Myxovirus Resistance Protein A (MxA) is an interferon-stimulated gene with antiviral activity directed towards a broad range of viruses. During infection, MxA localises to the cytoplasm, where it interacts with structural components of viruses, such as capsid and nucleocapsid proteins. While MxA effectively targets viruses with specific structural components that localise to the cytoplasm, it does not interact with those that localise to other organelles. Prior research has demonstrated that relocating MxA to different intracellular locations can increase its antiviral activity. For example, MxA retains its antiviral activity against influenza when relocated to the nucleus from the cytoplasm, and antiviral activity towards Kunjin virus was enhanced when MxA was relocated to the endoplasmic reticulum. We aim to enhance the breadth of MxA's antiviral activity by relocating it to different cellular organelles that are important for the replication of previously resistant viruses. Mammalian expression vectors encoding for MxA with N-terminal organelle-specific localisation sequences were used to direct MxA to the nucleus, endoplasmic reticulum, golgi apparatus, endosomes, and plasma membrane. Localisation to these specific cellular localisations was validated using immunofluorescence microscopy. Currently, we are exploring the extent of antiviral activity of each MxA construct towards a range of viruses. Increasing the breadth of MxA’s antiviral activity with relocation, in conjunction with developing optimal delivery approaches, may pave the way for MxA to be used as a novel therapeutic approach to reduce disease severity associated with infection by a diverse range of viruses.