HERPES-SIMPLEX VIRUS THYMIDINE KINASE AND SPECIFIC STAGES OF LATENCY IN MURINE TRIGEMINAL GANGLIA

From marker rescue, sequencing, transcript, and latency analyses of th e thymidine kinase-negative herpes simplex virus mutant dlsactk and st udies using the thymidine kinase inhibitor Ro 31-5140, we infer that t he virus-encoded thymidine kinase is required in murine trigeminal gan glia for acute replication and lytic gene expression, for increasing t he numbers of cells expressing latency-associated transcripts, and for reactivation from latent infection.