Herpes Simplex Virus (HSV) type I causes cold sores but may be associated with severe outcomes like encephalitis. A strong CD8+ T cell response develops following HSV-1 infection, curtailing the acute infection, after which time a latent infection persists. HSV-1 targets the CD8+ T cell response with the protein ICP47, further implying the importance of this arm of immunity. We have evidence ICP47 may be expressed during the establishment of latency, suggesting CD8+ T cell mediated immunity is important at this time. To explore the consequence of making virus-infected cells more visible to CD8+ T cells, we constructed HSV-1 that expresses an extra copy of the immunogenic peptide, gB498-505, which is efficiently presented by MHC-I on the surface of infected cells. This virus also expresses Cre to allow us to track the progression of infection in Cre/lox reporter mice. In this system, β-galactosidase (β-gal) expression is switched on permanently in any cell experiencing HSV-driven Cre expression. Mice infected with this virus mount a normal CD8+ T cell response to HSV-1, and the growth of the virus in vitro and in the skin and sensory ganglia of acutely infected mice was not impaired by the addition of the extra copy of gB498-505. However, mice infected with this virus had fewer β-gal+ cells than the control virus during the establishment phase of latency, although the number of β-gal+ cells was comparable during the acute infection. Further, the extra copy of gB498-505 did not significantly alter the number of cells in which latency is established or the stability of latency. Surprisingly, mice infected with this virus expressing an extra copy of gB498-505 develop significantly larger herpetic lesions than those infected with the control virus, which may be linked to increased immunopathology. Overall, this reveals new roles for CD8+ T cells in HSV-1 pathogenesis.