BST2 inhibits infection of influenza A virus by promoting apoptosis of infected cells

Eunbi Yi, Jinsoo Oh, Hye Ri Kang, Moon Jung Song, Se Ho Park

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)


BST2 is an antiviral factor that inhibits the release of enveloped virus at the plasma membrane via an unusual topology in which its N-terminal is in the cytosol while its C-terminal is anchored by glycophosphatidylinositol (GPI). BST2-deficient cells showed substantially higher release of virions than wild type cells. Influenza-infected BST2-deficient cells showed greatly reduced cytopathic effect (CPE) than wild type cells despite their generally robust virus production. This finding prompted us to determine whether BST2 was involved in the apoptotic process of virus-infected host cells. Our results revealed that BST2 might be involved in IRE1α-mediated ER stress pathway by increasing spliced form XBP-1. Consequently, levels of cytochrome C, caspase-3, caspase-9, and PARP as representative molecules of apoptosis were significantly increased in wild type cells than those in BST2-deficient cells. These results suggest that BST2 might participate in innate host defense by augmenting ER-stress-induced apoptotic signaling to inhibit the replication and spread of virus.

Original languageEnglish
Pages (from-to)414-420
Number of pages7
JournalBiochemical and biophysical research communications
Issue number2
Publication statusPublished - 2019 Feb 5

Bibliographical note

Funding Information:
This study was supported by a grant ( NRF-2018R1A2A2A05023297 ) of the Basic Science Research Program of the National Research Foundation of Korea and a grant from Korea University .

Publisher Copyright:
© 2018 The Authors


  • Apoptosis
  • BST2
  • ER stress
  • Influenza virus
  • Tetherin

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


Dive into the research topics of 'BST2 inhibits infection of influenza A virus by promoting apoptosis of infected cells'. Together they form a unique fingerprint.

Cite this