The host’s inflammatory response contributes to the pathophysiology and symptomatology. Host cells recognize RSV via toll-like receptors, and secrete inflammatory cytokines (e.g. IFN-y, IL-1B, IL-4, IL-8). These effectors influence the local tissue environment directly, and also further the inflammatory process by drawing immune cells from the periphery. Many cytokines have known roles in the pathogenesis of RSV bronchiolitis, and some are even implicated in sustaining the infection. For example, the helper T cell’s main cytokine, IL-17, enhances RSV infection by increasing mucus production, inhibiting CD8 T cell activation, and reducing viral clearance. (Jacobson & Van Meer, 2013, p. 56).