Paresthesia induced by cutaneous infection with herpes simplex virus in rats.

To assess the effects of herpetic infection on somatic sensations, herpes simplex virus type-1 was inoculated into the unilateral hind paw of the rat and its behavioral responses to noxious pressure and tactile stimulation were examined. Herpetic infection significantly increased the nociceptive threshold of the treated hind paw with a delay around 4 days. The increase in the nociceptive threshold continued at least until post-inoculation day 21 and was larger at night than in the morning. Any alterations in tactile responses were not observed during this period. Herpetic DNA was detected by polymerase chain reaction in the inoculated skin, but not in the dorsal root ganglia on the inoculated side, on the next day after inoculation. But on the following days it was detected in the dorsal root ganglia, but not in the skin. These results suggest that herpetic infection of the dorsal root ganglion produces paresthesia as a functional abnormality of the sensory neurons in rats.