Frequently, there are coinfections with respiratory viruses, including RSV, and bacteria that cause communityacquired respiratory diseases, such as Streptococcus pneumoniae and Haemophilus influenzae. There is evidence for a positive correlation between infections with S. pneumoniae and RSV in the pathogenesis of otitis media, pneumonia, and meningitis [8] [9] [10] [11] . S. pneumoniae and H. influenzae colonize to the host respiratory epithelium via host cell surface receptors, such as the platelet-activating factor (PAF) receptor [12] [13] [14] . These bacteria interact with the PAF receptor via phosphorylcholine, which is a component of the bacterial cell surface. Both live and heat-killed S. pneumoniae cells show an increased adhesion to human epithelial cells infected with RSV [15] . The upregulation of PAF receptor expression that is induced by respiratory virus infections, including those caused by RSV, results in the enhanced adhesion of S. pneumoniae and H. influenzae to respiratory epithelial cells [15] [16] [17] . PAF receptor expression and S. pneumoniae cell adhesion are also upregulated by exposure to acid, which causes tissue injury and an inflammatory response [18] .