The observations that endogenous cathelicidin expression had protective function against pulmonary RSV in mice in vivo, and that immediate interaction with LL-37 diminished the infectivity of RSV in vitro and in vivo, led to the hypothesis that higher constitutive, upper airway hCAP-18/LL-37 expression at the primary sites of infection with RSV may represent a protective barrier in humans in vivo. The gene discussed is CAMP; the disease is infection.