Herpes simplex virus (HSV) evades immune surveillance by expressing ICP47, a protein that binds the transporter associated with antigen presentation (TAP), blocking peptide transport for presentation on MHC I and ultimately recognition by CD8+ T cells. However, the full impact of this evasion on immunity to HSV has been impossible to assess in typical in vivo models because the binding of ICP47 to TAP is species-specific, with the affinity of this interaction being 100 times lower in mice than in humans. To address this gap we have made mice that express human instead of mouse TAP1 and TAP2 (HuTAP). HuTAP mice have a broadly similar immune profile to wild type mice and are able to control HSV infection. However, the ability of activated HSV-specific (gBT-I) CD8+ T cells to protect against HSV replication and lesions was greatly compromised, but not entirely abrogated in HuTAP mice. Importantly, this difference in efficacy of gBT-I cells was not seen when mice were infected with an ICP47 deletion mutant of HSV. Remarkably, the difference in clearance of HSV by CD8+ T cells in wild type and HuTAP mice was seen as early as one day after infection, demonstrating the capacity of these cells for rapid anti-viral activity. Taken together, this new mouse model faithfully renders the role of HSV ICP47 in evading CD8+ T cell reponses and will be an invaluable tool for assessing the impact of cellular immunotherapies that rely on harnessing these cells to treat HSV infections.