces progeny pseudotype virions bearing the MoMLV genome encapsulated by the envelope of the other virus. In this study, pseudotype formation between MoMLV and the prototype parainfluenza virus Sendai virus (SV) was investigated. We report for the first time that SV infection of MoMLV producer cells results in the formation of MoMLV(SV) pseudotypes, which display a largely extended host range compared to that of MoMLV particles. This could be associated with SV hemagglutinin-neuraminidase (SV-HN) glycoprotein incorporation into MoMLV envelopes. In contrast, solitary incorporation of the other SV glycoprotein, SV fusion protein (SV-F), resulted in a distinct and narrow extension of the MoMLV host range to asialoglycoprotein receptor (ASGP-R)-positive cells (e.g., cultured human hepatoma cells). Since stably ASGP-R cDNA-transfected MDCK cells, but not parental ASGP-R-negative MDCK cells, were found to be transduced by MoMLV(SV-F) pseudotypes and transduction of ASGP-R-expressing cells was found to be inhibited by ASGP-R antiserum, a direct proof for the ASGP-R-restricted tropism of MoMLV(SV-F) pseudotypes was provided. Cultivation of ASGP-R-positive HepG2 hepatoma cells on Transwell-COL membranes led to a significant enhancement of MoMLV(SV-F) titers in subsequent flowthrough transduction experiments, thereby suggesting the importance of ASGP-R accessibility at the basolateral domain for MoMLV(SV-F) pseudotype transduction. The availability of such ASGP-R-restricted MoMLV(SV-F)-pseudotyped vectors opens up new perspectives for future liver-restricted therapeutic gene transfer applications.

Host range conversion of murine leukemia virus resulting from recombination with endogenous virus

1997 ◽  
Vol 142 (1) ◽  
pp. 139-149 ◽  
Author(s):  
A. Kawana ◽  
A. Iwamoto ◽  
T. Odawara ◽  
H. Yoshikura
Keyword(s):  
Host Range ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Endogenous Virus ◽  
Murine Leukemia

scholarly journals Novel Host Range and Cytopathic Variant of Ecotropic Friend Murine Leukemia Virus

2004 ◽  
Vol 78 (22) ◽  
pp. 12189-12197 ◽  
Author(s):  
Yong Tae Jung ◽  
Tiyun Wu ◽  
Christine A. Kozak
Keyword(s):  
Host Range ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Syncytium Formation ◽  
Single Amino Acid ◽  
Receptor Binding Site ◽  
Mus Spicilegus ◽  
Novel Variant ◽  
Novel Host ◽  
Murine Leukemia

ABSTRACT A variant ecotropic Friend murine leukemia virus, F-S MLV, is capable of inducing the formation of large multinucleated syncytia in Mus dunni cells. This cytopathicity resembles that of Spl574 MLV, a novel variant recently isolated from the spleen of a Mus spicilegus mouse neonatally inoculated with Moloney MLV. F-S MLV is an N-tropic Friend MLV that also has the unusual ability to infect hamster cells, which are normally resistant to mouse ecotropic MLVs. Syncytium induction by both F-S MLV and Spl574 is accompanied by the accumulation of large amounts of unintegrated viral DNA, a hallmark of pathogenic retroviruses, but not previously reported for mouse ecotropic gammaretroviruses. Sequencing and site-specific mutagenesis determined that the syncytium-inducing phenotype of F-S MLV can be attributed to a single amino acid substitution (S84A) in the VRA region of the viral env gene. This site corresponds to that of the single substitution previously shown to be responsible for the cytopathicity of Spl574, S82F. The S84A substitution in F-S MLV also contributes to the ability of this virus to infect hamster cells, but Spl574 MLV is unable to infect hamster cells. Because this serine residue is one of the critical amino acids that form the CAT-1 receptor binding site, and because M. dunni and hamster cells have variant CAT-1 receptors, these results suggest that syncytium formation as well as altered host range may be a consequence of altered interaction between virus and receptor.

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