Latent infections in spinal ganglia with thymidine kinase-deficient herpes simplex virus.

摘要: A herpes simplex virus type 1 variant [C239(TK-)] harboring a deletion in the thymidine kinase (TK) gene was assessed for capacity to establish latent infections. Outbred Swiss Webster mice were inoculated on both hind footpads, and numbers of neurons expressing latency-associated transcript amounts viral DNA latently infected lumbosacral spinal ganglia scored. C239(TK-) established levels infection that only slightly lower than those found either TK rescued this agent or parent wild-type KOS. However, contrast TK+ viruses, could not be reactivated when cultured vitro. The results presented show expression plays no major role establishment state but it functions during reactivation from explanted maintained