1887

Abstract

Studies with replication-defective mutants of herpes simplex virus (HSV) have defined the minimum requirements for establishment of latency, but their behaviour may not reflect the course of events following infection by wild-type HSV, in which ability to express viral genes has not been precluded by a genetic lesion. To address this issue we devised a strategy for studying establishment of latency by a virulent strain of HSV, based on the distinctive molecular characteristics of latently infected neurons. By combining hybridization for detection of latency-associated transcripts with immunohistochemical analysis of viral proteins we demonstrate here that antigen-positive and latently infected neurons appear synchronously in spinal ganglia during the earliest stages of acute ganglionic infection. This is consistent with early divergence of the molecular pathways leading to productive and latent infection, supporting and extending the results obtained with viral mutants.

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1992-05-01
2022-01-18
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