Notably, IFN-γ induced a specific increase of Nup98 levels in HeLa cells that counteracts the inhibition of mRNA export by PV 2A pro [17, 201] . Collectively, these findings reflect the central role of Nup98 in PV infection and in antiviral response, since its overexpression by itself prevents, at least in part, blockade of nuclear RNA export. Therefore, secretion of IFN-γ by immune cells might allow the induction of antiviral response by neighbouring cells by increasing the levels of Nup98 in order to protect nuclearcytoplasmic protein and RNA trafficking pathways. The physiological relevance of the crosstalk between Nup98-PV 2A pro in PV (and other viruses) infection might be studied in the future with cellular and animal systems.