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Title: Determination of the minimal fusion peptide of bovine leukemia virus gp30

Abstract

In this study, we determined the minimal N-terminal fusion peptide of the gp30 of the bovine leukemia virus on the basis of the tilted peptide theory. We first used molecular modelling to predict that the gp30 minimal fusion peptide corresponds to the 15 first residues. Liposome lipid-mixing and leakage assays confirmed that the 15-residue long peptide induces fusion in vitro and that it is the shortest peptide inducing optimal fusion since longer peptides destabilize liposomes to the same extent but not shorter ones. The 15-residue long peptide can thus be considered as the minimal fusion peptide. The effect of mutations reported in the literature was also investigated. Interestingly, mutations related to glycoproteins unable to induce syncytia in cell-cell fusion assays correspond to peptides predicted as non-tilted. The relationship between obliquity and fusogenicity was also confirmed in vitro for one tilted and one non-tilted mutant peptide.

Authors:
 [1];  [1];  [2];  [3];  [1]
  1. Centre de Biophysique Moleculaire Numerique, Faculte Universitaire des Sciences Agronomiques, 2 Passage des deportes, B-5030 Gembloux (Belgium)
  2. Ludwig Institute for Cancer Research-Brussels Branch, 74 Avenue Hippocrate, B-1200 Brussels (Belgium)
  3. Centre de Biophysique Moleculaire Numerique, Faculte Universitaire des Sciences Agronomiques, 2 Passage des deportes, B-5030 Gembloux (Belgium). E-mail: brasseur.r@fsagx.ac.be
Publication Date:
OSTI Identifier:
20979875
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 355; Journal Issue: 3; Other Information: DOI: 10.1016/j.bbrc.2007.01.182; PII: S0006-291X(07)00258-6; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ABSORPTION SPECTROSCOPY; AIDS VIRUS; CATTLE; CELL MEMBRANES; FOURIER TRANSFORMATION; GLYCOPROTEINS; IN VITRO; INFRARED SPECTRA; LEUKEMIA VIRUSES; LIPIDS; LIPOSOMES; MUTANTS; MUTATIONS; PEPTIDES; SIMULATION

