References of "Rentier, Bernard"
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See detailParticipation in antibody dependent lymphocyte cytotoxicity of Fc bearing T lymphocytes
Wallen, W. C.; Rentier, Bernard ULg; Traub, R. G.

in Abstracts of the Annual Meeting of the American Society for Microbiology (1979)

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See detailElectron microscopic study of measles virus infection: unusual antibody-triggered redistribution of antigens on giant cells
Hooghe-Peters, Elisabeth L.; Rentier, Bernard ULg; Dubois-Dalcq, Monique

in Journal of Virology (1979), 29(2), 666-676

Vero cells infected with measles virus fuse to form multinucleated cells which incorporated virus- specific antigens in their membrane. The distribution of these antigens was analyzed after a brief ... [more ▼]

Vero cells infected with measles virus fuse to form multinucleated cells which incorporated virus- specific antigens in their membrane. The distribution of these antigens was analyzed after a brief treatment with human anti-measles immunoglobulin G, using autoradiography and immunoperoxidase labeling combined with transmission and scanning electron microscopy. Virus-specific antigens were distributed over the entire surface of giant cells treated at 4°C with human anti-measles immunoglobulin G and labeled Protein A. When cells were shifted to 37°C, labeled antigen-antibody complexes were redistributed in two stages. Patch formation occurred in 5 to 15 min. Later, antigen- antibody complexes became concentrated in a paracentral "ring" rather than typical caps. Patch formation occurred in the presence of metabolic inhibitors, whereas ring formation was inhibited by metabolic inhibitors. These rings contained membrane folds, villi, and viral buds, whereas the rest of the membrane was smooth. In addition, shedding, endocytosis of antigen-antibody complexes, and reexpression of antigens were observed. Antibodies to nonviral membrane antigens induced the same pattern of redistribution. Infected cells treated with anti-measles Fab' fragments maintained a homogeneous distribution of label throughout the experiments. In conclusion, intact immunoglobulins, but not Fab' fragments, were able to induce a dramatic redistribution of viral antigen on the membrane of giant cells infected with measles virus. [less ▲]

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See detailElectron microscopic study of measles virus infection: cell fusion and hemadsorption
Rentier, Bernard ULg; Hooghe-Peters, Elisabeth L.; Dubois-Dalcq, Monique

in Journal of Virology (1978), 28(2), 567-577

Virus-induced cell fusion has been studied after infection of Vero cells with measles virus. Scanning and transmission electron microscopy were combined with immunoperoxidase labeling of measles antigens ... [more ▼]

Virus-induced cell fusion has been studied after infection of Vero cells with measles virus. Scanning and transmission electron microscopy were combined with immunoperoxidase labeling of measles antigens to correlate viral production and distribution of virus-induced erythrocyte binding sites with progress of fusion-Release of infectious virus started before syncytia were detected and decreased while the number and size of syncytia were increasing. Most virions were seen budding from mononucleated cells or from the periphery of syncytia where cells were being recruited. Moving inward, the surfaces of syncytia were covered with numerous ridges containing viral antigen, but few viral buds were seen, suggesting that syncytia might be sites of defective viral formation. Hemadsorption occurred predominantly within the confines of syncytia. Erythrocytes were scattered sparsely over immature syncytia but were densely packed in the center of mature syncytia. Active binding sites for erythrocytes were located on cell villi and ridges covered with measles antigens. Hemadsorption was completely inhibited in measles virus-infected cultures pretreated with virus- specific immunoglobulin G for 1 h at 4°C. However, when these cultures were shifted to 37°C, hemadsorbing sites were recovered at the periphery of enlarging syncytia. Virus-induced sites for erythrocyte adsorption were found to move centripetally on syncytium membranes as fusion progressed. [less ▲]

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See detailStructural basis of hemadsorbing sites during the formation of syncytia in measles-infected cells
Rentier, Bernard ULg; Dubois-Dalcq, Monique

in Journal of Cell Biology (1977), 75

The surfaces of cells Infected with measles virus adsorb monkey red blood cells (RBC). In this study, the structure and localization of viral hemadsorbing (HAD) sites and their relationship with antigenic ... [more ▼]

