Epstein-Barr Virus Early Protein BFRF1 Suppresses IFN-β Activity by Inhibiting the Activation of IRF3.
EBV BFRF1
IFN-β
IRF3
ISG54
innate immunity
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
27
11
2019
accepted:
15
09
2020
entrez:
4
1
2021
pubmed:
5
1
2021
medline:
30
4
2021
Statut:
epublish
Résumé
Epstein-Barr virus (EBV) is the causative agent of infectious mononucleosis that is closely associated with several human malignant diseases, while type I interferon (IFN-I) plays an important role against EBV infection. As we all know, EBV can encode some proteins to inhibit the production of IFN-I, but it's not clear whether other proteins also take part in this progress. EBV early lytic protein BFRF1 is shown to be involved in viral maturation, however, whether BFRF1 participates in the host innate immune response is still not well known. In this study, we found BFRF1 could down-regulate sendai virus-induced IFN-β promoter activity and mRNA expression of IFN-β and ISG54 during BFRF1 plasmid transfection and EBV lytic infection, but BFRF1 could not affect the promoter activity of NF-κB or IRF7. Specifically, BFRF1 could co-localize and interact with IKKi. Although BFRF1 did not interfere the interaction between IKKi and IRF3, it could block the kinase activity of IKKi, which finally inhibited the phosphorylation, dimerization, and nuclear translocation of IRF3. Taken together, BFRF1 may play a critical role in disrupting the host innate immunity by suppressing IFN-β activity during EBV lytic cycle.
Identifiants
pubmed: 33391252
doi: 10.3389/fimmu.2020.513383
pmc: PMC7774019
doi:
Substances chimiques
BFRF1 protein, Human herpesvirus 4
0
IRF3 protein, human
0
Interferon Regulatory Factor-3
0
Membrane Proteins
0
Viral Proteins
0
Interferon-beta
77238-31-4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
513383Informations de copyright
Copyright © 2020 Wang, Deng, Guo, Xu, Li, Ou, Xie, Lu, Zhong, Li, Hu, Deng, Peng, Cai and Li.
Déclaration de conflit d'intérêts
TP was employed by South China Vaccine Corporation Limited. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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