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dc.contributor.authorZheng, Wenjin
dc.contributor.authorXu, Qing
dc.contributor.authorZhang, Yiyuan
dc.contributor.authorE, Xiaofei
dc.contributor.authorGao, Wei
dc.contributor.authorZhang, Mogen
dc.contributor.authorZhai, Weijie
dc.contributor.authorRajkumar, Ronaldjit Singh
dc.contributor.authorLiu, Zhijun
dc.date2022-08-11T08:09:58.000
dc.date.accessioned2022-08-23T16:50:49Z
dc.date.available2022-08-23T16:50:49Z
dc.date.issued2020-12-09
dc.date.submitted2021-02-18
dc.identifier.citation<p>Zheng W, Xu Q, Zhang Y, E X, Gao W, Zhang M, Zhai W, Rajkumar RS, Liu Z. Toll-like receptor-mediated innate immunity against herpesviridae infection: a current perspective on viral infection signaling pathways. Virol J. 2020 Dec 9;17(1):192. doi: 10.1186/s12985-020-01463-2. Erratum in: Virol J. 2020 Dec 31;17(1):199. PMID: 33298111; PMCID: PMC7726878. <a href="https://doi.org/10.1186/s12985-020-01463-2">Link to article on publisher's site</a></p>
dc.identifier.issn1743-422X (Linking)
dc.identifier.doi10.1186/s12985-020-01463-2
dc.identifier.pmid33298111
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41734
dc.description.abstractBACKGROUND: In the past decades, researchers have demonstrated the critical role of Toll-like receptors (TLRs) in the innate immune system. They recognize viral components and trigger immune signal cascades to subsequently promote the activation of the immune system. MAIN BODY: Herpesviridae family members trigger TLRs to elicit cytokines in the process of infection to activate antiviral innate immune responses in host cells. This review aims to clarify the role of TLRs in the innate immunity defense against herpesviridae, and systematically describes the processes of TLR actions and herpesviridae recognition as well as the signal transduction pathways involved. CONCLUSIONS: Future studies of the interactions between TLRs and herpesviridae infections, especially the subsequent signaling pathways, will not only contribute to the planning of effective antiviral therapies but also provide new molecular targets for the development of antiviral drugs.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=33298111&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rights© The Author(s) 2020, corrected publication 2020. Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectHerpesviridae
dc.subjectImmune mechanism
dc.subjectToll-like receptor
dc.subjectViral infection
dc.subjectImmunity
dc.subjectImmunology of Infectious Disease
dc.subjectVirology
dc.titleToll-like receptor-mediated innate immunity against herpesviridae infection: a current perspective on viral infection signaling pathways
dc.typeJournal Article
dc.source.journaltitleVirology journal
dc.source.volume17
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5556&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4526
dc.identifier.contextkey21712582
refterms.dateFOA2022-08-23T16:50:49Z
html.description.abstract<p>BACKGROUND: In the past decades, researchers have demonstrated the critical role of Toll-like receptors (TLRs) in the innate immune system. They recognize viral components and trigger immune signal cascades to subsequently promote the activation of the immune system.</p> <p>MAIN BODY: Herpesviridae family members trigger TLRs to elicit cytokines in the process of infection to activate antiviral innate immune responses in host cells. This review aims to clarify the role of TLRs in the innate immunity defense against herpesviridae, and systematically describes the processes of TLR actions and herpesviridae recognition as well as the signal transduction pathways involved.</p> <p>CONCLUSIONS: Future studies of the interactions between TLRs and herpesviridae infections, especially the subsequent signaling pathways, will not only contribute to the planning of effective antiviral therapies but also provide new molecular targets for the development of antiviral drugs.</p>
dc.identifier.submissionpathoapubs/4526
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.source.pages192


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© The Author(s) 2020, corrected publication 2020. Open Access. This article is licensed under a Creative Commons Attribution 4.0
International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
Except where otherwise noted, this item's license is described as © The Author(s) 2020, corrected publication 2020. Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.