Arenaviruses are part of the largest family of hemorrhagic fever-causing viruses. Infection with many arenaviruses results in expression of type I interferon (IFN) and upregulation of IFN-stimulated genes (ISGs). The IFN-inducible short isoform of human nuclear receptor coactivator 7 (NcoA7) has been identified as a host restriction factor of viruses that enter cells via endocytosis such as influenza A, hepatitis C and SARS-CoV-2. NcoA7 interacts with V-ATPase to increase vesicle acidification and endosomal degradation which restricts virus entry although there is currently no published data on the effect of NcoA7 on arenavirus infections.             Here we demonstrate that NcoA7 plays a dual role during arenavirus infection in cells stably overexpressing the protein. Using arenavirus-glycoprotein pseudotypes (GPpp) to assess viral entry and live Mopeia (MOPV) and lymphocytic choriomeningitis virus (LCMV) to evaluate virus replication, we show that NcoA7 acts as a restriction factor at the stage of viral entry. However, once infection is established, NcoA7 significantly enhances viral replication and spread, resulting in an overall proviral effect of NcoA7 that appears specific to arenaviruses.              Proteomic, transcriptomic and interactome analyses reveal NcoA7 expression results in changes to translation regulation, cellular transport and stress responses which increase arenavirus replication. These findings therefore highlight a mechanism of arenaviruses overcoming the antiviral effects of increased IFN and ISG expression: by exploiting the interactome of the IFN-induced NcoA7 to boost replication and infectious virus production.