The herpes simplex virus vector 17/LAT-RGUSB has previously been shown to express beta-glucuronidase enzyme activity stably in the trigeminal ganglia and brain stems of beta-glucuronidase-deficient mutant mice. However, the number of beta-glucuronidase expressing cells in trigeminal ganglia latently infected with 17/LAT-RGUSB was smaller than expected. Using normal mice for further characterization of 17/LAT-RGUSB latent infection, no appreciable differences were found between the vector and wild-type virus in: (1) their abilities to replicate in acutely infected ganglia; (2) their abilities to reactivate from latently infected ganglia: or (3) the quantities of viral DNA in tissues during the acute or the latent phases of infection. Using a minor LAT (mLAT)-specific probe to detect transcription by in situ hybridization, it was found that the intensity of the signal from individual cells latently-infected with 17/LAT-RGUSB or wild-type virus was similar. However, the vector-infected ganglia had only 20% as many positive cells as in wild-type infection. These data suggest that 17/LAT-RGUSB virus established latency similarly to wild-type virus, but that the LAT-promoter driven gene expression was compromised.