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Epstein‐Barr virus tegument protein BGLF2 inhibits NF‐κB activity by preventing p65 Ser536 phosphorylation
Author(s) -
Chen Tao,
Wang Yuanfang,
Xu Zuo,
Zou Xingmei,
Wang Ping,
Ou Xiaowen,
Li Yiwen,
Peng Tao,
Chen Daixiong,
Li Meili,
Cai Mingsheng
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201901196rr
Subject(s) - phosphorylation , lytic cycle , epstein–barr virus , p50 , biology , iκbα , microbiology and biotechnology , viral tegument , nf κb , virus , gene knockdown , immunoprecipitation , signal transduction , virology , gene , biochemistry , transcription factor
Epstein‐Barr virus (EBV), a ubiquitous gammaherpesvirus, can regulate the antiviral response of NF‐κB signaling, which is critical for cell survival, growth transformation, and virus latency. Here, we showed that tegument protein BGLF2 could inhibit TNF‐α‐induced NF‐κB activity. BGLF2 was shown to interplay with the NF‐κB subunits p65 and p50, and the Rel homology domain of p65 was the pivotal region to interact with BGLF2. Nonetheless, BGLF2 did not influence the development of p65‐p50 dimerization. Yet, overexpression of BGLF2 inhibited the phosphorylation of p65 Ser536 (but not Ser276) and blocked the nuclear translocation of p65. In addition, knockdown of BGLF2 during EBV lytic replication elevated NF‐κB activity and the phosphorylation of p65 Ser536. Taken together, these results suggest that the inhibition of NF‐κB activation may serve as a strategy to escape the host's antiviral innate immunity to EBV during its lytic infection.—Chen, T., Wang, Y., Xu, Z., Zou, X., Wang, P., Ou, X., Li, Y., Peng, T., Chen, D., Li, M., Cai, M. Epstein‐Barr virus tegument protein BGLF2 inhibits NF‐κB activity by preventing p65 Ser536 phosphorylation. FASEB J. 33, 10563–10576 (2019). www.fasebj.org