يعرض 1 - 10 نتائج من 42 نتيجة بحث عن '"Sadzot-Delvaux, Catherine"', وقت الاستعلام: 0.89s تنقيح النتائج
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    مؤتمر
  2. 2
    دورية أكاديمية

    المساهمون: GIGA-I3 - Giga-Infection, Immunity and Inflammation - ULiège

    المصدر: Journal of Virology (2014)

    الوصف: peer reviewed ; The protein encoded by the ORF9 is essential for Varicella-zoster virus (VZV) replication. Previous studies documented its presence in the trans-Golgi network and its involvement in secondary envelopment. In this work, we deleted the ORF9p acidic cluster, destroying its interaction with ORF47p and resulting in a nuclear accumulation of both proteins. This phenotype results to an accumulation of primary enveloped capsids in the perinuclear space, reflecting a capsid de-envelopment defect.

    العلاقة: urn:issn:0022-538X; urn:issn:1098-5514; https://orbi.uliege.be/handle/2268/183229Test; info:hdl:2268/183229; https://orbi.uliege.be/bitstream/2268/183229/1/J.%20Virol.-2015-Riva-2436-41.pdfTest; scopus-id:2-s2.0-84921689781; info:pmid:25473054

  3. 3
    دورية أكاديمية

    المساهمون: Giga-Signal Transduction - ULiège

    المصدر: PLoS ONE, 9 (2) (2011-02)

    الوصف: peer reviewed ; The innate immune response constitutes the first line of host defence that limits viral spread and plays an important role in the activation of adaptive immune response. Viral components are recognized by specific host pathogen recognition receptors triggering the activation of IRF3. IRF3, along with NF-kappaB, is a key regulator of IFN-beta expression. Until now, the role of IRF3 in the activation of the innate immune response during Varicella-Zoster Virus (VZV) infection has been poorly studied. In this work, we demonstrated for the first time that VZV rapidly induces an atypical phosphorylation of IRF3 that is inhibitory since it prevents subsequent IRF3 homodimerization and induction of target genes. Using a mutant virus unable to express the viral kinase ORF47p, we demonstrated that (i) IRF3 slower-migrating form disappears; (ii) IRF3 is phosphorylated on serine 396 again and recovers the ability to form homodimers; (iii) amounts of IRF3 target genes such as IFN-beta and ISG15 mRNA are greater than in cells infected with the wild-type virus; and (iv) IRF3 physically interacts with ORF47p. These data led us to hypothesize that the viral kinase ORF47p is involved in the atypical phosphorylation of IRF3 during VZV infection, which prevents its homodimerization and subsequent induction of target genes such as IFN-beta and ISG15.

    العلاقة: urn:issn:1932-6203; https://orbi.uliege.be/handle/2268/103006Test; info:hdl:2268/103006; https://orbi.uliege.be/bitstream/2268/103006/1/Vandevenne.pdfTest; scopus-id:2-s2.0-79951801158; info:pmid:21347389

  4. 4
    دورية أكاديمية
  5. 5
    دورية أكاديمية
  6. 6
    دورية أكاديمية

    المساهمون: GIGA-I3 - Giga-Infection, Immunity and Inflammation - ULiège

    المصدر: PLoS ONE, 4 (11), e7882 (2009-11-18)

    الوصف: peer reviewed ; Available data suggest that the Varicella-Zoster virus (VZV) IE4 protein acts as an important regulator on VZV and cellular genes expression and could exert its functions at post-transcriptional level. However, the molecular mechanisms supported by this protein are not yet fully characterized. In the present study, we have attempted to clarify this IE4-mediated gene regulation and identify some cellular partners of IE4. By yeast two-hybrid and immunoprecipitation analysis, we showed that IE4 interacts with three shuttling SR proteins, namely ASF/SF2, 9G8 and SRp20. We positioned the binding domain in the IE4 RbRc region and we showed that these interactions are not bridged by RNA. We demonstrated also that IE4 strongly interacts with the main SR protein kinase, SRPK1, and is phosphorylated in in vitro kinase assay on residue Ser-136 contained in the Rb domain. By Northwestern analysis, we showed that IE4 is able to bind RNA through its arginine-rich region and in immunoprecipitation experiments the presence of RNA stabilizes complexes containing IE4 and the cellular export factors TAP/NXF1 and Aly/REF since the interactions are RNase-sensitive. Finally, we determined that IE4 influences the export of reporter mRNAs and clearly showed, by TAP/NXF1 knockdown, that VZV infection requires the TAP/NXF1 export pathway to express some viral transcripts. We thus highlighted a new example of viral mRNA export factor and proposed a model of IE4-mediated viral mRNAs export.

