Vimentin plays a role in the release of the influenza A viral genome from endosomes.

Influenza A virus exploits the subcellular transport machinery during the early stages of infection. Actin filaments and microtubules facilitate the trafficking of virus-containing endosomes towards the perinuclear region; however, the role of vimentin remains to be determined. In this study, we followed influenza A virus infection in vimentin-null cells and found that vimentin depletion severely reduced influenza viral RNA and protein expression, and production of infectious progeny virions. Furthermore, we show that in vimentin-null cells endosomal distribution and acidification were affected, and incoming influenza virions accumulated in late endosomes of these cells. We propose that this accumulation resulted from the impaired acidification of late endosomes in vimentin-null cells, which blocked the release of the viral genome from these organelles. These findings are the first to demonstrate that vimentin is critical for influenza viral infection as it facilitates endosomal trafficking and acidification, and mediates viral genome penetration into the cytoplasm to propagate the infection.