References of "Rentier, Bernard"
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See detailPrise en charge des infections à VZV
Groupe de consensus; Rentier, Bernard ULiege

in Virologie (1998), 2(4), 317-323

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See detailSciences et Médecine à Liège à l'aube du troisième millénaire
Legros, Willy ULiege; Rentier, Bernard ULiege

in M S-Médecine Sciences (1998), 14(5), 535-536

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See detailLa régulation des cycles infectieux du virus de la varicelle et du zona
Piette, Jacques ULiege; Defechereux-Thibaut de Maisières, Patricia; Baudoux-Tebache, Laurence et al

in M S-Médecine Sciences (1998), 14(5), 556-565

Varicella-zoster virus (VZV) is an Alphaherpesvirus responsible for two human diseases: primary exposure to the virus results in chicken pox (varicella) and reactivation following a period of latency in ... [more ▼]

Varicella-zoster virus (VZV) is an Alphaherpesvirus responsible for two human diseases: primary exposure to the virus results in chicken pox (varicella) and reactivation following a period of latency in dorsal lia gives rise to shingles (zoster). Interestingly, several transcripts corresponding to regulatory proteins present during the lytic cycle can be found in latently infected cells. The IE62 protein, component of the viral tegument, is a nuclear phosphoprotein. IE62 may play a crucial role in triggering and regulating the replicative cycle of VZV since it transactivates all classes of VZV genes and is able to repress or activate its own promoter. Moreover, IE62 acts in synergy with IE4, another important regulatory protein, to stimulate VZV gene promoters and IE62 is responsible for the translocation of IE4 from the cytoplasm to the nucleus. IE4 is expressed at very early times of the VZV productive cycle, Predominantly localized in the cytoplasm, IE4 activates several VZV genes, either alone or in synergy with IE62, as well as heterologous viral genes. At the molecular level, IE4 seems to act both transcriptionally and post-transcriptionally. Another major VZV protein is a 45 kDa phosphorylated protein, called IE63, which is abundantly expressed at the onset of the productive cycle. It is also defected during latency in humans and in a rat animal model an unexpected observation in Alphaherpesviruses. IE63 displays little direct effect on VZV gene promoters, it shows no inhibitory effect on the transactivating functions of IE62 but it represses the IE4 mediated activation. Studies conducted to define the mode of action of three VZV regulatory proteins playing crucial roles in the latency and reactivation of the am-rus mil not only lead to a better understanding of the virus pathogenesis but will probably help define novel therapeutic tools. [less ▲]

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See detailVaricella-zoster virus open reading frame 4 encodes an immediate-early protein with posttranscriptional regulatory properties
Defechereux, Patricia; Debrus, Serge; Baudoux, Laurence et al

in Journal of Virology (1997), 71(9), 7073-7079

Varicella-zoster virus (VZV) encodes four putative immediate-early proteins based on sequence homology with herpes simplex virus type I: the products of ORF4, -61, -62, and -63. Until now, only two VZV ... [more ▼]

Varicella-zoster virus (VZV) encodes four putative immediate-early proteins based on sequence homology with herpes simplex virus type I: the products of ORF4, -61, -62, and -63. Until now, only two VZV proteins have been described as being truly expressed with immediate-early kinetics (IE62 and IE63). The ORF4-encoded protein can stimulate gene expression either alone or in synergy with the major regulatory protein IE62. Making use of a sequential combination of transcription and protein synthesis inhibitors (actinomycin D and cycloheximide, respectively), we demonstrated the immediate-early nature of the ORF4 gene product, which can thus be named IE4. The fact that IE4 is expressed with kinetics similar to that of IE62 further underlines the possible cooperation between these two VZV proteins in gene expression. Analysis of the IE4-mediated autologous or heterologous viral gene expression at the mRNA levels clearly indicated that IE4 may have several mechanisms of action. Activation of the two VZV genes tested could occur partly by a posttranscriptional mechanism, since increases in chloramphenicol acetyltransferase (CAT) mRNA levels do not account for the stimulation of CAT activity. On the other hand, stimulation of the human immunodeficiency virus type 1 long terminal repeat-or the cytomegalovirus promoter-associated CAT activity is correlated with an increase in the corresponding CAT mRNA. [less ▲]

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See detailChronic varicella-zoster virus skin lesions in patients with human immunodeficiency virus are related to decreased expression of gE and gB
Nikkels, Arjen ULiege; Rentier, Bernard ULiege; Pierard, Gérald ULiege

in Journal of Infectious Diseases (1997), 176(1), 261-264

The pathogenesis of chronic, verrucous varicella-zoster virus (VZV) cutaneous lesions in human immunodeficiency virus (HIV)-infected persons is unknown. It has been hypothesized that these lesions are due ... [more ▼]

