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.
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.