Abstract
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 and amounts of viral DNA in latently infected lumbosacral spinal ganglia were scored. C239(TK-) established levels of latent infection that were only slightly lower than those found for either a TK rescued variant of this agent or the parent wild-type KOS. However, in contrast to the TK+ viruses, C239(TK-) could not be reactivated when spinal ganglia were cultured in vitro. The results presented show that expression of the viral TK gene plays no major role in establishment of the latent state but that it functions during reactivation of latent virus from explanted ganglia maintained in vitro.
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