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.

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.