Avian influenza virus H5N1 induces rapid interferon-beta production but shows more potent inhibition to retinoic acid-inducible gene I expression than H1N1 in vitro

Virol J. 2012 Aug 3;9:145. doi: 10.1186/1743-422X-9-145.


Background: The mechanisms through which the avian influenza virus H5N1 modulate the host's innate immune defense during invasion, remains incompletely understood. RIG-I as a pattern recognition receptor plays an important role in mediating innate immune response induced by influenza virus. So, modulating RIG-I might be adopted as a strategy by influenza virus to antagonize the host's innate immune defense.

Methods: Here we chose an avian influenza virus A/tree sparrow/Henan/1/04 (H5N1) directly isolated from a free-living tree sparrow in Mainland China which is amplified in egg allantoic cavity, and researched its interferon induction and manipulation of RIG-I expression compared with influenza virus A/WSN/1933(H1N1), a well characterized mouse adapted strain, in human lung epithelial A549 cells and human embryonic kidney 293T cells.

Results: Although the avian influenza virus H5N1 infection initiated a rapid IFN-beta production early on, it eventually presented a more potent inhibition to IFN-beta production than H1N1. Correspondingly, the H5N1 infection induced low level expression of endogenous RIG-I, an Interferon Stimulating Gene (ISG), and showed more potent inhibition to the expression of endogenous RIG-I triggered by exogenous interferon than H1N1.

Conclusions: Manipulating endogenous RIG-I expression might constitute one of the mechanisms through which avian influenza virus H5N1 control the host's innate immune response during infection.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • China
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases / antagonists & inhibitors*
  • Epithelial Cells / virology
  • Humans
  • Influenza A Virus, H1N1 Subtype / immunology*
  • Influenza A Virus, H1N1 Subtype / pathogenicity*
  • Influenza A Virus, H5N1 Subtype / immunology*
  • Influenza A Virus, H5N1 Subtype / isolation & purification
  • Influenza A Virus, H5N1 Subtype / pathogenicity*
  • Interferon-beta / metabolism*


  • Interferon-beta
  • DDX58 protein, human
  • DEAD Box Protein 58
  • DEAD-box RNA Helicases