    العلاقة: urn:issn:1932-6203; https://orbi.uliege.be/handle/2268/33834Test; info:hdl:2268/33834; https://orbi.uliege.be/bitstream/2268/33834/1/OTE%202009.pdfTest; scopus-id:2-s2.0-70849134258; info:pmid:19924249

  7. 7
    دورية أكاديمية

    المساهمون: GIGA-I3 - Giga-Infection, Immunity and Inflammation - ULiège

    المصدر: BMC Molecular Biology, 8, 99 (2007-10)

    الوصف: peer reviewed ; Varicella Zoster Virus Immediate Early 63 protein (IE63) has been shown to be essential for VZV replication, and critical for latency establishment. The activity of the protein as a transcriptional regulator is not fully clear yet. Using transient transfection assays, IE63 has been shown to repress viral and cellular promoters containing typical TATA boxes by interacting with general transcription factors. In this paper, IE63 regulation properties on endogenous gene expression were evaluated using an oligonucleotide-based micro-array approach. We found that IE63 modulates the transcription of only a few genes in HeLa cells including genes implicated in transcription or immunity. Furthermore, we showed that this effect is mediated by a modification of RNA POL II binding on the promoters tested and that IE63 phosphorylation was essential for these effects. In MeWo cells, the number of genes whose transcription was modified by IE63 was somewhat higher, including genes implicated in signal transduction, transcription, immunity, and heat-shock signalling. While IE63 did not modify the basal expression of several NF-κB dependent genes such as IL-8, ICAM-1, and IκBα, it modulates transcription of these genes upon TNFα induction. This effect was obviously correlated with the amount of p65 binding to the promoter of these genes and with histone H3 acetylation and HDAC-3 removal. Conclusion While IE63 only affected transcription of a small number of cellular genes, it interfered with the TNF-inducibility of several NF-κB dependent genes by the accelerated resynthesis of the inhibitor IκBα.

  8. 8
    دورية أكاديمية

    المصدر: Journal of Virology, 79 (8), 5069-77 (2005)

    الوصف: peer reviewed ; Varicella-zoster virus (VZV) open reading frame 63 (ORF63) is one of the most abundant transcripts expressed during VZV latency in humans, and ORF63 protein has been detected in human ganglia by several laboratories. Deletion of over 90% of the ORF63 gene showed that the protein is required for efficient establishment of latency in rodents. We have constructed viruses with a series of mutations in ORF63. While prior experiments showed that transfection of cells with a plasmid expressing ORF63 but lacking the putative nuclear localization signal of the protein resulted in increased expression of the protein in the cytoplasm, we found that ORF63 protein remained in the nucleus in cells infected with a VZV ORF63 nuclear localization signal deletion mutant. This mutant was not impaired for growth in cell culture or for latency in rodents. Replacement of five serine or threonine phosphorylation sites in ORF63 with alanines resulted in a virus that was impaired for replication in vitro and for latency. A series of ORF63 carboxy-terminal mutants showed that the last 70 amino acids do not affect replication in vitro or latency in rodents; however, the last 108 amino acids are important for replication and latency. Thus, regions of ORF63 that are important for replication in vitro are also required for efficient establishment of latency.

