Mechanisms of respiratory syncytial virus modulation of airway immune responses

Abstract

Respiratory syncytial virus (RSV) most often causes severe respiratory disease in the very young and the elderly. Acute disease can also cause exacerbations of asthma in any age group. Recent findings provide insight into how the innate and adaptive immune systems respond to RSV infection and provide preliminary evidence that these effects vary significantly by RSV strain and host. Components of cell signaling pathways that induce inflammatory cytokine expression during the innate immune response and alter epithelial cell polarity through activating transcription factors, namely NF-κB, are now more clearly understood. New studies also reveal how RSV infection skews T helper (Th) cell differentiation away from the cell-mediated Th1 subset and towards the Th2 subset. There are also new data supporting preferential Th17 differentiation during RSV infection. In addition, effective immune system regulation of IL-10 expression and T regulatory cell (Treg) airway accumulation are essential for effective RSV clearance.