T cells are very important in the control of Herpes Simplex Virus (HSV) with CD8+T cells (with the help of CD4+ T cells) essential for HSV clearance. The dermal dendritic cells (dDCs, cross-presenting cDC1s and cDC2s) are suspected to play a key role in stimulating T cells. Our lab previously showed in human foreskin explants, that HSV-1 infection of Langerhans cells (LCs) caused apoptosis and the migration of these cells to the dermis, where they interacted with and were phagocytosed by dDCs. Little is known about the chemokines involved in facilitating attraction and clustering of dDCs with HSV-infected LCs, and the relative contribution of each dDC subset in these interactions. RNA-sequencing and surface phenotyping were conducted on human dDCs to determine their chemokine receptor profile, while bead-based immunoassays were used to determine the chemokines produced by HSV-1-infected LCs and HSV-1-infected keratinocytes. We found differential chemokine receptor expression on dDCs. cDC1s expressed CXCR3 and cDC2s expressed CCR2 and CCR5. HSV-1 infected LCs produced CXCL9/10/11 which binds to CXCR3, while keratinocytes produced CCL2, CCL3 and CCL5 which bind to CCR2 and CCR5 respectively. The importance of these chemokine axes was investigated using chemotaxis assays. Only cDC1s migrated towards HSV-1-infected LC supernatants. Additional chemotaxis assays are being conducted to determine whether CXCL9/10/11 (ligands of CXCR3) are facilitating cDC1 migration to HSV-1 infected LCs. We have shown CCL2, CCL3 and CCL5 are secreted by HSV infected keratinocytes and their relative roles in driving cDC2 migration is being investigated. By understanding the chemokine pathways that facilitate clustering of each dDC subset in HSV infected skin, and the role of each dDC subset in the HSV antigen relay between immune cells, we will determine which dDC subsets are crucial for CD8+ (and CD4+) T cell stimulation and aim to target them in developing vaccines.