The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.

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 wit...

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Autores principales:	Patricia Vandevenne, Marielle Lebrun, Nadia El Mjiyad, Isabelle Ote, Emmanuel Di Valentin, Yvette Habraken, Estelle Dortu, Jacques Piette, Catherine Sadzot-Delvaux
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/58181cad50584114a4df3604a3b1c1a0
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spelling	oai:doaj.org-article:58181cad50584114a4df3604a3b1c1a02021-11-18T06:59:03ZThe varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.1932-620310.1371/journal.pone.0016870https://doaj.org/article/58181cad50584114a4df3604a3b1c1a02011-02-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21347389/?tool=EBIhttps://doaj.org/toc/1932-6203The 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-κB, is a key regulator of IFN-β 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-β 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-β and ISG15.Patricia VandevenneMarielle LebrunNadia El MjiyadIsabelle OteEmmanuel Di ValentinYvette HabrakenEstelle DortuJacques PietteCatherine Sadzot-DelvauxPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 2, p e16870 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Patricia Vandevenne Marielle Lebrun Nadia El Mjiyad Isabelle Ote Emmanuel Di Valentin Yvette Habraken Estelle Dortu Jacques Piette Catherine Sadzot-Delvaux The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.
description	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-κB, is a key regulator of IFN-β 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-β 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-β and ISG15.
format	article
author	Patricia Vandevenne Marielle Lebrun Nadia El Mjiyad Isabelle Ote Emmanuel Di Valentin Yvette Habraken Estelle Dortu Jacques Piette Catherine Sadzot-Delvaux
author_facet	Patricia Vandevenne Marielle Lebrun Nadia El Mjiyad Isabelle Ote Emmanuel Di Valentin Yvette Habraken Estelle Dortu Jacques Piette Catherine Sadzot-Delvaux
author_sort	Patricia Vandevenne
title	The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.
title_short	The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.
title_full	The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.
title_fullStr	The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.
title_full_unstemmed	The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.
title_sort	varicella-zoster virus orf47 kinase interferes with host innate immune response by inhibiting the activation of irf3.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/58181cad50584114a4df3604a3b1c1a0
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The varicella-zoster virus ORF47 kinase interferes with host innate immune response by inhibiting the activation of IRF3.

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