Reactivation of herpes simplex virus type 1 (HSV-1) from neurons in sensory ganglia such as the trigeminal ganglia (TG) is influenced by virus-specific CD8+ T cells that infiltrate the ganglia at the onset of latency and contract to a stable activated tissue resident memory population. In C57Bl/6 mice, half of HSV-specific CD8+ T cells (gB-CD8s) recognize one dominant epitope on glycoprotein B (gB498-505), while the remainder (non-gB-CD8s) recognize 19 subdominant epitopes from 12 viral proteins. To address how expression by HSV-1 influences the formation and ganglionic retention of CD8+ T cell populations, we developed recombinant HSV-1 with the native immunodominant gB epitope disrupted, but then expressed ectopically from different viral promoters. Epitope expressed from the gB promoter restored full gB-CD8 immunodominance to 50%. Intriguingly, earlier expression from constitutive, immediate early and early promoters did not significantly increase immunodominance, indicating these promoters cannot elicit more than half of the CD8 compartment. Epitope expressed from candidate viral promoters of "true late" HSV-1 genes either delayed or reduced the priming efficiency of gB-CD8s and their levels in the TG at early times. HSV expressing the epitope from the full latency-associated transcript promoter did not efficiently prime gB-CD8s; however, gB-CD8s primed by a concurrent wild type flank infection infiltrated the TG and were retained long term at low levels, suggesting latent epitope expression is sufficient to retain gB-CD8s. Taken together the data indicate that viral promoters shape latent HSV-1 specific CD8+ T cell populations, and should be an important consideration in future vaccine design. [ABSTRACT FROM AUTHOR]