PIV serotypes differ in their kinetics of replication and cytokine secretion in human trachea-bronchial airway epithelium. PIV1 replicated to high titer yet did not induce cytokine secretion until late in infection, while PIV2 replicated less efficiently but induced an early cytokine peak. PIV3 replicated to high titer but induced a slower rise in cytokine secretion. The T cell chemoattractants CXCL10 and CXCL11 were the most abundant chemokines induced (127). The gene discussed is CXCL11; the disease is infection.