Disease relevance of Bxv1

• Nonecotropic murine leukemia viruses in BALB/c and NFS/N mice: characterization of the BALB/c Bxv-1 provirus and the single NFS endogenous xenotrope [1].
• Recombinant murine leukemia viruses from the highly leukemic mouse strains AKR, HRS, and C58 usually acquire pathogenic U3 region sequences fro the endogenous xenotropic virus, Bxv-1 [2].
• The Bxv-1 provirus and its flanking sequences also contain the same restriction sites as the provirus thought to contribute U3 long terminal repeat sequences to leukemogenic (class I) AKR MCF viruses [1].
• This transactivation may explain why the CWM-T15 and Bxv-1 U3 regions accelerate the onset of lymphoid neoplasms and why related enhancer core region sequences are preferentially incorporated into the genomes of recombinant MuLVs and are found in other leukemogenic mammalian retroviruses [3].
• In addition, the U3 region of CWM-S-5X contained a viral enhancer sequence that was identical to that found in MCF 247, a recombinant AKR virus that is thought to contain the Bxv-1 enhancer [4].

High impact information on Bxv1

• Bxv-1 is induced mainly by BrdU and only marginally by mitogen; in contrast, Bdv-1 is induced by mitogen and BrdU has little effect [5].
• In addition, we confirm previous reports that xenotropic virus is controlled by a locus, Bxv-1, mapping to chromosome 1 [5].
• This locus, designated Bxv-1, mapped to the same site on chromosome 1 in all strains: Id-1-Pep-3-[Bxv-1-Lp] [6].
• Virus expression in mice with Bxv-1 was induced by treatment of fibroblasts with 5-iododeoxyuridine or by exposure of spleen cells to a B cell mitogen, bacterial lipopolysaccharide [6].
• The genomes of most recombinant murine leukemia viruses (MuLVs) inherit pathogenic U3 region sequences from the endogenous xenotropic provirus Bxv-1 [3].

Biological context of Bxv1

• Three of these substitutions are located immediately 3' of the enhancer core, and two form part of an E-box motif that is also found in the Bxv-1 sequence [3].
• Recombinant murine leukemia viruses (MuLVs) from high-leukemia-incidence mouse strains typically acquire pathogenic U3 region sequences from the genome of the endogenous xenotropic virus, Bxv-1 [7].
• Comparison of DNA sequences suggests that the pathogenicity of the CWD virus U3 region was related to a sequence motif that is shared with Bxv-1 and is recognized by the basic helix-loop-helix class of transcription factors [7].
• The data imply that Bxv-1- and Bdv-1-dependent virus production require DNA synthesis and cell proliferation and, at least for Bxv-1, B-cell differentiation [8].

Anatomical context of Bxv1

• Mitogen treatment of murine (BALB/c) B-cells induces two different endogenous retroviruses involving two unlinked, presumably proviral, loci Bxv-1 and Bdv-1 [8].

Other interactions of Bxv1

• Sxv is closely linked to, but distinct from Bxv-1, the major locus for induction of xenotropic murine leukemia viruses in laboratory mice [9].
• Unlike that of Bxv-1, the restriction map of Nfxv-1 does not resemble that of any known infectious xenotropic virus including xenotropic viruses isolated from NFS mice [1].
• After induction, hybrids with Bxv-1 produced only a transient burst of virus, whereas those with Akv-2 continued to produce virus for periods in excess of 3 months [10].
• A single locus for inducibility of xenotropic murine leukemia virus was mapped to chromosome 1 close to, but possibly not allelic to, Bxv-1 [11].
• We have found that the final leukemogenic (MCF) virus is a recombinant of three different endogenous parents; an ecotropic virus, a polytropic virus that directs the gp70 region of env, and a xenotropic virus (identified as the inducible element Bxv-1) that directs the LTR [12].

Analytical, diagnostic and therapeutic context of Bxv1

• Restriction enzyme analysis of a hybrid cell DNA that contains only the Bxv-1 xenotropic provirus showed that the Bxv-1 provirus contains restriction enzyme sites characteristic of the infectious virus induced from BALB/c fibroblasts [1].
• In Southern blot experiments, these proviruses hybridized to probes that were specific for the xenotropic envelope and Bxv-1 U3 region sequences [4].

References