Viruses with their ability to effectively trigger and mediate potent immune responses have in recent years become desirable agents for anti-cancer therapeutics. ‘Oncolytic viruses’ have shown promise in their ability to target and kill cancer cells but are unable to maintain persistent immune response needed for tumour clearance.  Arenaviruses such as lymphocytic choriomeningitis virus (LCMV) are non-cytopathic and so do not kill the host cell upon infection and have been shown to preferentially replicate within cancer cells and induce and enhance a strong immune response with tumour clearance capabilities that can lead to tumour regression. In ‘immune cold’ cancer types with no real immunotherapy options, such as triple negative breast cancer (TNBC), this virus represents a strong contender as an effective viral immunotherapy.  We have investigated the relative levels of the viral host entry and fusion receptors for LCMV α-dystroglycan (α-DG), and the lysosomal mucin CD164, respectively across multiple breast cancer cell lines compared to the human mammary epithelial cell lines HMEC and MCF10a. We have shown via flow cytometry, western blotting and qPCR that, even though TNBC cell lines lack the usual receptors required for LCMV infection, the virus infects preferentially within these cell types compared to the healthy tissue type. We aim to further these investigations by analysing the effect of infected TNBC cell lines on the human monocyte cell line THP-1 to determine whether LCMV infection is able to render TNBC cells more responsive to the immune system, when otherwise they would remain undetected.