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Modulation of Innate Immune Signaling Pathways by Herpesviruses

Herpesviruses can be detected by pattern recognition receptors (PRRs), which then activate downstream adaptors, kinases and transcription factors (TFs) to induce the expression of interferons (IFNs) and inflammatory cytokines. IFNs further activate the Janus kinase-signal transducer and activator of...

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Autores principales: Liu, Qizhi, Rao, Youliang, Tian, Mao, Zhang, Shu, Feng, Pinghui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6630988/
https://www.ncbi.nlm.nih.gov/pubmed/31234396
http://dx.doi.org/10.3390/v11060572
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author Liu, Qizhi
Rao, Youliang
Tian, Mao
Zhang, Shu
Feng, Pinghui
author_facet Liu, Qizhi
Rao, Youliang
Tian, Mao
Zhang, Shu
Feng, Pinghui
author_sort Liu, Qizhi
collection PubMed
description Herpesviruses can be detected by pattern recognition receptors (PRRs), which then activate downstream adaptors, kinases and transcription factors (TFs) to induce the expression of interferons (IFNs) and inflammatory cytokines. IFNs further activate the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, inducing the expression of interferon-stimulated genes (ISGs). These signaling events constitute host innate immunity to defeat herpesvirus infection and replication. A hallmark of all herpesviruses is their ability to establish persistent infection in the presence of active immune response. To achieve this, herpesviruses have evolved multiple strategies to suppress or exploit host innate immune signaling pathways to facilitate their infection. This review summarizes the key host innate immune components and their regulation by herpesviruses during infection. Also we highlight unanswered questions and research gaps for future perspectives.
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spelling pubmed-66309882019-08-19 Modulation of Innate Immune Signaling Pathways by Herpesviruses Liu, Qizhi Rao, Youliang Tian, Mao Zhang, Shu Feng, Pinghui Viruses Review Herpesviruses can be detected by pattern recognition receptors (PRRs), which then activate downstream adaptors, kinases and transcription factors (TFs) to induce the expression of interferons (IFNs) and inflammatory cytokines. IFNs further activate the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, inducing the expression of interferon-stimulated genes (ISGs). These signaling events constitute host innate immunity to defeat herpesvirus infection and replication. A hallmark of all herpesviruses is their ability to establish persistent infection in the presence of active immune response. To achieve this, herpesviruses have evolved multiple strategies to suppress or exploit host innate immune signaling pathways to facilitate their infection. This review summarizes the key host innate immune components and their regulation by herpesviruses during infection. Also we highlight unanswered questions and research gaps for future perspectives. MDPI 2019-06-21 /pmc/articles/PMC6630988/ /pubmed/31234396 http://dx.doi.org/10.3390/v11060572 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Liu, Qizhi
Rao, Youliang
Tian, Mao
Zhang, Shu
Feng, Pinghui
Modulation of Innate Immune Signaling Pathways by Herpesviruses
title Modulation of Innate Immune Signaling Pathways by Herpesviruses
title_full Modulation of Innate Immune Signaling Pathways by Herpesviruses
title_fullStr Modulation of Innate Immune Signaling Pathways by Herpesviruses
title_full_unstemmed Modulation of Innate Immune Signaling Pathways by Herpesviruses
title_short Modulation of Innate Immune Signaling Pathways by Herpesviruses
title_sort modulation of innate immune signaling pathways by herpesviruses
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6630988/
https://www.ncbi.nlm.nih.gov/pubmed/31234396
http://dx.doi.org/10.3390/v11060572
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