The surfaces of cells Infected with measles virus adsorb monkey red blood cells (RBC). In this study, the structure and localization of viral hemadsorbing (HAD) sites and their relationship with antigenic sites and with cell fusion were investigated in measles virus infected Vero cells. Transmission and scanning electron microscopy were combined with immunolabeling, using human anti-measles IgG (Ab) and protein A from Staph, aureus coupled to peroxidase.. In the early syncytia (50-100 2 in diameter), HAD sites were clustered in the center but scattered at the periphery. In contrast, mature giant cells (400 to 500 2) had all HAD sites in the central area which displayed scattered villi. The periphery of the mature giant cells and the mononucleated cells did not hemadsorb but were covered with numerous villi. In the central area, RBC were firmly attached to villi and ridges over nucleocapsids but rarely to viral buds. Villi and ridges under the RBC were covered with antigenic sites which were not detected at the periphery of the mature syncytia. When living cells were treated with Ab at 4°C, complete inhibition of hemadsorption was only observed when RBC were applied to the cells in the cold. In other experiments, cells reacted with Ab at 4°C were washed, brought to 37°C and treated with RBC immediately or after 1-24 hrs. After 1-2 hrs, some HAD sites were present only at the periphery of immature giant cells, suggesting that RBC receptors had already emerged in membrane areas where fusion started again. After 24 hrs, the distribution of HAD and antigenic sites was the same as on cells not exposed to Ab. It seems that when fusion begins, HAD sites appeared on the periphery of the syncytia and then move spontaneously towards the center. With cessation of fusion, HAD sites disappear from the periphery of the giant cell. Receptors for RBC are closely associated with antigenic sites and correlated with viral induced fusion but not with virus production. [less ▲]

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See detailImpairment of the M-protein and unmasking of a superficial type-specific antigen by proteolytic treatment of influenza A virions with preservation of host-specific antigenicity
Reginster, Monique; Rentier, Bernard ULg; Dierickx, Louis

in Intervirology (1976), 6(4-5), 239-248

Influenza PR8 particles resulting from strong treatment with caseinase C are spikeless, devoid of neuraminidase and hemagglutinin 1 and 2 glycopeptides, and contain a Schiff-neg. polypeptide of about 13 ... [more ▼]

Influenza PR8 particles resulting from strong treatment with caseinase C are spikeless, devoid of neuraminidase and hemagglutinin 1 and 2 glycopeptides, and contain a Schiff-neg. polypeptide of about 13,000 mol. wt. which exists as traces in intact virions. Their M-protein polypeptide content is reduced to 50% of its original value, but there is no evidence of particle disruption nor of lipid release. They fix complement in the presence of both anti-M-protein and antiserum raised against a host polysaccharide. During exposure to caseinase C, an antigen is unmasked. It is type-specific and its identity with the M-protein is discussed [less ▲]

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See detailRecherches sur l'organisation de l'enveloppe des myxovirus
Rentier, Bernard ULg

Doctoral thesis (1976)

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See detailUnmasking of type-specific antigen on the outer face of the lipid layer of Influenza Virus
Rentier, Bernard ULg; Reginster, Monique

in Proceedings (1975)

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See detailOrganization of myxoviruses: structural basis of several biological properties of Newcastle Disease Virus
Rentier, Bernard ULg; Calberg-Bacq, C. M.; Reginster, Monique

in Proceedings (1973)

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See detailEffets de la caséinase C et de l'iturine sur le virus grippal Lee
Rentier, Bernard ULg

Master's dissertation (1970)

Treating influenza B virus (Lee strain) by proteases caseinase C and iturin in a soft action provokes the "shaving" of surface projections ("spikes"). It modifies the sedimentation speed of the particles ... [more ▼]

Treating influenza B virus (Lee strain) by proteases caseinase C and iturin in a soft action provokes the "shaving" of surface projections ("spikes"). It modifies the sedimentation speed of the particles and allows for antigenic exploration of the envelope below the spikes. [less ▲]

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