Our laboratory is interested in understanding the mechanisms of disease in flaviviral encephalitis. In our murine model of West Nile virus (WNV) encephalitis, inflammatory monocytes migrate from the bone marrow into the infected central nervous system (CNS), where they release toxic mediators that ultimately lead to death of the animal. We have been able to abrogate this response using antibody blockade, which prevents monocyte infiltration into the CNS, leading to increased survival and reduced pathology (Getts et al., 2012). More recently, we have described an exciting novel therapeutic approach to treating monocyte-mediated diseases. Infusion of synthetic immune-modulating microparticles (IMP) prevents monocyte infiltration into the brain, resulting in the removal of these monocytes by the spleen. Increased survival and reduced pathology were not only seen in WNV-infected animals, but also in a wide variety of other disease models including experimental autoimmune encephalomyelitis (EAE) and cardiac infarction (Getts et al., 2014). My research is focused on analysing cellular infiltration in the infected CNS, and understanding how monocyte progenitors in the bone marrow are mobilised in response to infection. The soluble mediators and other cell signals that mobilise these populations are unknown, but these signals results in both the release of existing monocytes and the generation of new monocytes from progenitor populations. As such, my interest here is to analyse the infiltration of cells into the CNS during infection, and to characterise differentiation of cells across the haematopoietic continuum in the bone marrow, from stem cells through to mature monocytes.