The type I interferon (IFN) system is one of the most powerful innate defenses of vertebrate cells, which limits replication and spread of viral pathogens including avian and human influenza viruses. Influenza virus propagation is sensitive to IFN activities and therefore, like other viral pathogens, these viruses do not only induce type I IFN but also antagonize the production and effects of these cytokines at the same time [55] . For influenza A and B viruses, this is accomplished through their non-structural NS1 proteins that are structurally related polypeptides of 26 kDa (A/ NS1) and 32 kDa (B/NS1), which are abundantly expressed in infected cells [55] . NS1 proteins predominantly act on the level of IFN gene induction in infected cells by obstructing RIG-Idependent signaling through interaction with cellular factor(s) and/or sequestration of RNAs generated during virus replication [1, 2, 57] . Some NS1 proteins were also described to inhibit the maturation of cellular pre-mRNAs raising the possibility that this activity additionally reduces production of IFNa/b in infected cells [58, 59] . While NS1 also interferes with the activity of some ISGs, such as the dsRNA dependent kinase PKR [5, 60] , so far no type I IFN antagonistic mechanism was described for influenza viruses that act on the level of IFN signaling rather than gene induction. Here we present data, showing that RNA-induced expression of SOCS-3 in early phases of infection leads to a functional inhibition of IFN-induced STAT activation and gene expression. This is a novel mechanism by which influenza virus suppresses the antiviral response of the host and paves the path to efficient virus replication.