In vivo imaging studies using reporters, such as hRLuc and GFP, may provide a more complete picture of the spatiotemporal progression of a viral disease [47, 48] . In this study, we report the use of recombinant RVFV-hRLuc and RVFV-GFP strains to investigate the in vivo dynamics of RVFV infection progression in living mice and identify the virus-expressing cells. The recombinant viruses were generated by replacing the NSs gene with the reporter gene. Hence, these viruses were avirulent in immunocompetent mice when compared with wild-type virus but they were highly pathogenic in mice lacking interferon-a/b receptor, enabling to use them for pathogenesis studies in this mouse model. We were able to detect luciferase reporter expression at early stages of infection in the main known sites of viral replication, the liver, the spleen, the thymus and the brain [18, 21, 49, 50, 51] . The pancreas appeared as an unexpected site of virus replication. Using ex vivo imaging and histological examination, we primarily identified macrophages infiltrating the adipose tissue surrounding the pancreas as primarily virus-expressing cells. Similarly, RVFVexpressing macrophages were identified in the stroma of the ovary. The RVFV-GFP confirmed the importance of macrophages as specific host cells for the virus in Ifnar1 2/2 mice. It further allowed the identification of dendritic cells and granulocytes as target cells for RVFV replication. Interestingly, only a low number of B-, T-and NK-cells expressed the GFP reporter. Viral antigens have been previously detected in mononuclear phagocytic cells and dendritic cells in the lymph nodes, spleen and thymus from infected wild-type mice [21] and in macrophages in the lymph nodes from infected rats [51] . Interestingly, Smith and colleagues [21] also noticed that lymphocytes did not appear stained with the RVFV antibody in agreement with our observations. Although RVFV replication in the human macrophage-like cell line U937 [52] and in cultured peritoneal macrophages from susceptible rats [53] have been previously documented, this is, to our knowledge, the first study to evaluate the infection rates of various subsets of cells of the myeloid lineage in vivo. Because the level of fluorescent GFP directly reflects the extent of transcription and replication of the recombinant virus, we assume that the virus is highly expressed in GFP-positive cells. However, since macrophages, dendritic cells and granulocytes are able to uptake cell debris, it is possible that some of these cells are GFP-positive following phagocytosis of debris of RVFV-GFPinfected cells in vivo.