 The purpose of this study is to explore the role of histoblood group antigens in virus-induced asthma exacerbations. These antigens ABH and Lewis decorate O- and N-linked glycans on mucin and epithelial glycoproteins, respectively. Glycan synthesis involves glycosyltransferases, including fucosyltransferases FUT encoded by FUT genes. Glycan degradation involves glycosidases, including fucosidase. Secretor status is defined by FUT2 activity in epithelial cells, which forms the H antigen and allows subsequent synthesis and secretion of A, B, and Lewis B antigens. In preliminary studies it was found that: 1 asthmatic patients with frequent exacerbations are more likely than non-exacerbated patients to be secretors; 2 secretors report more frequently that a cold causes asthma; and 3 sputum in stable asthma has abnormally high fucosidase activity. These findings suggest that airway glycans are subjected to the following two competing homoeostatic influences: 1 the diversity and activity of glycosyltransferases within cells that synthesize glycans; and 2 the diversity and activity of glycosidases that turn over and remodel glycans in the airway lumen. This study will test the hypothesis that secretor positive asthmatic patients are susceptible to virus-induced asthma exacerbation and that abnormal glycosidase activity in secretions modifies the glycan coat and promotes virus-induced exacerbation. 