    العلاقة: urn:issn:0022-538X; urn:issn:1098-5514; https://orbi.uliege.be/handle/2268/1637Test; info:hdl:2268/1637; https://orbi.uliege.be/bitstream/2268/1637/1/Cohen%2063%3a10M.pdfTest; scopus-id:2-s2.0-16244395803; info:pmid:15795292

  9. 9
    دورية أكاديمية

    المصدر: Virology, 289 (2), 218-23 (2001)

    الوصف: peer reviewed ; Latent infection of human ganglia with Varicella-Zoster virus (VZV) is characterized by a highly restricted pattern of viral gene expression. To enhance understanding of this process we used in situ hybridization (ISH) in a rat model of VZV latency to examine expression of RNA corresponding to eight different VZV genes in rat dorsal root ganglia (DRG) at various times after footpad inoculation with wild-type VZV. PCR in situ amplification was also used to determine the cell specificity of latent VZV DNA. It was found that the pattern of viral gene expression at 1 week after infection was different from that observed at the later times of 1 and 18 months after infection. Whereas multiple genes were expressed at 1 week after infection, gene expression was restricted at the later time points when latency had been established. At the later time points after infection the RNA transcripts expressed most frequently were those for VZV genes 21, 62, and 63. Gene 63 was expressed more than any other gene studied. While VZV DNA was detected almost exclusively in 5-10% of neurons, VZV RNA was detected in both neurons and nonneuronal cells at an approximate ratio of 3:1. A newly described monoclonal antibody to VZV gene 63-encoded protein was used to detect this protein in neuronal nuclei and cytoplasm in almost half of the DRG studied. These results demonstrate that (1) this rat model of latency has close similarities in terms of viral gene expression to human VZV latency which makes it a useful tool for studying this process and its experimental modulation and (2) expression of VZV gene 63 appears to be the single most consistent feature of VZV latency.

    العلاقة: urn:issn:0042-6822; urn:issn:1096-0341; https://orbi.uliege.be/handle/2268/17279Test; info:hdl:2268/17279; https://orbi.uliege.be/bitstream/2268/17279/1/Kennedy%202001.pdfTest; scopus-id:2-s2.0-0035950610; info:pmid:11689044

  10. 10
    دورية أكاديمية

    المساهمون: GIGA-I3 - Giga-Infection, Immunity and Inflammation - ULiège

    المصدر: Journal of Virology, 92 (15) (2018-07-17)

    الوصف: peer reviewed ; ORF9p (homologous to HSV-1 VP22) is a varicella-zoster virus (VZV) tegument protein essential for viral replication. Even though its precise functions are far from being fully described, a role in the secondary envelopment of the virus has long been suggested. We performed a yeast two-hybrid screen to identify cellular proteins interacting with ORF9p that might be important for this function. We found thirty-one ORF9p interaction partners, among which AP1M1, the mu subunit of the adaptor protein complex-1 (AP-1). AP-1 is a heterotetramer involved in intracellular vesicle-mediated transport and regulates the shuttling of cargo proteins between endosomes and the TGN via clathrin-coated vesicles. We confirmed that AP-1 interacts with ORF9p in infected cells and mapped potential interaction motifs within ORF9p. We generated VZV mutants in which each of these motifs is individually impaired and identified leucine 231 in ORF9p as critical to interact with AP-1. Disrupting ORF9p binding to AP-1 by mutating leucine 231 to alanine in ORF9p strongly impaired viral growth, most likely by preventing efficient secondary envelopment of the virus. Leucine 231 is part of a di-leucine motif conserved among alphaherpesviruses and we showed that VP22 of MDV and HSV-2 also interact with AP-1. This indicates that the function of this interaction in the secondary envelopment might be conserved as well.IMPORTANCE Herpesviruses are responsible for infections that, especially in immunocompromised patients, can lead to severe complications, including neurological symptoms and strokes. The constant emergence of viral strains resistant to classical antivirals (mainly acyclovir and its derivatives) pleads for the identification of new targets for future antiviral treatments. Cellular adaptor protein complexes (AP) have been implicated in the correct addressing of herpesvirus glycoproteins in infected cells and the discovery that a major constituent of varicella-zoster virus tegument is interacting with AP-1 reveals a ...

    العلاقة: urn:issn:0022-538X; urn:issn:1098-5514; https://orbi.uliege.be/handle/2268/224498Test; info:hdl:2268/224498; scopus-id:2-s2.0-85050152155; info:pmid:29793951