Ebolavirus VP24 binding to karyopherins is required for inhibition of interferon signaling

Mathieu Mateo, St Patrick Reid, Lawrence W. Leung, Christopher F. Basler, Viktor E. Volchkov

Research output: Contribution to journalArticle

90 Scopus citations

Abstract

The Ebolavirus VP24 protein counteracts alpha/beta interferon (IFN-α/β) and IFN-γ signaling by blocking the nuclear accumulation of tyrosine-phosphorylated STAT1 (PY-STAT1). According to the proposed model, VP24 binding to members of the NPI-1 subfamily of karyopherin alpha (KPNα) nuclear localization signal receptors prevents their binding to PY-STAT1, thereby preventing PY-STAT1 nuclear accumulation. This study now identifies two domains of VP24 required for inhibition of IFN-β-induced gene expression and PY-STAT1 nuclear accumulation. We demonstrate that loss of function correlates with loss of binding to KPNα proteins. Thus, the VP24 IFN antagonist function requires the ability of VP24 to interact with KPNα.

Original languageEnglish (US)
Pages (from-to)1169-1175
Number of pages7
JournalJournal of virology
Volume84
Issue number2
DOIs
StatePublished - Jan 2010

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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