Are latent, immediate-early genes of herpes simplex virus-1 essential in causing trigeminal neuralgia?

Abstract

The etiology and pathogenesis of major trigeminal neuralgia remain largely unknown, but are believed to result from an irritative lesion near the semilunar ganglion. We suggest that its primary cause is a single, active DNA sequence in the persistent but non-integrated genome of latent herpes simplex virus type 1 commonly observed in a few infected A-delta nerve fibers of the cheek. Facial pain occurs as a result of herpes virus reactivation and when supplies of neurotrophins controlling normal transport functions of axolemmal ion channels become depleted.