L-sel−/−, B6, and LΔP polyclonal mice were infected intranasally with two different strains of influenza A viruses, and lungs were harvested for virus titer 8 days p.i. Virus titers were significantly lower in wild-type mice than in L-selectin-deficient mice following infection with the pathogenic PR8 (H1N1) or the non-pathogenic H17 (H3N2) strains of influenza virus, demonstrating a role for L-selectin in the clearance of virus from the lungs (Figures 7A and 7B). This evidence concerns the gene SELL and infection.