Background
A vast majority of asthma exacerbations are linked to viral infections, most of which are caused by rhinovirus (RV). We hypothesize that eosinophils are key effector cells in asthma exacerbations. As such, using an in vitro model of human cells, we have shown that respiratory syncytial virus (RSV) and RV induce eosinophil degranulation when co-cultured with T-cells and autologous monocyte-derived dendritic cells (moDC), concurrent with moDC-dependent CD4+ CD45RO+ T-cell activation. While our original hypothesis has been that such activation is mediated solely by antigen-presentation (AP), our recent data also suggest that RV may be the major pathogen associated with asthma attacks because of its unique ability to interact directly with T-cells.