In studies of tracheal infection, ciliated cells and goblet cells have been shown to be the major target cells of IBV [1, 22] . Our results with primary ATE cells also showed that IBV viral protein can be detected in both ciliated cells and goblet cells. This cell tropism may account for the pathogenesis of IBV, such as the ciliostasis in observed IBV-infected TOC and the reduction of sialic acid secretion [3, 22] . In addition, we are the first to demonstrate that IBV does not appear to infect K14-positive basal cells. In an uncomplicated IBV-infected chick, clinical signs such as gasping, coughing, tracheal rales and nasal discharge persist for only 5-to-7 days and disappear within 2 weeks [3, 22] . In the recovery stage, unaffected basal cells may be responsible for epithelial hyperplasia after desquamation of the ciliated and goblet cells and reconstruction of the epithelium of the injured respiratory tract to reestablish normal physiological functioning [12, 13, 22] . The insensitivity of basal cells to IBV infection also suggests that coinfection with other viral or bacterial pathogens is required to disrupt basal membrane integrity and cause hemorrhage in IBV-infected tracheas. At present, quantification of the virulence of IBV is still a problem [3, 22] . Measuring ciliostasis in TOC is not a sensitive approach for determining the severity of respiratory tract injury caused by IBV infection [21] . In addition, different species of chicken may also vary in the vulnerability of their respiratory tissue to IBV infection [2, 22] . In our ATE system, IBV shows high affinity for ciliated cells and goblet cells. Cell tropism, viral replication and viral spread can be determined and quantified by immunocytostaining, suggesting that ATE cells could serve as a quantitative platform to determine the pathogenesis of IBV. It has been shown that sialic acid and HS may help IBV bind to its receptor on the cell membrane of target cells [18, 32] . Receptor binding triggers endocytosis and delivers the viral genome into the cytosol through pHdependent membrane fusion [4] . In this study, we demonstrate that none of the tested GAG interfered with IBV binding to ATE cells. Further investigation is required to test whether this ineffectiveness is due to a lack of the XBBXBX H consensus sequence in the S protein sequences of TW IBV.