Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction

Abstract Herpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1) infection, is the commonest cause of infectious blindness in the developed world. Following infection the virus is initially suspended in the tear film, where it encounters a multi-pronged immune response comprisi...

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Autores principales:	David Shahnazaryan, Rana Khalil, Claire Wynne, Caroline A. Jefferies, Joan Ní Gabhann-Dromgoole, Conor C. Murphy
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ce3c1ce58bd24780879b3e7ca5fe90f2
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spelling	oai:doaj.org-article:ce3c1ce58bd24780879b3e7ca5fe90f22021-12-02T11:57:57ZHerpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction10.1038/s41598-020-77725-42045-2322https://doaj.org/article/ce3c1ce58bd24780879b3e7ca5fe90f22020-12-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-77725-4https://doaj.org/toc/2045-2322Abstract Herpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1) infection, is the commonest cause of infectious blindness in the developed world. Following infection the virus is initially suspended in the tear film, where it encounters a multi-pronged immune response comprising enzymes, complement, immunoglobulins and crucially, a range of anti-viral and pro-inflammatory cytokines. However, given that HSV-1 can overcome innate immune responses to establish lifelong latency throughout a susceptible individual’s lifetime, there is significant interest in understanding the mechanisms employed by HSV-1 to downregulate the anti-viral type I interferon (IFN) mediated immune responses. This study aimed to investigate the interactions between infected cell protein (ICP)0 and key elements of the IFN pathway to identify possible novel targets that contribute to viral immune evasion. Reporter gene assays demonstrated the ability of ICP0 to inhibit type I IFN activity downstream of pathogen recognition receptors (PRRs) which are known to be involved in host antiviral defences. Further experiments identified interferon regulatory factor (IRF)7, a driver of type I IFN, as a potential target for ICP0. These findings increase our understanding of the pathogenesis of HSK and suggest IRF7 as a potential therapeutic target.David ShahnazaryanRana KhalilClaire WynneCaroline A. JefferiesJoan Ní Gabhann-DromgooleConor C. MurphyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-10 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q David Shahnazaryan Rana Khalil Claire Wynne Caroline A. Jefferies Joan Ní Gabhann-Dromgoole Conor C. Murphy Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction
description	Abstract Herpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1) infection, is the commonest cause of infectious blindness in the developed world. Following infection the virus is initially suspended in the tear film, where it encounters a multi-pronged immune response comprising enzymes, complement, immunoglobulins and crucially, a range of anti-viral and pro-inflammatory cytokines. However, given that HSV-1 can overcome innate immune responses to establish lifelong latency throughout a susceptible individual’s lifetime, there is significant interest in understanding the mechanisms employed by HSV-1 to downregulate the anti-viral type I interferon (IFN) mediated immune responses. This study aimed to investigate the interactions between infected cell protein (ICP)0 and key elements of the IFN pathway to identify possible novel targets that contribute to viral immune evasion. Reporter gene assays demonstrated the ability of ICP0 to inhibit type I IFN activity downstream of pathogen recognition receptors (PRRs) which are known to be involved in host antiviral defences. Further experiments identified interferon regulatory factor (IRF)7, a driver of type I IFN, as a potential target for ICP0. These findings increase our understanding of the pathogenesis of HSK and suggest IRF7 as a potential therapeutic target.
format	article
author	David Shahnazaryan Rana Khalil Claire Wynne Caroline A. Jefferies Joan Ní Gabhann-Dromgoole Conor C. Murphy
author_facet	David Shahnazaryan Rana Khalil Claire Wynne Caroline A. Jefferies Joan Ní Gabhann-Dromgoole Conor C. Murphy
author_sort	David Shahnazaryan
title	Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction
title_short	Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction
title_full	Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction
title_fullStr	Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction
title_full_unstemmed	Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction
title_sort	herpes simplex virus 1 targets irf7 via icp0 to limit type i ifn induction
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/ce3c1ce58bd24780879b3e7ca5fe90f2
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Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction

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