Document Type
Article
Publication Date
1-1-2014
Abstract
Respiratory syncytial virus (RSV) infection is the number one cause of bronchiolitis in infants, yet no vaccines are available because of a lack of knowledge of the infant immune system. Using a neonatal mouse model, we previously revealed that mice initially infected with RSV as neonates develop Th2-biased immunopathophysiologies during reinfection, and we demonstrated a role for enhanced interleukin-4 receptor α (IL-4Rα) expression on T helper cells in these responses. Here we show that RSV infection in neonates induced limited type I interferon (IFN) and plasmacytoid dendritic cell (pDC) responses. IFN alpha (IFN-α) treatment or adoptive transfer of adult pDCs capable of inducing IFN-α prior to neonatal RSV infection decreased Th2-biased immunopathogenesis during reinfection. A reduced viral load and downregulation of IL-4Rα on Th2 cells were observed in IFN- α-treated neonatal mice, suggesting dual mechanisms of action. © 2014, American Society for Microbiology.
Publication Source (Journal or Book title)
Journal of Virology
First Page
9350
Last Page
9360
Recommended Citation
Cormier, S., Shrestha, B., Saravia, J., Lee, G., Shen, L., DeVincenzo, J., Kim, Y., & You, D. (2014). Limited type I interferons and plasmacytoid dendritic cells during neonatal respiratory syncytial virus infection permit immunopathogenesis upon reinfection. Journal of Virology, 88 (16), 9350-9360. https://doi.org/10.1128/JVI.00818-14