Peter S. Askovich

TL;DR: This study demonstrates, for the first time, that in addition to its direct antiviral role, 25HC also regulates transcriptional responses and acts as an amplifier of inflammation via AP-1 and that the resulting alteration in inflammatory response leads to increased tissue damage in mice following infection with influenza.

TL;DR: The data suggest that viral infection specifically induces a miRNA that directs a negative regulatory cascade to tune DC cytokine production, and this work determined that miR-451 regulates a subset of proinflammatory cytokine responses.

TL;DR: By comparing data from mutant versus wild-type virus and host strains, RNA versus protein differential expression, and infection with genetically similar strains, these data can be used to further investigate genetic and physiological determinants of host responses to viral infection.

TL;DR: The results indicate that the type I epithelial cell can play a major role in restricting influenza virus infection without contribution from the haematopoietic compartment.

TL;DR: This study measured the growth rate of three strains of varying pathogenicity in the mouse airway epithelium and simultaneously examined the global host transcriptional response over the first 24 hours, identifying separate networks of genes in both the lung and tracheal tissues whose rapid up-regulation at early time points correlated with a reduced viral replication rate of those strains.