We previously demonstrated that HSV-1 preferentially establishes latent infection of murine sensory ganglia in A5+ neurons and HSV-2 preferentially establishes latent infection in KH10+ neurons, as identified by dual fluorescent in situ hybridization (FISH) for LAT and immunofluorescent (IF) staining with mAbs A5 and KH10 for neuronal markers [2], [3]. The gene discussed is LAT; the disease is disease arising from reactivation of latent virus.