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See detailLe virus de la varicelle et du zona dans le système nerveux : retraite silencieuse ou guérilla permanente ?
Rentier, Bernard ULg; Sadzot-Delvaux, Catherine ULg

in Virologie (2000), 4(3), 207-216

Varicella-zoster virus is a Herpesvirus responsible for three distinct clinical features : chicken pox (varicella), shingles (herpes zoster) and post-zosterian pain (post-herpetic neuralgia). Neurological ... [more ▼]

Varicella-zoster virus is a Herpesvirus responsible for three distinct clinical features : chicken pox (varicella), shingles (herpes zoster) and post-zosterian pain (post-herpetic neuralgia). Neurological aspects of these diseases such as complications of chicken pox, viral latency in sensory gan-glia and reactivation as shingles with concurrent and at times subsequent prolonged pain, are the sequels of the invasion of the peripheral nervous system during primary infection. Prevention is achieved by vaccination with a live attenuated virus strain and therapy calls for specific antiviral agents. In many respects, VZV behaves differently from close relatives. In particular, viral latency in the nervous system is quite different from that of other Herpesviri-dae. The recent discovery of the expression and accumulation of some viral regulatory proteins during latency, although VZV latency had always been considered silent, as well as the demonstration that these proteins are immu-nogenic are opening new avenues to investigate the mechanisms of VZV latency and the immune control of VZV reactivation. [less ▲]

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See detailAnimal models of VZV infection
Sadzot-Delvaux, Catherine ULg; Rentier, Bernard ULg

in Gershon, Anne A.; Arvin, Ann M. (Eds.) Varicella-Zoster Virus : Virological and Clinical Management (2000)

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See detailOverview of the replication cycle of varicella-zoster virus
Sadzot-Delvaux, Catherine ULg; Baudoux, Laurence; Defechereux, Patricia et al

in Schmidt, A.; Wolff, M. H.; Schünemann, S. (Eds.) Varicella-Zoster Virus : Molecular Biology, Pathogenesis and Clinical Aspects (1999)

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See detailVaricella-zoster virus IE63, a virion component expressed during latency and acute infection, elicits humoral and cellular immunity
Sadzot-Delvaux, Catherine ULg; Arvin, Ann M.; Rentier, Bernard ULg

in Journal of Infectious Diseases (1998), 178(Suppl. 1), 43-47

Varicella-zoster virus (VZV) latency in human dorsal root ganglia is characterized by the transcription of large regions of its genome and by the expression of large amounts of some polypeptides, which ... [more ▼]

Varicella-zoster virus (VZV) latency in human dorsal root ganglia is characterized by the transcription of large regions of its genome and by the expression of large amounts of some polypeptides, which are also expressed during lytic cycles. The immediate early 63 protein (IE63) is a virion component expressed very early in cutaneous lesions and the first viral protein detected during latency. Immune response against IE63 has been evaluated among naturally immune adults with a history of chickenpox: Specific antibodies were detected in serum, and most subjects who had a T cell proliferation with unfractionated VZV antigens had T cell recognition of purified IE63. The cytotoxic T cell (CTL) response to IE63 was equivalent to CTL recognition of IE62, the major tegument component of VZV, whose immunogenicity has been previously described. T cell recognition of IE63 and other VZV proteins is one of the likely mechanisms involved in controlling VZV reactivation from latency. [less ▲]

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See detailLow-productive alpha-herpesviridae infection in chronic lichenoid dermatoses
Nikkels, Arjen ULg; Sadzot-Delvaux, Catherine ULg; Rentier, Bernard ULg et al

in Dermatology : International Journal for Clinical & Investigative Dermatology (1998), 196(4), 442-446

BACKGROUND: Herpes simplex virus (HSV) and Varicella-zoster virus (VZV) are responsible for various atypical mucocutaneous manifestations in the immunosuppressed population. One of the causative ... [more ▼]

BACKGROUND: Herpes simplex virus (HSV) and Varicella-zoster virus (VZV) are responsible for various atypical mucocutaneous manifestations in the immunosuppressed population. One of the causative pathomechanisms suggests an altered virus-host cell relationship. OBJECTIVE/METHODS: This report investigates by histology, immunohistochemistry and in situ hybridization the histological and virological features of 6 protracted, indolent HSV infections and 2 prolonged zoster infections. RESULTS: Histopathology revealed a lichenoid dermatitis in all patients. Specific HSV-1, HSV-2 and VZV in situ hybridization proved the viral origin of the cutaneous lesions. Immunohistochemical assessment demonstrated the intracellular presence of the HSV glycoproteins gB, gC and gD in epidermal keratinocytes which did not exhibit cytolysis. Similar findings were obtained for the VZV gE and gB. CONCLUSION: These results suggest that in some instances HSV and VZV infections may present a protracted disease course associated with a lichenoid inflammatory pattern and a non-cytolytic virus-host cell relationship. [less ▲]

