Reference : Varicella-zoster virus modulates NF-kappaB recruitment on selected cellular promoters.
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/3664
Varicella-zoster virus modulates NF-kappaB recruitment on selected cellular promoters.
English
El Mjiyad, Nadia mailto [Université de Liège - ULg > Département des sciences de la vie > Virologie - Immunologie >]
Bontems, Sébastien mailto [Université de Liège - ULg > > Virologie - Immunologie >]
Gloire, Geoffrey mailto [Université de Liège - ULg > > Virologie - Immunologie >]
Horion, Julie mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Anatomie et cytologie pathologiques >]
Vandevenne, P. mailto [Université de Liège - ULg > Département des sciences de la vie > Virologie et immunologie >]
Dejardin, Emmanuel mailto [Université de Liège - ULg > > Virologie - Immunologie >]
Piette, Jacques mailto [Université de Liège - ULg > Département des sciences de la vie > Virologie - Immunologie - GIGA-Research >]
Sadzot-Delvaux, Catherine mailto [Université de Liège - ULg > Département des sciences de la vie > Virologie et immunologie - GIGA-M : Coordination scientifique >]
2007
Journal of Virology
American Society for Microbiology (ASM)
81
23
13092-104
Yes (verified by ORBi)
International
0022-538X
1098-5514
Washington
DC
[en] Cell Line ; Cell Nucleus/chemistry ; Gene Expression Regulation ; Herpesvirus 3, Human/immunology ; Humans ; Intercellular Adhesion Molecule-1/biosynthesis/genetics ; NF-kappa B/metabolism ; NF-kappa B p50 Subunit/analysis ; NF-kappa B p52 Subunit/analysis ; Promoter Regions (Genetics) ; Protein Binding ; RNA, Messenger/biosynthesis ; Transcription Factor RelA/metabolism ; Tumor Necrosis Factor-alpha/immunology
[en] Intercellular adhesion molecule 1 (ICAM-1) expression is down-regulated in the center of cutaneous varicella lesions despite the expression of proinflammatory cytokines such as gamma interferon and tumor necrosis factor alpha (TNF-alpha). To study the molecular basis of this down-regulation, the ICAM-1 induction of TNF-alpha was analyzed in varicella-zoster virus (VZV)-infected melanoma cells (MeWo), leading to the following observations: (i) VZV inhibits the stimulation of icam-1 mRNA synthesis; (ii) despite VZV-induced nuclear translocation of p65, p52, and c-Rel, p50 does not translocate in response to TNF-alpha; (iii) the nuclear p65 present in VZV-infected cells is no longer associated with p50 and is unable to bind the proximal NF-kappaB site of the icam-1 promoter, despite an increased acetylation and accessibility of the promoter in response to TNF-alpha; and (iv) VZV induces the nuclear accumulation of the NF-kappaB inhibitor p100. VZV also inhibits icam-1 stimulation of TNF-alpha by strongly reducing NF-kappaB nuclear translocation in MRC5 fibroblasts. Taken together, these data show that VZV interferes with several aspects of the immune response by inhibiting NF-kappaB binding and the expression of target genes. Targeting NF-kappaB activation, which plays a central role in innate and adaptive immune responses, leads to obvious advantages for the virus, particularly in melanocytes, which are a site of viral replication in the skin.
Giga-Signal Transduction
http://hdl.handle.net/2268/3664
10.1128/JVI.01378-07
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17855547

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