Abstract
It has been almost 20 years since herpes simplex virus type 1 (HSV-1) was first shown to establish latent infections in the neurons of sensory ganglia (1). As might be expected, a considerable amount of work on the latent state followed this finding. In spite of the volume of work which has been published, the mechanisms employed by the agent and cell in establishing, maintaining, and reactivating from this state are just now beginning to be understood. The reasons for this extended period of relative ignorance relate principally to the complexities and difficulties of manipulating both virus and host cell. The virus has a complex morphological structure with a unique DNA arrangement, and it replicates in an involved fashion in which there is a temporal appearance of transcripts and protein products that arise from some 72 different viral genes (reviewed in [2]). The host cell is a member of a group of cells which is among the most poorly understood within the mammalian body, and they continue to be difficult to isolate, maintain, and study in vitro.
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© 1990 Plenum Press, New York
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Stevens, J.G. (1990). Transcripts Associated with Herpes Simplex Virus Latency. In: Lopez, C., Mori, R., Roizman, B., Whitley, R.J. (eds) Immunobiology and Prophylaxis of Human Herpesvirus Infections. Advances in Experimental Medicine and Biology, vol 278. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5853-4_20
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DOI: https://doi.org/10.1007/978-1-4684-5853-4_20
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