Citation Formats

Lorin, Aurelien, Lins, Laurence, Stroobant, Vincent, Brasseur, Robert, and Charloteaux, Benoit. Determination of the minimal fusion peptide of bovine leukemia virus gp30. United States: N. p., 2007. Web. doi:10.1016/j.bbrc.2007.01.182.
Lorin, Aurelien, Lins, Laurence, Stroobant, Vincent, Brasseur, Robert, & Charloteaux, Benoit. Determination of the minimal fusion peptide of bovine leukemia virus gp30. United States. doi:10.1016/j.bbrc.2007.01.182.
Lorin, Aurelien, Lins, Laurence, Stroobant, Vincent, Brasseur, Robert, and Charloteaux, Benoit. Fri . "Determination of the minimal fusion peptide of bovine leukemia virus gp30". United States. doi:10.1016/j.bbrc.2007.01.182.
@article{osti_20979875,
title = {Determination of the minimal fusion peptide of bovine leukemia virus gp30},
author = {Lorin, Aurelien and Lins, Laurence and Stroobant, Vincent and Brasseur, Robert and Charloteaux, Benoit},
abstractNote = {In this study, we determined the minimal N-terminal fusion peptide of the gp30 of the bovine leukemia virus on the basis of the tilted peptide theory. We first used molecular modelling to predict that the gp30 minimal fusion peptide corresponds to the 15 first residues. Liposome lipid-mixing and leakage assays confirmed that the 15-residue long peptide induces fusion in vitro and that it is the shortest peptide inducing optimal fusion since longer peptides destabilize liposomes to the same extent but not shorter ones. The 15-residue long peptide can thus be considered as the minimal fusion peptide. The effect of mutations reported in the literature was also investigated. Interestingly, mutations related to glycoproteins unable to induce syncytia in cell-cell fusion assays correspond to peptides predicted as non-tilted. The relationship between obliquity and fusogenicity was also confirmed in vitro for one tilted and one non-tilted mutant peptide.},
doi = {10.1016/j.bbrc.2007.01.182},
journal = {Biochemical and Biophysical Research Communications},
number = 3,
volume = 355,
place = {United States},
year = {Fri Apr 13 00:00:00 EDT 2007},
month = {Fri Apr 13 00:00:00 EDT 2007}
}
  • Bovine leukemia virus (BLV) is the causative agent of enzootic bovine lymphosarcoma. Much speculation continues to be directed at the role of BLV in human leukemia. To test this hypothesis rigorously, a case-control study of childhood acute lymphoblastic leukemia and non-Hodgkin's lymphoma was conducted between December 1983 and February 1986. Cases (less than or equal to 16 years at diagnosis) derived from patients diagnosed at the primary institutions and affiliated hospitals were matched (age, sex, and race) with regional population controls. DNA samples from bone marrow or peripheral blood from 157 cases (131 acute lymphoblastic leukemia, 26 non-Hodgkin's lymphoma) andmore » peripheral blood from 136 controls were analyzed by Southern blot technique, under highly stringent conditions, using cloned BLV DNA as a probe. None of the 157 case or 136 control DNA samples hybridized with the probe. The high statistical power and specificity of this study provide the best evidence to date that genomic integration of BLV is not a factor in childhood acute lymphoblastic leukemia/non-Hodgkin's lymphoma.« less
  • Bovine peripheral blood lymphocytes from a cow with persistent lymphocytosis were separated on nylon wool columns into nylon-adherent and nonadherent populations. Nylon-adherent cells were highly enriched for surface immunoglobulin (SIg) bearing B lymphocytes (95.5%) and nonadherent cells for SIg negative non-B cells, presumably T lymphocytes (96.3%). The B lymphocytes were found to be the major producers for bovine leukemia virus. A total of 39% of the B-enriched cells, surviving after 72 hours in culture, produced bovine leukemia virus as compared with 0.5% of the non-B cells.
  • A microculture syncytia assay for the detection of bovine leukemia virus (BLV) has been described and compared with the conventional macroculture assay. The microculture assay required fewer indicator cells, was as sensitive as the macroculture assay and provided a reproducible test for the detection and titration of BLV.
  • Peripheral blood lymphocytes from 3 cows with persistent lymphocytosis were separated on nylon wool columns into nylon wool-adherent and nonadherent populations. The percentage of cells coated with surface immunoglobulin (B-cells) and the frequency of lymphocytic nuclear pockets in each subpopulation were then determined. In each case the adherent population consisted predominantly of B-cells with an increased nuclear pocket frequency, whereas the nonadherent cells were 98.99% negative for surface immunoglobulin (non-B-cells) and contained essentially no nuclear pockets. These findings provided additional evidence that the B-subpopulation of cells was highly involved in bovine leukemia oncogenesis.
  • Previously, we found an up-regulation of tumor necrosis factor alpha (TNF)-{alpha} and an imbalance of TNF receptors in sheep experimentally infected with bovine leukemia virus (BLV). In order to investigate the different TNF-{alpha}-induced responses, in this study we examined the TNF-{alpha}-induced proliferative response and the expression levels of two distinct TNF receptors on peripheral blood mononuclear cells (PBMC) derived from BLV-uninfected cattle and BLV-infected cattle that were aleukemic (AL) or had persistent lymphocytosis (PL). The proliferative response of PBMC isolated from those cattle with PL in the presence of recombinant bovine TNF-{alpha} (rTNF-{alpha}) was significantly higher than those from ALmore » cattle and uninfected cattle and the cells from PL cattle expressed significantly higher mRNA levels of TNF receptor type II (TNF-RII) than those from AL and BLV-uninfected cattle. No difference was found in TNF-RI mRNA levels. Most cells expressing TNF-RII in PL cattle were CD5{sup +} or sIgM{sup +} cells and these cells showed resistance to TNF-{alpha}-induced apoptosis. Additionally, there were significant positive correlations between the changes in provirus load and TNF-RII mRNA levels, and TNF-{alpha}-induced proliferation and TNF-RII mRNA levels. These data suggest that imbalance in the expression of TNF receptors could at least in part contribute to the progression of lymphocytosis in BLV infection.« less