Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung.

ABSTRACT: Recently, we demonstrated that influenza A virus (IAV)-infected murine neonates lacking a functional IFN-I receptor (IFNAR^-/-) had significantly improved survival and reduced lung pathology relative to wild-type (WT) neonates. In direct contrast, adult IFNAR^-/- mice display enhanced morbidity following IAV infection relative to WT adults. We hypothesized that IAV-induced IFN-I signaling in primary neonatal type II alveolar epithelial cells (TIIECs), the main cell type of IAV infection and initiator of host response in the lung, contributed to age-specific viral pathogenesis. Multifactorial transcriptional analysis of purified TIIECs revealed age, not infection status, as the primary driver of transcriptional differences in TIIECs. Subsequent pathway analysis demonstra

SUBMITTER: Onufer AP 

PROVIDER: S-EPMC12710878 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature