RNAseq analysis identifies involvement of EBNA2 in PD-L1 induction during Epstein-Barr virus infection of primary B cells

Yusuke Yanagi, Yusuke Okuno, Yohei Narita, H. M.Abdullah Al Masud, Takahiro Watanabe, Yoshitaka Sato, Teru Kanda, Hiroshi Kimura, Takayuki Murata

Research output: Contribution to journalArticlepeer-review

Abstract

Epstein-Barr virus (EBV) is a causative agent of infectious mononucleosis and several types of malignancy. RNAseq of peripheral blood primary B cell samples infected with wild-type EBV revealed that expression of programmed cell death ligand-1 (PD-L1) is markedly induced by infection. This induction of PD-L1 was alleviated by knockout of the EBNA2 gene, but knockout of LMP1 had little effect. ChIPseq, ChIA-PET, and reporter assays further confirmed that EBNA2-binding sites in the promoter region and at 130 kb downstream of the PD-L1 gene played important roles in PD-L1 induction. Our results indicate that EBV mainly utilizes the EBNA2 gene for induction of PD-L1 and to evade host immunity on infection of primary B cells. Furthermore, pathway analysis revealed that genes involved in the cell cycle, metabolic processes, membrane morphogenesis, and vesicle regulation were induced by EBNA2, and that EBNA2 suppressed genes related to immune signaling.

Original languageEnglish
Pages (from-to)44-54
Number of pages11
JournalVirology
Volume557
DOIs
Publication statusPublished - 05-2021

All Science Journal Classification (ASJC) codes

  • Virology

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