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Article: Epstein–Barr Virus and Innate Immunity: Friends or Foes?

TitleEpstein–Barr Virus and Innate Immunity: Friends or Foes?
Authors
KeywordsEpstein–Barr virus
EBV
interferon
inflammasome
caspase
Issue Date2019
PublisherMDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/microorganisms
Citation
Microorganisms, 2019, v. 7 n. 6, p. article no. 183 How to Cite?
AbstractEpstein–Barr virus (EBV) successfully persists in the vast majority of adults but causes lymphoid and epithelial malignancies in a small fraction of latently infected individuals. Innate immunity is the first-line antiviral defense, which EBV has to evade in favor of its own replication and infection. EBV uses multiple strategies to perturb innate immune signaling pathways activated by Toll-like, RIG-I-like, NOD-like, and AIM2-like receptors as well as cyclic GMP-AMP synthase. EBV also counteracts interferon production and signaling, including TBK1-IRF3 and JAK-STAT pathways. However, activation of innate immunity also triggers pro-inflammatory response and proteolytic cleavage of caspases, both of which exhibit proviral activity under some circumstances. Pathogenic inflammation also contributes to EBV oncogenesis. EBV activates NFκB signaling and induces pro-inflammatory cytokines. Through differential modulation of the proviral and antiviral roles of caspases and other host factors at different stages of infection, EBV usurps cellular programs for death and inflammation to its own benefits. The outcome of EBV infection is governed by a delicate interplay between innate immunity and EBV. A better understanding of this interplay will instruct prevention and intervention of EBV-associated cancers.
Persistent Identifierhttp://hdl.handle.net/10722/277966
ISSN
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorJangra, S-
dc.contributor.authorYuen, KS-
dc.contributor.authorBotelho, MG-
dc.contributor.authorJin, D-Y-
dc.date.accessioned2019-10-04T08:04:49Z-
dc.date.available2019-10-04T08:04:49Z-
dc.date.issued2019-
dc.identifier.citationMicroorganisms, 2019, v. 7 n. 6, p. article no. 183-
dc.identifier.issn2076-2607-
dc.identifier.urihttp://hdl.handle.net/10722/277966-
dc.description.abstractEpstein–Barr virus (EBV) successfully persists in the vast majority of adults but causes lymphoid and epithelial malignancies in a small fraction of latently infected individuals. Innate immunity is the first-line antiviral defense, which EBV has to evade in favor of its own replication and infection. EBV uses multiple strategies to perturb innate immune signaling pathways activated by Toll-like, RIG-I-like, NOD-like, and AIM2-like receptors as well as cyclic GMP-AMP synthase. EBV also counteracts interferon production and signaling, including TBK1-IRF3 and JAK-STAT pathways. However, activation of innate immunity also triggers pro-inflammatory response and proteolytic cleavage of caspases, both of which exhibit proviral activity under some circumstances. Pathogenic inflammation also contributes to EBV oncogenesis. EBV activates NFκB signaling and induces pro-inflammatory cytokines. Through differential modulation of the proviral and antiviral roles of caspases and other host factors at different stages of infection, EBV usurps cellular programs for death and inflammation to its own benefits. The outcome of EBV infection is governed by a delicate interplay between innate immunity and EBV. A better understanding of this interplay will instruct prevention and intervention of EBV-associated cancers.-
dc.languageeng-
dc.publisherMDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/microorganisms-
dc.relation.ispartofMicroorganisms-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectEpstein–Barr virus-
dc.subjectEBV-
dc.subjectinterferon-
dc.subjectinflammasome-
dc.subjectcaspase-
dc.titleEpstein–Barr Virus and Innate Immunity: Friends or Foes?-
dc.typeArticle-
dc.identifier.emailYuen, KS: samyuen@hku.hk-
dc.identifier.emailBotelho, MG: botelho@hkucc.hku.hk-
dc.identifier.emailJin, D-Y: dyjin@hku.hk-
dc.identifier.authorityBotelho, MG=rp00033-
dc.identifier.authorityJin, D-Y=rp00452-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/microorganisms7060183-
dc.identifier.pmid31238570-
dc.identifier.pmcidPMC6617214-
dc.identifier.scopuseid_2-s2.0-85072551096-
dc.identifier.hkuros306751-
dc.identifier.volume7-
dc.identifier.issue6-
dc.identifier.spagearticle no. 183-
dc.identifier.epagearticle no. 183-
dc.publisher.placeSwitzerland-

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