Flavivirus Capsid Proteins Inhibit the Interferon Response

Zika virus (ZIKV) establishes persistent infections in multiple human tissues, a phenomenon that likely plays a role in its ability to cause congenital birth defects and neurological disease. Multiple nonstructural proteins encoded by ZIKV, in particular NS5, are known to suppress the interferon (IF...

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Main Authors: Adriana M. Airo, Alberto Felix-Lopez, Valeria Mancinelli, Danyel Evseev, Joaquin Lopez-Orozco, Kathy Shire, Patrick Paszkowski, Lori Frappier, Katharine E. Magor, Tom C. Hobman
Format: Article
Language:English
Published: MDPI AG 2022-05-01
Series:Viruses
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Online Access:https://www.mdpi.com/1999-4915/14/5/968
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author Adriana M. Airo
Alberto Felix-Lopez
Valeria Mancinelli
Danyel Evseev
Joaquin Lopez-Orozco
Kathy Shire
Patrick Paszkowski
Lori Frappier
Katharine E. Magor
Tom C. Hobman
author_facet Adriana M. Airo
Alberto Felix-Lopez
Valeria Mancinelli
Danyel Evseev
Joaquin Lopez-Orozco
Kathy Shire
Patrick Paszkowski
Lori Frappier
Katharine E. Magor
Tom C. Hobman
author_sort Adriana M. Airo
collection DOAJ
description Zika virus (ZIKV) establishes persistent infections in multiple human tissues, a phenomenon that likely plays a role in its ability to cause congenital birth defects and neurological disease. Multiple nonstructural proteins encoded by ZIKV, in particular NS5, are known to suppress the interferon (IFN) response by attacking different steps in this critical antiviral pathway. Less well known are the potential roles of structural proteins in affecting the host immune response during ZIKV infection. Capsid proteins of flaviviruses are of particular interest because a pool of these viral proteins is targeted to the nuclei during infection and, as such, they have the potential to affect host cell gene expression. In this study, RNA-seq analyses revealed that capsid proteins from six different flaviviruses suppress expression of type I IFN and IFN-stimulated genes. Subsequent interactome and in vitro ubiquitination assays showed that ZIKV capsid protein binds to and prevents activating ubiquitination of RIG-I CARD domains by TRIM25, a host factor that is important for the induction arm of the IFN response. The other flavivirus capsid proteins also interacted with TRIM25, suggesting that these viral proteins may attenuate antiviral signaling pathways at very early stages of infection, potentially even before nonstructural proteins are produced.
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spelling doaj.art-e9dd4fea08f24773acb3200a539d23442023-11-23T13:31:07ZengMDPI AGViruses1999-49152022-05-0114596810.3390/v14050968Flavivirus Capsid Proteins Inhibit the Interferon ResponseAdriana M. Airo0Alberto Felix-Lopez1Valeria Mancinelli2Danyel Evseev3Joaquin Lopez-Orozco4Kathy Shire5Patrick Paszkowski6Lori Frappier7Katharine E. Magor8Tom C. Hobman9Department of Medical Microbiology & Immunology, University of Alberta, Edmonton, AB T6G 2E1, CanadaDepartment of Medical Microbiology & Immunology, University of Alberta, Edmonton, AB T6G 2E1, CanadaDepartment of Cell Biology, University of Alberta, Edmonton, AB T6G 2H7, CanadaDepartment of Biological Sciences, University of Alberta, Edmonton, AB T6G 2E9, CanadaHigh Content Analysis Core, University of Alberta, Edmonton, AB T6G 2E1, CanadaDepartment of Molecular Genetics, University of Toronto, Toronto, ON M5G 1M1, CanadaDepartment of Medical Microbiology & Immunology, University of Alberta, Edmonton, AB T6G 2E1, CanadaDepartment of Molecular Genetics, University of Toronto, Toronto, ON M5G 1M1, CanadaDepartment of Biological Sciences, University of Alberta, Edmonton, AB T6G 2E9, CanadaDepartment of Medical Microbiology & Immunology, University of Alberta, Edmonton, AB T6G 2E1, CanadaZika virus (ZIKV) establishes persistent infections in multiple human tissues, a phenomenon that likely plays a role in its ability to cause congenital birth defects and neurological disease. Multiple nonstructural proteins encoded by ZIKV, in particular NS5, are known to suppress the interferon (IFN) response by attacking different steps in this critical antiviral pathway. Less well known are the potential roles of structural proteins in affecting the host immune response during ZIKV infection. Capsid proteins of flaviviruses are of particular interest because a pool of these viral proteins is targeted to the nuclei during infection and, as such, they have the potential to affect host cell gene expression. In this study, RNA-seq analyses revealed that capsid proteins from six different flaviviruses suppress expression of type I IFN and IFN-stimulated genes. Subsequent interactome and in vitro ubiquitination assays showed that ZIKV capsid protein binds to and prevents activating ubiquitination of RIG-I CARD domains by TRIM25, a host factor that is important for the induction arm of the IFN response. The other flavivirus capsid proteins also interacted with TRIM25, suggesting that these viral proteins may attenuate antiviral signaling pathways at very early stages of infection, potentially even before nonstructural proteins are produced.https://www.mdpi.com/1999-4915/14/5/968flavivirusesglobal transcriptioncapsid proteininterferon responseTRIM25Zika virus
spellingShingle Adriana M. Airo
Alberto Felix-Lopez
Valeria Mancinelli
Danyel Evseev
Joaquin Lopez-Orozco
Kathy Shire
Patrick Paszkowski
Lori Frappier
Katharine E. Magor
Tom C. Hobman
Flavivirus Capsid Proteins Inhibit the Interferon Response
Viruses
flaviviruses
global transcription
capsid protein
interferon response
TRIM25
Zika virus
title Flavivirus Capsid Proteins Inhibit the Interferon Response
title_full Flavivirus Capsid Proteins Inhibit the Interferon Response
title_fullStr Flavivirus Capsid Proteins Inhibit the Interferon Response
title_full_unstemmed Flavivirus Capsid Proteins Inhibit the Interferon Response
title_short Flavivirus Capsid Proteins Inhibit the Interferon Response
title_sort flavivirus capsid proteins inhibit the interferon response
topic flaviviruses
global transcription
capsid protein
interferon response
TRIM25
Zika virus
url https://www.mdpi.com/1999-4915/14/5/968
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