Herpes simplex viruses (HSV) are highly successful human pathogens that have long provided the paradigm for latency/reactivation as a strategy for survival in a host population. It is now clear that HSV lytic gene transcription persists at a low level into latency, but whether this leads to protein production has not been shown. We examined HSV activity during the establishment of HSV latency in mice (between 5 and 30 days after infection) and then later using a mouse model in which LacZ expression is switched on permanently in cells experiencing HSV-driven Cre recombinase expression. A panel of viruses with Cre under the control of various promoters in HSV enabled counting of infected sensory neurons that had experienced different types of HSV activity: Entry of a virus genome was examined by driving Cre from the CMV IE promoter and we chose four lytic gene promoters (ICP0, ICP47, RR1 and gB) to track expression of these HSV genes. Surprisingly, the appearance of marked neurons and spread of virus to sensory ganglia not innervating the infected dermatome continued to increase for 5-6 days beyond the time when infectious virus load peaked. In addition the promoters for ICP47, RR1 and gB (an immediate early, an early and a late gene, respectively), but not ICP0 (a second immediate early gene) were active and able to drive Cre protein expression during latency. ICP47 was especially interesting, being highly active during the establishment of latency. These data suggest that i) the traditional kinetic classes of HSV genes are a poor guide to HSV gene expression in neurons in vivo and ii) residual lytic gene expression leads to protein production, providing antigen to drive ongoing adaptive immune responses. We conclude that lytic gene expression needs to be understood as a part of any unified model of HSV latency.