References of "Rentier, Bernard"
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See detailDetection by PCR of varicella zoster virus DNA during primary infection in mice
Plumier, Jean-Christophe ULg; Sadzot-Delvaux, Catherine ULg; Debrus, Serge et al

in Archives Internationales de Physiologie et de Biochimie (1992), 100

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See detailEtude ultrastructure de l'organisation du nucléoïde du virus de la varicelle et du zona
Schoonbroodt, Sonia; Piette, Jacques ULg; Rentier, Bernard ULg

in Bulletin de la Société Royale des Sciences de Liège (1992), 60(6), 373-383

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See detailHuman papillomavirus type 33 upstream regulatory elements can control gene expression in human cervical keratinocytes
Lauricella-Lefèbvre, M. A.; Rentier, Bernard ULg; Piette, Jacques ULg

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1992), 100

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See detailLa régulation de l'expression des gènes du virus de la varicelle et du zona
Piette, Jacques ULg; Defechereux, Patricia; Baudoux, Laurence et al

in Annales de Médecine Vétérinaire (1992), 136(8), 627-635

Varicella-zoster virus (VZV) belongs to the alphaherpesvirus family and shares many important structural and functional similarities with other members of the family such as herpes simplex virus type 1 ... [more ▼]

Varicella-zoster virus (VZV) belongs to the alphaherpesvirus family and shares many important structural and functional similarities with other members of the family such as herpes simplex virus type 1 (HSV-1). VZV is responsible for two different clinical syndromes, varicella which is the result of the primary infection and zoster which is due to virus reactivation remaining latent in the peripheral nervous system. VZV DNA is 124,884 base pair long and encodes four regulatory proteins (IE4, IE61, IE62 and IE63). Using transient expression systems, we have shown that IE4, IE62 and IE63 can regulate the expression of an indicator gene driven by various VZV promoter regions, demonstrating that these proteins play important roles in the infectious cycle. [less ▲]

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See detailAntibodies to varicella-zoster virus modulate antigen distribution but fail to induce viral persistence in vitro.
Sadzot-Delvaux, Catherine ULg; Marc, Philippe; Lebon, Linda et al

in Journal of Virology (1992), 66(12), 7499-504

Varicella-zoster virus (VZV) persists in human sensory ganglia. One of the hypotheses to explain the induction or the maintenance of VZV latency is that it could be promoted by the immune response itself ... [more ▼]

Varicella-zoster virus (VZV) persists in human sensory ganglia. One of the hypotheses to explain the induction or the maintenance of VZV latency is that it could be promoted by the immune response itself. It is known that in the case of viruses which bud off the infected cell membrane, virus-specific antibodies can induce antigenic modulation, i.e., spatial redistribution of viral antigens and modulation of their synthesis. To determine whether antigenic modulation occurs during VZV infection in vitro and could possibly be involved in viral persistence, we have grown infected cells in the presence of anti-VZV antibodies either transiently or permanently. The distribution of immune complexes and viral proteins was then analyzed. In transient immunomodulation experiments, the distribution of one or more viral antigens was modified not only in the cytoplasmic membranes but also in the cytoplasm and nucleoplasm of infected cells. When infected cells were kept permanently in the presence of antibodies, the same pattern of redistribution of immune complexes was observed and the localization of internal viral glycoproteins was significantly modified. However, antibodies did not prevent the lytic effect of infection; they altered neither the infectious virus yield nor the Western immunoblot pattern of viral proteins, suggesting that immunomodulation is not the primary effector of viral persistence. [less ▲]

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See detailTwo-dimensional study of varicella-zoster virus proteins
Debrus, S.; Duquesne, Patricia ULg; Sadzot-Delvaux, Catherine ULg et al

Poster (1992)

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See detailGranulomatous reactions following herpes-zoster contain varicella-zoster glycoprotein GPI
Nikkels, Arjen ULg; Sadzot-Delvaux, Catherine ULg; Cloes, Jean-Michel et al

in Journal of Investigative Dermatology (1992), 98(4), 522

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See detailCharacterization of regulatory functions of the varicella-zoster virus gene-63-encoded protein
Jackers, Pascale ULg; Defechereux, Patricia; Baudoux, Laurence et al

in Journal of Virology (1992), 66(6), 3899-3903

Varicella-zoster virus (VZV) gene 63 encodes a protein (IE63) with a predicted molecular mass of 30.5 kDa which has amino acid similarities to the immediate-early (IE) protein 22 (ICP22) of herpes simplex ... [more ▼]

