title: 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.
abstract: 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.
authors.affiliation: Beijing Institute of Microbiology and Epidemiology, 20 Dong-Da Street, Beijing, Fengtai District, 100071, China.
authors.forename: Zhiqiang
authors.initials: Z
authors.lastname: Mi
authors.forename: Yonghong
authors.initials: Y
authors.lastname: Ma
authors.forename: Yigang
authors.initials: Y
authors.lastname: Tong
mesh_terms: D000818:Animals; D002460:Cell Line; D002681:China; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases / Q000037:antagonists & inhibitors*; D004847:Epithelial Cells / Q000821:virology; D006801:Humans; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology* / Q000472:pathogenicity*; D053124:Influenza A Virus, H5N1 Subtype / Q000276:immunology* / Q000302:isolation & purification / Q000472:pathogenicity*; D016899:Interferon-beta / Q000378:metabolism*; D011971:Receptors, Immunologic
chemical_list: D011971:Receptors, Immunologic; D016899:Interferon-beta; C452820:RIGI protein, human; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases