Reactivation of the virus in the trigeminal ganglion seeds to the oral or nasal mucosae, most commonly at the vermillion border of the lip, to produce characteristic vesicles.
During primary infection, virus enters sensory nerve terminals and is transported retrogradely via axons to neuronal cell bodies i n the trigeminal ganglion where latency is established (see below).
The pain usually commences in the maxillary and mandibular divisions of the trigeminal nerve and in less than 5% of cases begins in the ophthalmic division.
In these studies it has been shown that vocalizations can be elicited from cranial nuclei in the brainstem, such as the solitary nucleus, trigeminal motor nucleus, and the reticular formation.
We focused our studies particularly on the trigeminal ganglion, a cranial sensory ganglion that receives a contribution from neural crest cells derived from the midbrain and rostral hindbrain.
These investigators found latent viral genomes in about 3% of sensory neurons in positive trigeminal ganglia and calculated that the average copy number of latent genomes per cell was 16.
After over-expression by electroporation into the cranial neural tube and neural crest, we observed a marked redistribution of electroporated neural crest cells in the vicinity of the trigeminal ganglion.
Expressing the gene in neural crest cells by electroporation, inhibits migration of neural crest cells into the trigeminal ganglia, and prevents differentiation into neurons or other differentiated cells.
