In this study, we used genetic approaches that revealed that endophilin B2 is not required for embryonic development <i>in vivo</i> but that endophilin B2 deficiency impairs endosomal trafficking <i>in vitro</i>, as evidenced by suppressed endosome acidification, EGFR degradation, autophagic flux, and influenza A viral RNA nuclear entry and replication.
Disruption of B2 enhanced recovery from severe influenza infection as indicated by swift body weight recovery and significantly better survival of endophilin B2-deficient mice compared to WT mice.
WT and B2-deficient mice were infected with H1N1 PR8 by intranasal administration and course of influenza pneumonia, inflammatory, and tissue responses were monitored over time.