A recombinant NiV lacking the V protein induced more IFNβ in primary human microvascular lung endothelial cells in a late step of infection than the wild-type virus48, suggesting that the stabilization of UBXN1 by the V protein may contribute to the suppression of IFNβ induction in addition to its many reported IFN-suppressive functions. Here, UBXN1 is linked to infection.