Disease relevance of Emv2

• MelARV probably emerged as a result of recombination between Emv-2 and an endogenous nonecotropic provirus [1].
• Loss of Fv-1 restriction in Balb/3T3 cells following infection with a single N tropic murine leukemia virus particle [2].
• The subject of this study was to test whether in vivo thymocytes in the preleukemic and leukemic periods also bear receptors specific for N-tropic, recombinant MCF and SL AKR retroviruses [3].
• The pseudotype prepared with MuLV-RF or another NB-tropic MuLV-F, but not the virus obtained by rescue with N-tropic MuLV-F, induced erythroleukemia that spontaneously regressed [4].
• After infecting these mice with N-tropic FV complex, we followed the replication of spleen focus-forming virus (SFFV) and the generation of SFFV-transformed tumor colony-forming cells (CFC) in their spleens [5].

High impact information on Emv2

• Examination of hybrids of BALB/c and of B6 with other strains indicates that strains related in pedigree to BALB/c carry Inc-1, whereas those related to B6 carry Inb-1 [6].
• AKR mice regularly begin expressing N-tropic retroviruses (as assayed on NIH fibroblasts by the XC plaque assay) in several tissues early in life; thymic lymphocytes also express these viruses, but are not autonomously transformed [3].
• The resulting dose-response curves indicate that productive infection of a single Balb/3T3 cell with N tropic MSV requires co-infection with two MuLV particles [2].
• These observations suggested that neuropathogenic strains of LDV elicit the disease only in those strains of mice that carry multiple copies of N-tropic C-type retroviruses in their genomes and that are permissive for retrovirus replication [7].
• Previously, we identified two genes, termed Inc-1 and Inb-1, that interact to enhance ecotropic murine leukemia virus induction in low virus strains of mice [8].

Chemical compound and disease context of Emv2

• Induction of B-tropic and N-tropic murine leukemia virus from B10.BR/SgLi mouse embryo cell lines by 5-iodo-2'-deoxyuridine [9].
• N-tropic endogenous murine retrovirus of C type with buoyant density in the saccharose density gradient of 1.18 g/cm3 and a reverse transcriptase activity was expressed in the transformed cells [10].

Biological context of Emv2

• Here, we show that mice related to BALB/c in origin, i.e., A, C3H/He, and SEC, have an Inc-1 locus that is allelic with that of BALB/c. The C57BR mouse strain has an Inb-1 locus that is allelic with that of B6, located on chromosome 8, 30 cM from Es-1 [8].
• Our data show that MelARV has a typical full-length retroviral genome with high homology (98.54%) to Emv-2, indicating a close relationship between both viruses [1].
• Southern analysis and hybridization with an ecotropic MuLV DNA-specific probe showed that DNA of normal BXH-2 tissues contained both parental N-tropic MuLV proviruses but lacked endogenous B-tropic MuLV DNA sequences [11].
• In C58 and AKR mice, endogenous N-tropic, ecotropic murine leukemia virus (MuLV) proviruses become activated in rare cells during embryogenesis [12].
• By typing thymocytes of Fv-1-congenic mice for Ec+ gp70 was found that manifestation of the Ec+ gp70 phenotype requires the Fv-1n allele, which is permissive for replication of N-tropic virus produced by AKR and other virus-producing mouse strains [13].

Anatomical context of Emv2

• DNA dose-response studies in NIH-3T3 cells revealed a one-hit mechanism for both the [B-tropic MuLV]SC-1 cell DNA and the [N-tropic MuLV]SC-1 cell DNA preparation [14].
• C57BL/6 (B6) mice injected with B- or NB-fibrotropic clones, but not with TV or N-tropic viral clones, developed reactive T lymphocytes (Tr), capable of differentiating into anti-tumor cytotoxic cells [15].

Associations of Emv2 with chemical compounds

• However, a pre-adipocyte line established following simultaneous exposure to retinoic acid and 5-azacytidine showed strong restriction of both B-tropic and endogenous N-tropic MuLV [16].

Other interactions of Emv2

• Mice related to BALB/c in origin carry a locus termed Inc-1, whereas mice related to B6 carry an Inb-1 locus [8].
• The relationship between Myls, expansion of Mac1+/GR1+ cells, and Emv2 was investigated [17].
• Analysis of the segregation patterns closely linked Agt to Aprt and Emv-2, which places the angiotensinogen locus on the distal end of mouse Chr 8 [18].
• Efficiency of transfection for all DNAs was better in the NIH-3T3 cells than in C57BL/6 or SV-A31 cells; and an [N-tropic MuLV]SC-1 cell DNA preparation was slightly more infectious than a [B-tropic MuLV]SC-1 cell DNA preparation in all three cell cultures, regardless of their Fv-1 genotypes [14].
• Nucleotide sequences of gag-pol regions that determine the Fv-1 host range property of BALB/c N-tropic and B-tropic murine leukemia viruses [19].

Analytical, diagnostic and therapeutic context of Emv2

• It seems probable that a requirement for abrogation of Fv-1b restriction by a single infectious particle of N tropic MuLV, which does not itself replicate, is responsible for the two-hit dose-response relationship observed in infectivity titrations of N tropic MuLV in Balb/3T3 cells [2].
• Fv-1 determinants in xenotropic murine leukemia viruses studied with biological assay systems: Isolation of xenotropic virus with N-tropic Fv-1 activity in the cryptic form [20].
• A type-specific radioimmunoassay for p30 was developed which uniformly discriminated all B-tropic viruses from N-tropic viruses of BALB/c origin [21].
• Sequence analysis and site-specific mutagenesis of N-tropic MLVs identified a single amino acid difference responsible for this restriction that is distinct from the site that governs N or B tropism [22].
• Molecular cloning of B- and N-tropic endogenous BALB/c murine leukemia virus circular DNA intermediates: isolation and characterization of infectious recombinant clones [23].

References