Epstein-Barr Virus LF2: an Antagonist to Type 1 Interferon

L. Wu, Even Fossum, Chul Hyun Joo, Kyung-Soo Inn, Young Chul Shin, Eric Johannsen, Lindsay M. Hutt-Fletcher, Juergen Haas, Jae U. Jung

Research output: Contribution to journalArticlepeer-review


Upon viral infection, the major defense mounted by the host immune system is activation of the interferon (IFN)-mediated antiviral pathway, which is mediated by IFN regulatory factors (IRFs). In order to complete their life cycle, viruses must modulate host IFN-mediated immune responses. Despite its association with significant human health problems, activities of Epstein-Barr virus (EBV), a human tumor-inducing herpesvirus, to evade host IFN-mediated innate immunity have not been well characterized. To search for EBV genes that block IFN signal transduction, we carried out a screening of EBV open reading frames for their abilities to block IFN-alpha/beta-mediated luciferase expression upon Sendai virus infection. This screening demonstrates that EBV LF2 tegument protein specifically interacts with the central inhibitory association domain of IRF7, and this interaction leads to inhibition of the dimerization of IRF7, which suppresses IFN-alpha production and IFN-mediated immunity. This demonstrates a novel immune evasion mechanism of EBV LF2 in blocking cellular IRF7-mediated innate immunity.

Original languageEnglish
Pages (from-to)1140-1146
Number of pages6
JournalJournal of Virology
Issue number2
Early online date5 Nov 2008
Publication statusPublished - Jan 2009


  • cell line
  • Genes, Reporter
  • Glycoproteins
  • Herpesvirus 4, Human
  • Humans
  • Interferon Regulatory Factor-7
  • Interferon Type I
  • Luciferases
  • Protein Binding
  • Viral Proteins


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