Varicella-zoster virus (VZV) gene 63 encodes a protein (IE63) with a predicted molecular mass of 30.5 kDa which has amino acid similarities to the immediate-early (IE) protein 22 (ICP22) of herpes simplex virus type 1. ICP22 is a polypeptide synthesized in herpes simplex virus type 1-infected cells, and as is the case for its VZV counterpart, its regulatory functions are unknown. On the basis of the VZV DNA sequence, it has been shown that IE63 exhibits hydrophilic and acidic properties, suggesting that this protein could play a regulatory role during the infectious cycle. We report in this article cotransfection experiments which demonstrate that the VZV gene 63 protein strongly represses, in a dose-dependent manner, the expression of VZV gene 62. On the other hand, transient expression of the VZV gene 63 protein can promote activation of the thymidine kinase gene but cannot affect the expression of the genes encoding glycoproteins I and II. The results of transient expression experiments strongly suggest that the VZV gene 63 protein could play a pivotal role in the repression of IE gene expression as well as in the activation of early gene expression [less ▲]

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See detailVaricella-zoster gene 63 encoded protein is an important regulatory factor
Jackers, Pascale ULg; Defechereux, Patricia; Baudoux, Laurence et al

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1992), 100

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See detailStudy of a new presumed mitochondrial carrier, the product of the yeast RIM 2 gene
Hellin, E.; Van Dyck, E.; Duyckaerts, Claire ULg et al

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1992), 100

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See detailHIV-1 reactivation after an oxidative stress
Legrand, Sylvie ULg; Vaira, Dolorès ULg; Rentier, Bernard ULg et al

in LinkVIII International Conference on AIDS/III STD World Congress, Amsterdam, the Netherlands 19-24 July 1992 (1992)

OBJECTIVES: A common denominator shared by several HIV-1 reactivation agents such as certain cytokines, UV irradiation and heat shock is their ability to cause stress response. Consequently, we have ... [more ▼]

OBJECTIVES: A common denominator shared by several HIV-1 reactivation agents such as certain cytokines, UV irradiation and heat shock is their ability to cause stress response. Consequently, we have investigated the effects of oxidative stress on HIV-1 reactivation, knowing that HIV-1 latently infected T cells can be exposed in vivo to such a stress when blood phagocytes are stimulated during inflammatory reactions. METHODS: The promonocytic (U1) and lymphocytic (ACH-2) cell lines, both HIV-1 chronically infected, were used to study the reactivation phenomenon. To test wether HIV-1 reactivation is mediated by LTR transactivation, the HeLa HIV-1 CAT cell line, which carries an integrated DNA cartridge containing CAT gene under control of HIV-1 LTR, was also exposed to an oxidative stress. RESULTS: Hydrogen peroxide exposure of U1 cells leads to an increased reverse transcriptase (RT) activity in supernatant fluid. Over the optimal concentrations range (0.5 to 1 mM), a four to fivefold stimulation level is reached. Below these concentrations, stress conditions are not sufficient and above, they induce a too important lethal effect. Immunofluorescence carried out on stressed U1 cells shows that H2O2 leads to HIV-1 gene expression activation and not to a release of viral particles from damaged cells. H2O2 also induces a stimulation of CAT activity in HeLa HIV-1 CAT cells. Intracellular singulet oxygen (1O2) is also able to induce an increase of RT activity in supernatant fluid of U1 and ACH-2 cells and a stimulation of CAT activity in HeLa HIV-1 CAT cells. A dose-response curve can also be demonstrated. In order to transpose these in vitro experiments to situations encountered in vivo, activated phagocytes were cocultivated with HeLa HIV-1 CAT cells. A weak stimulation of CAT activity was detected. CONCLUSIONS: Cellular oxidative damages induce HIV-1 LTR transactivation leading to viral gene expression and consequently to a burst of virus production. DNA damages induced by oxidative stress could be at the onset of HIV-1 reactivation. Experiments are now in progress to elucidate the mechanisms leading to HIV-1 reactivation after an oxidative stress. [less ▲]

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See detailHIV-1 reactivation after an oxidative stress
Legrand, Sylvie ULg; Hoebeke, Maryse ULg; Vaira, Dolorès ULg et al

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1992), 100

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See detailVaricella-zoster virus: an ultrastructural study of the assembly phases
Schoonbroodt, Sonia; Piette, Jacques ULg; Rentier, Bernard ULg

