Most of our understanding of responses to pneumovirus infection has emerged from studies of RSV infection of human epithelial target cells in vitro; a list of genes and/or gene products produced by epithelial cells in response to RSV infection in vitro is provided in Table 1 . At the cellular level, epithelial cells initially respond to RSV infection by reducing their ciliary beat frequency. Production and release of chemoattractant cytokines (chemokines) can be observed as early as 12 h after infection, leading to the recruitment of specific leukocyte subsets to the lung tissue. RSV-infected epithelial cells become resistant to tumor necrosis factor (TNF)-α-induced apoptosis, but later fuse to form giant-cell syncytia and die by cellular necrosis. We review the molecular bases (to the extent that they