Whilst these data are consistent with previous work describing decreasing reporter gene expression during latent infection from both HSV-1 promoters and heterologous promoters such as the HCMV MIEP [15, 18–20], the greater loss of luciferase expression during LAT-negative virus infection may indicate: a) that neurons harbouring transcriptionally active HSV-1 are destroyed, or conversely b) that LAT expression may aid the maintenance of gene expression in SC16CMVluc and SC16CMVlucREV viruses over time. The gene discussed is LAT; the disease is disease arising from reactivation of latent virus.