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1992), 100

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See detailTwo-dimensional study of varicella-zoster virus proteins
Debrus, S.; Lebon, L.; Schoonbroodt, Sonia et al

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1992), 100(2), 39

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See detailMolecular characterization of varicella-zoster virus gene expression
Defechereux, Patricia; Baudoux, Laurence; Jackers, Pascale ULg et al

in Archives Internationales de Physiologie, de Biochimie et de Biophysique (1992), 100

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See detailVZV glycoproteins gpI and gpII are present in dermal cells without their corresponding genome
Nikkels, Arjen ULg; Delvenne, Philippe ULg; Debrus, S. et al

in Journal of Cutaneous Pathology (1992), 19

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See detailParasite communities: Patterns and Processes
Rentier, Bernard ULg

in Book Reviews, Biochemical Systematics and Ecology (G. Esch, A. Bush & J. Aho, eds., Chapman & Hall, 1990) (1991)

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See detailAn in vivo model of varicella-zoster virus latent infection of dorsal root ganglia
Sadzot-Delvaux, Catherine ULg; Merville, Marie-Paule ULg; Delrée, P. et al

in Journal of Neuroscience Research (1990), 26(1), 83-89

We describe here the first in vivo model of varicella-zoster virus (VZV) latent infection in the adult rat peripheral nervous system. Infected Mewo cells were injected subcutaneously along the spine of ... [more ▼]

We describe here the first in vivo model of varicella-zoster virus (VZV) latent infection in the adult rat peripheral nervous system. Infected Mewo cells were injected subcutaneously along the spine of healthy adult rats. No clinical sign of infection was observed even 9 months after inoculation. Humoral immune response to VZV was detected in all infected animals throughout the study (9 months). The presence of viral material in dissociated and cultured dorsal root ganglia (DRG) from inoculated animals was studied by immunoperoxidase and in situ hybridization. When DRGs from infected animals were plated in culture from 1 month and up to 9 months after inoculation, viral nucleic acids and proteins were detected in neurons. Furthermore, trypsinization and subcultivation of infected neurons in culture is needed to reactivate infectious virus at least in some of the neurons. This model provides a useful tool for studying 1) the molecular mechanisms leading to an in vivo latency, 2) the role of the immune system, in particular cellular immunity, on the establishment, maintenance, and reactivation of latency, 3) the neurotropism of mutant viruses, and 4) the effects of antiviral agents. [less ▲]

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See detailAcute and persistent varicella-zoster virus infection of human and murine neuroblastoma cell lines
Bourdon-Wouters, C.; Merville, Marie-Paule ULg; Sadzot-Delvaux, Catherine ULg et al

in Journal of Neuroscience Research (1990), 26(1), 90-97

Human and murine neuroblastoma cell lines were infected in vitro with varicella-zoster virus (VZV). Infected human neuroblastoma cells (IMR-32) supported the synthesis of abundant viral antigens as ... [more ▼]

Human and murine neuroblastoma cell lines were infected in vitro with varicella-zoster virus (VZV). Infected human neuroblastoma cells (IMR-32) supported the synthesis of abundant viral antigens as detected by indirect immunoperoxidase labeling using human serum rich in anti-VZV antibodies and did not survive the infection. In situ hybridization (ISH) with VZV-cloned probes revealed a strong hybridization signal in these infected cells. During cultivation, the virus was released in the culture medium, and viral polypeptides were revealed by Western blotting of infected cells, using either a monoclonal anti-gpI antibody or a rabbit antiserum. All these findings indicate that IMR-32 cells support a productive and lytic infection by VZV, whether infected by cell-free virus or by cocultivation with infected cells. Murine neuroblastoma cells (neuro-2A) survived VZV infection and did not produce any infectious virus. No VZV-specific proteins were detected in infected cells either by immunolabeling or by Western blotting. However, viral nucleic acids could be detected by ISH, indicating that mouse neuroblastoma cells displayed a nonproductive, nonlytic infection. Infected neuro-2A cells have been examined by ISH using probes corresponding to immediate early (IE) genes 4, 62, and 63 and late (L) gene 31 encoding gpII. A strong hybridization signal was detected when infected cells were probed with a fragment containing the IE genes 62 and 63. Lower levels of hybridization were detected with the other probes, corresponding to IE or L genes. These systems allow comparative molecular analysis of persistent and acute infection of nerve cells by VZV. [less ▲]

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