Prevalence of HSV‐1 LAT in Human Trigeminal, Geniculate, and Vestibular Ganglia and Its Implication for Cranial Nerve Syndromes

Abstract

Herpes simplex virus type 1 (HSV-1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV-1 gene expression takes place in the form of latency-associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in allTG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT-PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV-1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG.

Incidence, seasonality and comorbidity in vestibular neuritis

“…Several studies have suggested that a viral agent may be the underlying cause of VN, either by demonstrating the presence of herpes simplex virus DNA within vestibular nerve fibers and "Scarpa's" ganglion or by demonstrating histologic changes within the vestibular nerve suggestive of viral-induced atrophy and inflammation. [11][12][13][14][15] On the other hand, an uncertain proportion of acute peripheral vestibular disorders are likely due to a vascular lesion of the nerve, and patients with such lesions may be at increased risk for future vascular events. [16] One study has suggested that age difference (50 years) plays an important role in differentiating between these two possible pathologies, however we were not able to confirm these results.…”

Glucocorticoids improve acute dizziness symptoms following acute unilateral vestibulopathy

“…The aetiology of vestibular neuritis remains controversial and whilst labyrinthine ischaemia has been proposed, for the majority of patients, the natural history of the condition hints at an inflammatory cause, possibly due to reactivation of neurotropic viruses [2,22]. One study probed the effects of corticosteroids with and without antivirals and concluded that methylprednisolone, but not valacyclovir, improves the recovery of vestibular function in these patients [21].…”

About the pathophysiology of acute unilateral vestibular deficit – vestibular neuritis (VN) or peripheral vestibulopathy (PVP)?

“…The many terms -vestibular neuritis / neuronitis / neuropathy / neuronopathy, acute vestibulopathy, acute vestibular neurolabyrinthitis, acute labyrinthitis 1 -often used interchangeably to describe PVP, testify to the fact that there is still much to be discovered about the nature of the disease.A less disputed issue is the fact that PVP is often preceded by a viral infection of the upper respiratory tract [37] or the higher prevalence (compared to controls) of Herpes viruses in the eighth and other cranial nerves and their neurons [1,12,17,41] as well as in the saliva of patients with PVP [33]. One animal study also supports the etiopathogenetic role of Herpes viruses, but points to histopathological changes in both the vestibular nerve and labyrinth [13].…”