When HSV-1 infects human epidermal Langerhans cells (LCs) and Epidermal (Epi-) DCs, both cell types undergo apoptosis[1]. We have shown in foreskin explants and herpetic lesion biopsies that HSV-infected LCs migrate to the dermis and cluster with dermal conventional DCs type 1 (cDC1s) and macrophages, which phagocytose LC fragments containing HSV antigen- a “viral antigen relay”[2]. However, the role of the more prevalent dermal cDC2s in interactions with HSV-infected LCs and Epi-DCs is unknown. Here we defined the interactions of dermal cDC1s and cDC2s with HSV-infected LCs by cyclic immunofluorescence. At 24 h.p.i. we analysed cell clusters in the upper dermis beneath foci of infection and found 19% of these cell clusters contained LCs. Of these “LC clusters” 77% contained CD11c+ cDC2s and 23% contained XCR1+ cDC1s. “Non-LC” clusters contained predominantly CD11c+ cDC2s, which may have included Epi-DCs (to be confirmed). LCs were not observed in the occasional small clusters in regions far from HSV foci or in mock samples. We investigated which chemokines may be responsible for the attraction and clustering of dermal DCs with HSV-infected LCs (and Epi-DCs). Dermal cDC1s expressed higher CXCR3 RNA and surface protein than cDC2s, while cDC2s expressed CCR2 and CCR5 exclusively. HSV-infected LCs and Epi-DCs produced (CXCR3-binding) CXCL9/10, and Epi-DCs also produced increased (CCR5-binding) CCL3/4. By chemotaxis assays we found that cDC1s migrated towards CXCL9/10, while cDC2s migrated towards CXCL9 and a combination of all CXCR3- and CCR5-binding chemokines. Thus, chemokines produced by HSV-infected LCs and Epi-DCs could induce attraction and clustering of both cDC1s and cDC2s. Significance: Dermal DCs play a key role in the stimulation of primary T cell responses, cDC1s cross-present antigens to CD8 T cells and cDC2s primarily stimulate CD4 T cells. Understanding the pathways to stimulate both T cell subsets is critical for designing improved vaccine candidates.