References of "Vanderplasschen, Alain"
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See detailAttachment but Not Penetration of Bovine Herpesvirus 1 Is Necessary to Induce Apoptosis in Target Cells
Hanon, Emmanuel; Meyer, Gilles; Vanderplasschen, Alain ULg et al

in Journal of Virology (1998), 72(9), 7638-41

Bovine herpesvirus 1 (BHV-1) induces apoptotic cell death in bovine peripheral blood mononuclear cells and B-lymphoma cells. Using a BHV-1 glycoprotein H null mutant, we have demonstrated that although ... [more ▼]

Bovine herpesvirus 1 (BHV-1) induces apoptotic cell death in bovine peripheral blood mononuclear cells and B-lymphoma cells. Using a BHV-1 glycoprotein H null mutant, we have demonstrated that although penetration of BHV-1 is not required, attachment of BHV-1 viral particles is essential for the induction of apoptosis. [less ▲]

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See detailIntracellular and extracellular vaccinia virions enter cells by different mechanisms
Vanderplasschen, Alain ULg; Hollinshead, M.; Smith, G. L.

in Journal of General Virology (The) (1998), 79(Pt 4), 877-887

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See detailExtracellular enveloped vaccinia virus is resistant to complement because of incorporation of host complement control proteins into its envelope
Vanderplasschen, Alain ULg; Mathew, E.; Hollinshead, M. et al

in Proceedings of the National Academy of Sciences of the United States of America (1998), 95

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See detailExtracellular enveloped vaccinia virus. Entry, egress, and evasion
Smith, G. L.; Vanderplasschen, Alain ULg

in Advances in Experimental Medicine and Biology (1998), 440

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See detailStudy of vaccinia virus binding and entry using confocal microscopy, an original approach
Vanderplasschen, Alain ULg; Smith, G. L.

in Biology of the Cell (1998), 90

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See detailOptimization of murine CD8+ cytotoxic T-lymphocyte responses to pseudorabies virus
Depierreux, C.; Graff, I.; Lancelot, V. et al

in Journal of Immunological Methods (1997), 203

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See detailAntibodies against vaccinia virus do not neutralize extracellular enveloped virus but prevent virus release from infected cells and comet formation
Vanderplasschen, Alain ULg; Hollinshead, M.; Smith, G. L.

in Journal of General Virology (The) (1997), 78(Pt 8), 2041-2048

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See detailA novel virus blinding assay using confocal microscopy: demonstration that the intracellular and extracellular vaccinia virions bind to different cellular receptors
Vanderplasschen, Alain ULg; Smith, G. L.

in Journal of Virology (1997), 71

Vaccinia virus (VV) produces two antigenically and structurally distinct infectious virions, intracellular mature virus (IMV) and extracellular enveloped virus (EEV), which bind to unidentified and ... [more ▼]

Vaccinia virus (VV) produces two antigenically and structurally distinct infectious virions, intracellular mature virus (IMV) and extracellular enveloped virus (EEV), which bind to unidentified and possibly different cellular receptors. Studies of VV binding have been hampered by having two infectious virions and by the rupture of the EEV outer membrane in the majority of EEV virions during purification. To overcome these problems, we have developed a novel approach to study VV binding that is based on confocal microscopy and does not require EEV purification. In this assay, individual virus particles adsorbed to the cell are simultaneously distinguished and quantified by double immunofluorescence labelling with antibody markers for EEV and IMV. By this method, we show unequivocally that IMV and EEV bind to different cellular receptors. Three independent observations allow this conclusion. First, the efficiencies with which IMV and EEV bind to different cell lines are unrelated; second, cell surface digestion with some enzymes affects IMV and EEV binding differently; and third, the binding of a monoclonal antibody to cells prevents IMV binding but not EEV binding. This technique may be widely applicable for studying the binding of different viruses. [less ▲]

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See detailTwo centuries of vaccination
Vanderplasschen, Alain ULg; Smith, G. L.

in Annales de Médecine Vétérinaire (1997), 141

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See detailVaccinia virus immune evasion
Smith, G. L.; Symons, J. A.; Khanna, A. et al

in Immunological Reviews (1997), 159

Vaccinia virus and other poxviruses express a wide variety of proteins which are nonessential for virus replication in culture but help the virus to evade the host response to infection. Examples include ... [more ▼]

Vaccinia virus and other poxviruses express a wide variety of proteins which are nonessential for virus replication in culture but help the virus to evade the host response to infection. Examples include proteins which oppose apoptosis. Synthesise steroids, capture chemokines, counteract complement, interfere with interferon and intercept interleukins. This review provides an overview of such proteins, with an emphasis on work from our laboratory, and illustrates how the study of these proteins can increase our understanding of virus pathogenesis, the function of the immune system and how to make safer and more immunogenic poxvirus-based vaccines. [less ▲]

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See detailBovine herpesvirus type 4. In Lymphotropicherpesviruses: Epstein-Barr virus and Human herpesvirus 8
Thiry, Etienne ULg; Lomonte, P.; Vanderplasschen, Alain ULg et al

in International Agency for research on cancer (1997)

