Cell entry by influenza virus depends on the recognition of a terminal SA-capped glycosylated molecules by the viral hemag-glutinin (HA) protein [3] . Generally, human influenza viruses preferentially bind to cell surface oligosaccharides that have the SAa2-6Gal linkage, while avian influenza viruses (AIVs) prefer SAa2-3Gal [3] . Especially, the glycans containing the SAa2-3Galb1-4GalNAc or SAa2-3Galb1-4(6OSO3)GalNAc, show a high affinity to MAA/MAL-I [4] and AIVs [7, 8] . Tracheal/ bronchial epithelium, mainly consisting of ciliated cells, goblet cells and basal cells, is the initially attacked tissue by the invading influenza viruses. The infected chicken trachea shows necrosis and detachment of ciliated cells, suggesting that ciliated cell is one of the cells targeted by AIV [9] . Previous analyses of the expression of SAs in chicken have revealed that a2,3-linked SA was localized on tracheal ciliated cells and a2,6-linked SAs was also present in the tracheal tissues [10, 11, 12] . However, the detailed distribution of SAs among chicken tracheal epithelial (CTE) cells remains unclear. Clarification of the distribution and the expression intensity of influenza receptor on CTE cells will help us to understand the viral tropism, viral spreading and the pathogenesis of avian influenza viruses. Here, the SA distribution on CTE cells were identified by the staining of biotin-labeled plant lectins. A Taiwan-isolated AIV H6N1 was applied to characterize the cell tropism of AIV and the correlation of the cell tropism of AIV to the SA distribution on CTE cells was also explored.