Bone marrow (BM) has previously been demonstrated to proliferate in response to exogenous type I interferon (IFN) treatment in vivo, supporting an immunoregulatory role for IFNs in hematopoietic stem / progenitor cell responses. To investigate the role of type I IFN signalling on BM during the dynamics of an immune response to infection, we investigated BM stem / progenitor populations and their response to IFN during lung tropic viral infection using a novel IFN signalling reporter mouse. While IFN signalling was minimal in naïve mice, influenza A virus (IAV) infected mice markedly upregulated DsRed fluorescent protein expression. Interestingly, multipotent progenitors demonstrated a much higher response to IFN than stem cell and lymphoid progenitors, suggesting that IFN responsiveness in the bone marrow is not homogenous among cell types. Furthermore, infection did not lead to enhanced stem cell proliferation, suggesting that infection induced changes in the BM are distinct from those reported in mice treated with exogenous type I IFN . Overall, this work demonstrates that IFN produced at the site of infection directly signals on bone marrow cells which may influence their function during immunological stresses.