Insufficiency in airway interferon activation defines clinical severity to infant RSV infection

Chin-Yi Chu; Xing Qiu; Matthew N. McCall; Lu Wang; Anthony Corbett; Jeanne Holden-Wiltse; Christopher Slaunwhite; Qian Wang; Christopher Anderson; Alex Grier; Steven R. Gill; Gloria S. Pryhuber; Ann R. Falsey; David J. Topham; Mary T. Caserta; Edward E. Walsh; Thomas J Mariani

While interferon production is known to be a ubiquitous host response to suppress viral infection, its role in mediating the severity of RSV illness in infants is unclear, as the virus actively suppresses this host protection mechanism via the RSV NS1 and NS2 gene products 49 . Further, since our data are from the upper respiratory system, they may not accurately reflect the importance of this pathway in the lower airway as a disease mechanism contributing to clinical severity. We sought to test whether this pathway was were evident at the RNA level. We tested for the induction of expression of our severity associated biomarkers in PHLEs. Not surprisingly, as we are only modeling a portion of the in vivo responses to infection, we found that some but not all genes were regulated.