Localised herpes simplex virus (HSV-1) infection leads to the activation and expansion of antigen-specific CD8+ T cells and the subsequent generation of a population of tissue-resident memory CD8+ T cells (TRM) that persist in the skin epidermis. CD8+ TRM can provide enhanced protection against reinfection and may prevent viral recrudescence. To directly examine recall responses by HSV-specific skin TRM we induced a stable population of memory CD8+ T cells in the epidermis following non-specific inflammation. Using intravital 2-photon microscopy combined with fluorescent HSV-specific CD8+ TCR transgenic gBT-I T cells and fluorescent HSV constructs, we found that TRM interact with skin cells infected with recrudescent virus and display reduced motility. We imaged the kinetics of effector memory CD8+ T cell (TEM) recruitment from the circulation, using T cells expressing the photoconvertible fluorescent protein KAEDE, and were able to distinguish epidermal TRM from recruited, dermal TEM. We found that TRM remain localized in the epidermis throughout viral recrudescence, whereas recruited TEM were able to circulate in both dermal in epidermal compartments. Finally, to understand the contribution of TEM to the recall response, we depleted circulating TEM and analysed the migratory behaviour of TRM during viral recrudescence in the absence of TEM. Interestingly, we found that TRM interacted dynamically with epidermal HSV-infected keratinocytes and were able to protect against infection while remaining in the epidermis. Here we show previously unappreciated response dynamics of epidermal TRM upon recall during recrudescent viral infection, thus providing further insights into the mechanisms of local protection by memory T cells resident in the skin.