The pathogenesis of chronic, verrucous varicella-zoster virus (VZV) cutaneous lesions in human immunodeficiency virus (HIV)-infected persons is unknown. It has been hypothesized that these lesions are due to an altered pattern of virus gene expression. Immediate early and late (L) gene expression in five chronic verrucous VZV lesions, four full-blown herpes zoster vesicular lesions in HIV-infected persons, and eight vesicular herpes zoster lesions in immunocompetent individuals was semiquantitatively assessed immunohistochemically using specific antibodies to the IE63, gE (L), and gB (L) proteins. All patients had evidence of IE63 expression in keratinocytes; however, gE expression was either weak or absent in keratinocytes of three verrucous lesions, and gB was either weak or absent in two. These results suggest that chronic VZV skin lesions are associated with diminished gE and gB expression. It is inferred that the VZV behavior in keratinocytes may vary from a latency-like state to a fully developed, productive infection. [less ▲]

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See detailVaricella-zoster virus immediate early proteins 4 and 62 interact with cellular transcription factors
Defechereux, Patricia; Baudoux, Laurence; Rentier, Bernard ULiege et al

Poster (1997)

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See detailBinding sites analysis of the major varicella-zoster virus regulatory IE62 protein
Baudoux, Laurence; Remacle, V.; Defechereux, Patricia et al

Poster (1997)

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See detailQu'est-ce qu'un virus?
Rentier, Bernard ULiege

Conference (1997)

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See detailLes recherches sur la biologie moléculaire du virus de la varicelle et du zona (VZV) ont-elles des applications cliniques ?
Rentier, Bernard ULiege

in Annales de Dermatologie et de Vénéréologie (1997), 124(Suppl. 2), 4-8

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See detailDe l’acyclovir au valacyclovir: la biodisponibilité en plus de l’efficacité et de la tolérance
Rentier, Bernard ULiege

in Virologics (1997), (Septembre), 10-11

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See detailRecognition of the latency-associated immediate early protein IE63 of varicella-zoster virus by human memory T-lymphocytes
Sadzot-Delvaux, Catherine ULiege; Kinchington, Paul R.; Debrus, Serge et al

in Journal of Immunology (1997), 159(6), 2802-2806

Varicella-zoster virus (VZV) is a human alpha herpesvirus that establishes latency in sensory ganglia. Latency is characterized by the abundant expression of the immediate early protein 63 (IE63), whereas ... [more ▼]

Varicella-zoster virus (VZV) is a human alpha herpesvirus that establishes latency in sensory ganglia. Latency is characterized by the abundant expression of the immediate early protein 63 (IE63), whereas other viral proteins have not yet been detected during the quiescent phase of VZV infection. The IE63 protein is a component of the virion and is expressed very early in the infectious cycle. The IE63 protein is also expressed in skin during episodes of varicella and herpes zoster. We have evaluated the cell-mediated immune response against IE63 in naturally immune adults with a history of chickenpox, by T lymphoproliferation and cytotoxicity assays. Among donors who had T cell proliferation to unfractionated VZV Ags from infected cell extract, 59% had T cell recognition of purified IE63. The CTL response to IE63 was equivalent to CTL recognition of IE62, the major tegument component of VZV whose immunogenicity has been previously described. IgG Abs against IE63 were detected in serum from healthy immune adults. These results indicate that IE63 is an important target of immunity to VZV. T cell recognition of IE63 is likely to be involved in controlling VZV reactivation from latency. [less ▲]

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See detailThe VZV IE63, expressed during latency, is an efficient target for the immune system
Sadzot-Delvaux, Catherine ULiege; Debrus, Serge; Kinchington, P. et al

Conference (1997)

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See detailThe VZV IE63, expressed during latency, is an efficient target for the immune system
Sadzot-Delvaux, Catherine ULiege; Debrus, Serge; Kinchington, P. et al

Conference (1997)

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See detailIn vitro models of non persistent and persistent infection of human and murine neuroblastoma cell lines by the varicella zoster virus
Schlabertz, Tania; Sadzot-Delvaux, Catherine ULiege; Piette, Jacques ULiege et al

in Archives Internationales de Physiologie et de Biochimie (1997)

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See detailAssessment of pain in herpes zoster: lessons learned from antiviral trials
Dworkin, R. H.; Carrington, D.; Cunningham, A. et al

in Antiviral Research (1997), 33(2), 73-85

Pain typically accompanies acute herpes zoster and, in a proportion of patients, it persists well beyond rash healing. Pain must therefore be analyzed in trials of antiviral agents in herpes zoster, but ... [more ▼]

Pain typically accompanies acute herpes zoster and, in a proportion of patients, it persists well beyond rash healing. Pain must therefore be analyzed in trials of antiviral agents in herpes zoster, but different methods have been used to analyze pain in recent published trials. These reports are reviewed and their methodological strengths and weaknesses examined. Based on this review, recommendations for the design and analysis of future trials of antiviral agents in herpes zoster are proposed. The principal recommendation is that antiviral efficacy should be evaluated both by distinguishing post-herpetic neuralgia from acute pain and by considering pain as a continuum. The primary endpoint should address both the prevalence and duration of post-herpetic neuralgia and should be examined in those patients who have post-herpetic neuralgia. Adopting the proposed recommendations in design and analysis of future trials should facilitate comparison across trials of the efficacy of antiviral agents in the treatment of herpes zoster. [less ▲]

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