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See detailLa régulation des cycles infectieux du virus de la varicelle et du zona
Piette, Jacques ULg; 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 detailRecognition of the latency-associated immediate early protein IE63 of varicella-zoster virus by human memory T-lymphocytes
Sadzot-Delvaux, Catherine ULg; 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 ULg; 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 ULg; 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 ULg; Piette, Jacques ULg et al

in Archives Internationales de Physiologie et de Biochimie (1997)

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See detailLessons to be learned from varicella-zoster virus
Rentier, Bernard ULg; Piette, Jacques ULg; Baudoux, Laurence et al

in Veterinary Microbiology (1996), 53(1-2), 55-66

Varicella-zoster virus (VZV) is an alphaherpesvirus responsible for two human diseases: chicken pox and shingles. The virus has a respiratory port of entry. After two successive viremias, it reaches the ... [more ▼]

Varicella-zoster virus (VZV) is an alphaherpesvirus responsible for two human diseases: chicken pox and shingles. The virus has a respiratory port of entry. After two successive viremias, it reaches the skin where it causes typical lesions. There, it penetrates the peripheral nervous system and it remains latent in dorsal root ganglia. It is still debatable whether VZV persists in neurons or in satellite cells. During latency, VZV expresses a limited set of transcripts of its immediate early (IE) and early (E) genes but no protein has been detected. Mechanisms of reactivation from ganglia have not been identified. However, dysfunction of the cellular immune system appears to be involved in this process. The cell-associated nature of VZV has made it difficult to identify a temporal order of gene expression, but there appears to be a cascade mechanism as for HSV-1. The lack of high titre cell-free virions or recombination mutants has hindered so far the understanding of VZV gene functions. Five genes, ORFs 4, 10, 61, 62, and 63 that encode regulatory proteins could be involved in VZV latency. ORF4p activates gene promoters with basal activities. ORF10p seems to activate the ORF 62 promoter. ORF61p has trans-activating and trans-repressing activities. The major IE protein ORF62p, a virion component, has DNA-binding and regulatory functions, transactivates many VZV promoters and even regulates its own expression. ORF63p is a nuclear IE protein of yet unclear regulatory functions, abundantly expressed very early in infection. We have established an animal model of VZV latency in the rat nervous system, enabling us to study the expression of viral mRNA and protein expression during latency, and yielding results similar to those found in humans. This model is beginning to shed light on the molecular events in VZV persistent infection and on the regulatory mechanisms that maintain the virus in a latent stage in nerve cells. [less ▲]

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See detailDistribution of varicella-zoster virus and herpes simplex virus in disseminated fatal infections
Nikkels, Arjen ULg; Delvenne, Philippe ULg; Sadzot-Delvaux, Catherine ULg et al

in Journal of Clinical Pathology (1996), 49(3), 243-248

AIMS: To study the cutaneous and visceral distribution of herpes simplex virus (HSV) and varicella zoster virus (VZV) in fatal infections. METHODS: Standard histology, immunohistochemistry (monoclonal ... [more ▼]

AIMS: To study the cutaneous and visceral distribution of herpes simplex virus (HSV) and varicella zoster virus (VZV) in fatal infections. METHODS: Standard histology, immunohistochemistry (monoclonal antibodies VL8 and VL2 and polyclonal antibody IE63 directed against VZV; monoclonal antibodies IBD4 and HH2 and polyclonal antibodies directed against HSVI and HSVII) and in situ hybridisation (anti-HSV and anti-VZV probes) were applied to formalin fixed, paraffin wax sections. RESULTS: On histological examination, Herpesviridae infection was evident in various organs including the lungs, liver and skin. In addition, immunohistochemistry and in situ hybridisation revealed the presence of HSV and VZV antigens and nucleic acids in several cell types and tissues showing no cytopathological alterations suggestive of Herpesviridae infection. The organs with histological evidence of infection also contained VZV or HSV antigens and their genes. CONCLUSIONS: These findings suggest that organ failure in disseminated VZV and HSV infections is primarily caused by HSV or VZV induced cell damage and lysis. They also indicate that immunohistochemistry and in situ hybridisation can provide an accurate, type-specific diagnosis on formalin fixed, paraffin wax embedded tissue even when classic histological and cytological characteristics are lacking. [less ▲]

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