Herpes simplex virus infection induces a selective increase in the proportion of galanin-positive neurons in mouse sensory ganglia.

We examined the effects of herpes simplex virus type 2 (HSV-2) infection on host neuropeptide content in mouse dorsal root ganglia (DRG) neurons following unilateral hind footpad inoculation. At selected survival times following infection, adjacent tissue sections of decalcified spine containing the paired 4th and 5th lumbar DRGs were immunoreacted to detect HSV-2, calcitonin gene-related peptide (CGRP), or galanin antigen. Labeled and unlabeled neurons were counted and the somal areas for all neurons in the infected and the contralateral uninfected DRG in each mouse were compared. HSV-positive neurons were small. HSV-2 antigen was present in neurons at Day 5; by Day 14 the antigen had disappeared. Galanin positivity was first seen at Day 8, peaked at Day 14, gradually declined on Days 21 and 28, and returned to control values by Day 42. The mean soma size of the labeled population was small. Galanin antigen was not seen in DRG at any time following sham inoculation. At all times after infection, equal numbers of CGRP-positive neurons were seen in infected and uninfected ganglia and in sham-operated mice. These results show that HSV-2 infection differentially affects host neuropeptide production and that nervous system effects are not restricted to the acute stage of infection. These events are consistent with those seen in other injury/regeneration paradigms.