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Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection

Herpes simplex virus-1 (HSV-1) is a double-stranded DNA virus that causes life-long infections. HSV-1 infections may lead to herpetic stromal keratitis that may advance to corneal blindness. HSV-1 infections can also cause fatal conditions, such as herpes encephalitis, or neonatal disease. A major v...

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Detalles Bibliográficos
Autores principales: Yakoub, Abraam M., Shukla, Deepak
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4929686/
https://www.ncbi.nlm.nih.gov/pubmed/25856282
http://dx.doi.org/10.1038/srep09730
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author Yakoub, Abraam M.
Shukla, Deepak
author_facet Yakoub, Abraam M.
Shukla, Deepak
author_sort Yakoub, Abraam M.
collection PubMed
description Herpes simplex virus-1 (HSV-1) is a double-stranded DNA virus that causes life-long infections. HSV-1 infections may lead to herpetic stromal keratitis that may advance to corneal blindness. HSV-1 infections can also cause fatal conditions, such as herpes encephalitis, or neonatal disease. A major virulence mechanism of HSV-1 is the control of autophagy, an innate immune defense strategy that could otherwise degrade viral particles. Here, to investigate a new mechanism for antiviral therapy, we tested the effect of various autophagy inducers (physiological and pharmacological) on infection. Autophagy stimulation was confirmed to significantly suppress HSV-1 infection in various cell types, without affecting cell viability. This study establishes the importance of autophagy for regulating HSV-1 infection, and provides a proof-of-principle evidence for a novel antiviral mechanism.
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spelling pubmed-49296862016-07-06 Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection Yakoub, Abraam M. Shukla, Deepak Sci Rep Article Herpes simplex virus-1 (HSV-1) is a double-stranded DNA virus that causes life-long infections. HSV-1 infections may lead to herpetic stromal keratitis that may advance to corneal blindness. HSV-1 infections can also cause fatal conditions, such as herpes encephalitis, or neonatal disease. A major virulence mechanism of HSV-1 is the control of autophagy, an innate immune defense strategy that could otherwise degrade viral particles. Here, to investigate a new mechanism for antiviral therapy, we tested the effect of various autophagy inducers (physiological and pharmacological) on infection. Autophagy stimulation was confirmed to significantly suppress HSV-1 infection in various cell types, without affecting cell viability. This study establishes the importance of autophagy for regulating HSV-1 infection, and provides a proof-of-principle evidence for a novel antiviral mechanism. Nature Publishing Group 2015-04-09 /pmc/articles/PMC4929686/ /pubmed/25856282 http://dx.doi.org/10.1038/srep09730 Text en Copyright © 2015, Macmillan Publishers Limited. All rights reserved http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Yakoub, Abraam M.
Shukla, Deepak
Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection
title Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection
title_full Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection
title_fullStr Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection
title_full_unstemmed Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection
title_short Autophagy Stimulation Abrogates Herpes simplex Virus-1 Infection
title_sort autophagy stimulation abrogates herpes simplex virus-1 infection
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4929686/
https://www.ncbi.nlm.nih.gov/pubmed/25856282
http://dx.doi.org/10.1038/srep09730
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