Revealing the distribution and the expression intensity of influenza virus receptor on the tracheal basal cells will help us to understand the cell tropism of influenza virus and the pathogenesis of AIV infected tissues. Our previous study indicated that the replication of infectious bronchitis virus (IBV) is restricted to ciliated cells and goblet cells, but not basal cells [21] . The tracheal/bronchial basal cells, assumed as multipotent stem cells, are responsible for epithelial recovery and reestablish normal respiratory function after desquamation of the ciliated and goblet cells [14, 15] . In an uncomplicated IBV-infected chick, clinical signs persist for only 1 week and the unaffected basal cells may be responsible for epithelial reconstruction of the injured respiratory tract [22] . In contrast, basal cells are susceptible to the infection of avian influenza virus at a MOI of 1. The susceptibility of basal cells to AIV infection suggests that infection with AIV alone may cause the cell death of basal cells, and consequently affect basal membrane integrity and severe inflammation in the AIV infected trachea.