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See detailBovine Herpesvirus 1-Induced Apoptosis Occurs At The G0/G1 Phase Of The Cell Cycle
Hanon, Emilien ULg; Hoornaert, S.; Dequiedt, Franck ULg et al

in Virology (1997), 232(2), 351-358

We have previously shown that bovine herpesvirus 1 (BHV-1), even when inactivated, induces apoptotic cell death in mitogen-stimulated bovine peripheral blood mononuclear cells (PBMCs) (Hanon et al., 1996 ... [more ▼]

We have previously shown that bovine herpesvirus 1 (BHV-1), even when inactivated, induces apoptotic cell death in mitogen-stimulated bovine peripheral blood mononuclear cells (PBMCs) (Hanon et al., 1996, J. Virol. 70, 4116-4120). In order to gain insight into this process, we have investigated the cell cycle phase at which BHV-1 induces apoptosis in PBMCs. Our results show that the percentage of cells that progress through the S phase was always lower in BHV-1-infected PBMCs than in control cells. This effect was not due to a defective activation of mitogen-stimulated PBMCs since BHV-1 only slightly affected the percentage of cells expressing BoCD25, a well-known lymphocyte activation marker. Furthermore, mimosine and cyclosporine A, two chemicals that inhibit entry into the S phase of the cell cycle by different pathways, did not affect the ability of BHV-1 to induce apoptosis. BHV-1-induced apoptosis also occurred in unstimulated PBMCs and interestingly, this was associated with the expression of c-myc and BoCD25 proteins both of which are related to cell cycle progression. All together, these data provide evidence demonstrating that BHV-1-induced apoptosis occurs at the G0/G1 phase of the cell cycle. [less ▲]

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See detailInactivated Bovine Herpesvirus 1 Induces Apoptotic Cell Death of Mitogen-Stimulated Bovine Peripheral Blood Mononuclear Cells
Hanon, E.; Vanderplasschen, Alain ULg; Lyaku, S. et al

in Journal of Virology (1996), 70(6), 4116-4120

Bovine herpesvirus 1 (BHV-1) is able to inhibit the proliferation of bovine peripheral blood mononuclear cells. Here, we have demonstrated that live BHV-1 and, interestingly, inactivated BHV-1 can induce ... [more ▼]

Bovine herpesvirus 1 (BHV-1) is able to inhibit the proliferation of bovine peripheral blood mononuclear cells. Here, we have demonstrated that live BHV-1 and, interestingly, inactivated BHV-1 can induce apoptosis of mitogen-stimulated bovine peripheral blood mononuclear cells in vitro. [less ▲]

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See detailThe Replication in Vitro of the Gammaherpesvirus Bovine Herpesvirus 4 Is Restricted by Its DNA Synthesis Dependence on the S Phase of the Cell Cycle
Vanderplasschen, Alain ULg; Goltz, M.; Lyaku, J. et al

in Virology (1995), 213(2), 328-40

Because several observations have suggested that replication of the gammaherpesvirus bovine herpesvirus 4 (BHV-4) is influenced by the physiological state of the host cell, a study was carried out to ... [more ▼]

Because several observations have suggested that replication of the gammaherpesvirus bovine herpesvirus 4 (BHV-4) is influenced by the physiological state of the host cell, a study was carried out to determine the relationship between BHV-4 infection and the cell cycle. The temporal expression of BHV-4 late (L) proteins in unsynchronized cell cultures was first investigated by flow cytometry. Interestingly, L protein expression occurred in a limited number of cells infected with a high multiplicity of infection, and a reciprocal correlation between the percentage of positive cells and the cell density at the time of infection was demonstrated. Moreover, the finding that a BHV-4 early-late protein was expressed in nearly all the cells suggested that a blockage in the viral replication cycle occurred in some infected cells at the stage of viral DNA synthesis or L protein expression. Because this blockage could be the consequence of the dependence of one or both of these events on the cell cycle, they were investigated after infection of synchronized cell cultures. The following findings were made. (i) Cell transition through the S phase quantitatively increased the rate of BHV-4 DNA replication. (ii) BHV-4 DNA synthesis could not be detected in cells arrested in G0. (iii) Synchronization of MDBK cells with Lovastatin before infection increased the percentage of cells expressing L proteins. (iv) In contrast, infection of cells arrested in G0 led to few positive cells. Taken together these results showed that BHV-4 DNA replication and consequently the expression of L proteins are dependent on the S phase of the cell cycle. This dependence could be of importance for several biological properties of BHV-4 infection in vitro and might have implications for the biology of the virus in vivo. [less ▲]

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See detailLes herpèsvirus bovins : biologie et implications
Pastoret, Paul-Pierre ULg; Lemaire, Mylène; Denis, Martine et al

Part of book (1994)

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See detailImmunological detection of beta-galactosidase-expressing cells by flow cytometry
Vanderplasschen, Alain ULg; Goltz, M.; Hanon, E.

in Biochemica (1994), 3

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