Section of the sciatic nerve during the period of herpes simplex virus (HSV) latent infection was performed to evaluate residual latency in mouse dorsal root ganglion. In control mice without sciatic neurectomy, latency was present in 90-100%, while in those which underwent a neurectomy procedure, latent infection was surprisingly decreased to 28-50%. To investigate the hypothesis that the decrease of latency resulted from HSV reactivation and replication (with subsequent neuron destruction), groups of mice were treated with acyclovir to inhibit HSV reactivation, after having undergone a neurectomy procedure. Acyclovir treatment largely prevented the neurectomy-related elimination of latency and supported the hypothesized mechanism.
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