Immunosuppression, whether due to underlying disease or therapeutic intervention, significantly alters the host's ability to mount effective immune responses against viral pathogens. This is particularly relevant in the context of emerging infectious diseases such as COVID-19, where immunosuppressive treatments (e.g., corticosteroids) are employed to mitigate hyperinflammation. However, the precise effects of these therapies on antiviral immunity remain incompletely understood. Understanding how immunosuppressive drugs modulate immune cell function at the molecular level is critical for optimizing treatment strategies and minimizing infection-related complications. This research addresses a pressing clinical challenge: balancing the benefits of immunosuppressive therapy with the risks of impaired antiviral defence. Insights from this study could inform the development of safer immunomodulatory regimens and improve outcomes for patients receiving such treatments, especially during viral outbreaks or pandemics. Furthermore, the findings may have broader implications for transplant medicine, autoimmune diseases, and cancer therapy, where immunosuppression is routinely employed. To elucidate the effects of immunosuppressive therapy on the antiviral immune response, peripheral blood immune cells from healthy donors were stimulated in presence or absence of immunosuppressive drugs and subjected to single-cell RNA sequencing (scRNA-seq). Specific research objectives involve: characterisation and comparison of the transcriptional profiles of peripheral blood immune cells from healthy donors under immunosuppressive treatment; identifying shared and distinct molecular pathways of immunoinhibition across different immune cell subsets; determining temporal dynamics of immune modulation by analysing responses at multiple timepoints post-stimulation; and generating a systems-level map of how immunosuppressive agents alter antiviral signalling pathways. Collectively, this project will give insight into the effect of immunosuppressive treatment on the antiviral host response.