In:
Frontiers in Immunology, Frontiers Media SA, Vol. 11 ( 2020-12-17)
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
1664-3224
DOI:
10.3389/fimmu.2020.513383
DOI:
10.3389/fimmu.2020.513383.s001
DOI:
10.3389/fimmu.2020.513383.s002
DOI:
10.3389/fimmu.2020.513383.s003
DOI:
10.3389/fimmu.2020.513383.s004
DOI:
10.3389/fimmu.2020.513383.s005
DOI:
10.3389/fimmu.2020.513383.s006
DOI:
10.3389/fimmu.2020.513383.s007
DOI:
10.3389/fimmu.2020.513383.s008
DOI:
10.3389/fimmu.2020.513383.s009
DOI:
10.3389/fimmu.2020.513383.s010
DOI:
10.3389/fimmu.2020.513383.s011
Language:
Unknown
Publisher:
Frontiers Media SA
Publication Date:
2020
detail.hit.zdb_id:
2606827-8
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