To investigate the mechanism that regulates dysplastic KRT5+ cell expansion following influenza A virus (IAV) (H1N1 PR8 strain) infection, we first compared the lung histology in mice subjected to IAV to that of those challenged by bleomycin, a chemotherapy reagent that can also induce severe alveolar damage, but that has a limited extent of alveolar KRT5+ cell formation (8). This evidence concerns the gene KRT5 and infection.