Viperin is an important host restriction factor in control of Zika virus infection

Abstract Zika virus (ZIKV) infection has emerged as a global health threat and infection of pregnant women causes intrauterine growth restriction, spontaneous abortion and microcephaly in newborns. Here we show using biologically relevant cells of neural and placental origin that following ZIKV infe...

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Autores principales: Kylie H. Van der Hoek, Nicholas S. Eyre, Byron Shue, Onruedee Khantisitthiporn, Kittirat Glab-Ampi, Jillian M. Carr, Matthew J. Gartner, Lachlan A. Jolly, Paul Q. Thomas, Fatwa Adikusuma, Tanja Jankovic-Karasoulos, Claire T. Roberts, Karla J. Helbig, Michael R. Beard
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Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/31b52a34fd5a49c7bd204c6693170547
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spelling oai:doaj.org-article:31b52a34fd5a49c7bd204c66931705472021-12-02T15:05:25ZViperin is an important host restriction factor in control of Zika virus infection10.1038/s41598-017-04138-12045-2322https://doaj.org/article/31b52a34fd5a49c7bd204c66931705472017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04138-1https://doaj.org/toc/2045-2322Abstract Zika virus (ZIKV) infection has emerged as a global health threat and infection of pregnant women causes intrauterine growth restriction, spontaneous abortion and microcephaly in newborns. Here we show using biologically relevant cells of neural and placental origin that following ZIKV infection, there is attenuation of the cellular innate response characterised by reduced expression of IFN-β and associated interferon stimulated genes (ISGs). One such ISG is viperin that has well documented antiviral activity against a wide range of viruses. Expression of viperin in cultured cells resulted in significant impairment of ZIKV replication, while MEFs derived from CRISPR/Cas9 derived viperin−/− mice replicated ZIKV to higher titers compared to their WT counterparts. These results suggest that ZIKV can attenuate ISG expression to avoid the cellular antiviral innate response, thus allowing the virus to replicate unchecked. Moreover, we have identified that the ISG viperin has significant anti-ZIKV activity. Further understanding of how ZIKV perturbs the ISG response and the molecular mechanisms utilised by viperin to suppress ZIKV replication will aid in our understanding of ZIKV biology, pathogenesis and possible design of novel antiviral strategies.Kylie H. Van der HoekNicholas S. EyreByron ShueOnruedee KhantisitthipornKittirat Glab-AmpiJillian M. CarrMatthew J. GartnerLachlan A. JollyPaul Q. ThomasFatwa AdikusumaTanja Jankovic-KarasoulosClaire T. RobertsKarla J. HelbigMichael R. BeardNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Kylie H. Van der Hoek
Nicholas S. Eyre
Byron Shue
Onruedee Khantisitthiporn
Kittirat Glab-Ampi
Jillian M. Carr
Matthew J. Gartner
Lachlan A. Jolly
Paul Q. Thomas
Fatwa Adikusuma
Tanja Jankovic-Karasoulos
Claire T. Roberts
Karla J. Helbig
Michael R. Beard
Viperin is an important host restriction factor in control of Zika virus infection
description Abstract Zika virus (ZIKV) infection has emerged as a global health threat and infection of pregnant women causes intrauterine growth restriction, spontaneous abortion and microcephaly in newborns. Here we show using biologically relevant cells of neural and placental origin that following ZIKV infection, there is attenuation of the cellular innate response characterised by reduced expression of IFN-β and associated interferon stimulated genes (ISGs). One such ISG is viperin that has well documented antiviral activity against a wide range of viruses. Expression of viperin in cultured cells resulted in significant impairment of ZIKV replication, while MEFs derived from CRISPR/Cas9 derived viperin−/− mice replicated ZIKV to higher titers compared to their WT counterparts. These results suggest that ZIKV can attenuate ISG expression to avoid the cellular antiviral innate response, thus allowing the virus to replicate unchecked. Moreover, we have identified that the ISG viperin has significant anti-ZIKV activity. Further understanding of how ZIKV perturbs the ISG response and the molecular mechanisms utilised by viperin to suppress ZIKV replication will aid in our understanding of ZIKV biology, pathogenesis and possible design of novel antiviral strategies.
format article
author Kylie H. Van der Hoek
Nicholas S. Eyre
Byron Shue
Onruedee Khantisitthiporn
Kittirat Glab-Ampi
Jillian M. Carr
Matthew J. Gartner
Lachlan A. Jolly
Paul Q. Thomas
Fatwa Adikusuma
Tanja Jankovic-Karasoulos
Claire T. Roberts
Karla J. Helbig
Michael R. Beard
author_facet Kylie H. Van der Hoek
Nicholas S. Eyre
Byron Shue
Onruedee Khantisitthiporn
Kittirat Glab-Ampi
Jillian M. Carr
Matthew J. Gartner
Lachlan A. Jolly
Paul Q. Thomas
Fatwa Adikusuma
Tanja Jankovic-Karasoulos
Claire T. Roberts
Karla J. Helbig
Michael R. Beard
author_sort Kylie H. Van der Hoek
title Viperin is an important host restriction factor in control of Zika virus infection
title_short Viperin is an important host restriction factor in control of Zika virus infection
title_full Viperin is an important host restriction factor in control of Zika virus infection
title_fullStr Viperin is an important host restriction factor in control of Zika virus infection
title_full_unstemmed Viperin is an important host restriction factor in control of Zika virus infection
title_sort viperin is an important host restriction factor in control of zika virus infection
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/31b52a34fd5a49c7bd204c6693170547
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