A SAP30 complex inhibits IFN-beta expression in Rift Valley fever virus infected cells.

Rift Valley fever virus (RVFV) nonstructural protein NSs acts as the major determinant of virulence by antagonizing interferon beta (IFN-beta) gene expression. We demonstrate here that NSs interacts with the host protein SAP30, which belongs to Sin3A/NCoR/HDACs repressor complexes and interacts with...

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Autores principales: Nicolas Le May, Zeyni Mansuroglu, Psylvia Léger, Thibaut Josse, Guillaume Blot, Agnès Billecocq, Ramon Flick, Yves Jacob, Eliette Bonnefoy, Michèle Bouloy
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Publicado: Public Library of Science (PLoS) 2008
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Acceso en línea:https://doaj.org/article/9b0c71d7d3274feb8a4452e85870730c
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spelling oai:doaj.org-article:9b0c71d7d3274feb8a4452e85870730c2021-11-25T05:46:46ZA SAP30 complex inhibits IFN-beta expression in Rift Valley fever virus infected cells.1553-73661553-737410.1371/journal.ppat.0040013https://doaj.org/article/9b0c71d7d3274feb8a4452e85870730c2008-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18225953/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Rift Valley fever virus (RVFV) nonstructural protein NSs acts as the major determinant of virulence by antagonizing interferon beta (IFN-beta) gene expression. We demonstrate here that NSs interacts with the host protein SAP30, which belongs to Sin3A/NCoR/HDACs repressor complexes and interacts with the transcription factor YY1 that regulates IFN-beta gene expression. Using confocal microscopy and chromatin immunoprecipitation, we show that SAP30, YY1, and Sin3A-associated corepressor factors strongly colocalize with nuclear NSs filaments and that NSs, SAP30 and Sin3A-associated factors are recruited on the IFN-beta promoter through YY1, inhibiting CBP recruitment, histone acetylation, and transcriptional activation. To ascertain the role of SAP30, we produced, by reverse genetics, a recombinant RVFV in which the interacting domain in NSs was deleted. The virus was unable to inhibit the IFN response and was avirulent for mice. We discuss here the strategy developed by the highly pathogenic RVFV to evade the host antiviral response, affecting nuclear organization and IFN-beta promoter chromatin structure.Nicolas Le MayZeyni MansurogluPsylvia LégerThibaut JosseGuillaume BlotAgnès BillecocqRamon FlickYves JacobEliette BonnefoyMichèle BouloyPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 4, Iss 1, p e13 (2008)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Nicolas Le May
Zeyni Mansuroglu
Psylvia Léger
Thibaut Josse
Guillaume Blot
Agnès Billecocq
Ramon Flick
Yves Jacob
Eliette Bonnefoy
Michèle Bouloy
A SAP30 complex inhibits IFN-beta expression in Rift Valley fever virus infected cells.
description Rift Valley fever virus (RVFV) nonstructural protein NSs acts as the major determinant of virulence by antagonizing interferon beta (IFN-beta) gene expression. We demonstrate here that NSs interacts with the host protein SAP30, which belongs to Sin3A/NCoR/HDACs repressor complexes and interacts with the transcription factor YY1 that regulates IFN-beta gene expression. Using confocal microscopy and chromatin immunoprecipitation, we show that SAP30, YY1, and Sin3A-associated corepressor factors strongly colocalize with nuclear NSs filaments and that NSs, SAP30 and Sin3A-associated factors are recruited on the IFN-beta promoter through YY1, inhibiting CBP recruitment, histone acetylation, and transcriptional activation. To ascertain the role of SAP30, we produced, by reverse genetics, a recombinant RVFV in which the interacting domain in NSs was deleted. The virus was unable to inhibit the IFN response and was avirulent for mice. We discuss here the strategy developed by the highly pathogenic RVFV to evade the host antiviral response, affecting nuclear organization and IFN-beta promoter chromatin structure.
format article
author Nicolas Le May
Zeyni Mansuroglu
Psylvia Léger
Thibaut Josse
Guillaume Blot
Agnès Billecocq
Ramon Flick
Yves Jacob
Eliette Bonnefoy
Michèle Bouloy
author_facet Nicolas Le May
Zeyni Mansuroglu
Psylvia Léger
Thibaut Josse
Guillaume Blot
Agnès Billecocq
Ramon Flick
Yves Jacob
Eliette Bonnefoy
Michèle Bouloy
author_sort Nicolas Le May
title A SAP30 complex inhibits IFN-beta expression in Rift Valley fever virus infected cells.
title_short A SAP30 complex inhibits IFN-beta expression in Rift Valley fever virus infected cells.
title_full A SAP30 complex inhibits IFN-beta expression in Rift Valley fever virus infected cells.
title_fullStr A SAP30 complex inhibits IFN-beta expression in Rift Valley fever virus infected cells.
title_full_unstemmed A SAP30 complex inhibits IFN-beta expression in Rift Valley fever virus infected cells.
title_sort sap30 complex inhibits ifn-beta expression in rift valley fever virus infected cells.
publisher Public Library of Science (PLoS)
publishDate 2008
url https://doaj.org/article/9b0c71d7d3274feb8a4452e85870730c
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