Detection of herpes simplex virus type 1 in human vestibular nuclei

Arbusow, Viktor; Strupp, Michael; Wasicky, R.; Horn, Anja K. E.; Schulz, Peter; Brandt, Thomas

doi:10.1212/wnl.55.6.880

Cited by 50 publications

(32 citation statements)

References 9 publications

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“…It is widely accepted that after primary infection (stomatitis herpetica) HSV-1 ascends to associated sensory ganglia by retrograde axonal transport, e.g., via chorda tympani in the GG and via faciovestibular anastomosis to the VG [Bergström, 1973;Whitley, 1988]. A recent study reported the presence of HSV-1 not only in VGs but also in vestibular nuclei, thus indicating that viral migration can also occur via the vestibular nerve to the pontomedullary brainstem [Arbusow et al, 2000] ( fig. 1).…”

Section: Introductionmentioning

confidence: 99%

HSV-1 Not Only in Human Vestibular Ganglia but Also in the Vestibular Labyrinth

et al. 2001

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Reactivation of herpes simplex virus type 1 (HSV-1) in the vestibular ganglion (VG) is the suspected cause of vestibular neuritis (VN). Recent studies reported the presence of HSV-1 DNA not only in human VGs but also in vestibular nuclei, a finding that indicates the possibility of viral migration to the human vestibular labyrinth. Distribution of HSV-1 DNA was determined in geniculate ganglia, VGs, semicircular canals, and macula organs of 21 randomly obtained human temporal bones by nested PCR. Viral DNA was detected in 48% of the labyrinths, 62% of the VGs, and 57% of the geniculate ganglia. The potential significance of this finding is twofold: (1) Inflammation in VN could also involve the labyrinth and thereby cause acute unilateral vestibular deafferentation. (2) As benign paroxysmal positional vertigo often occurs in patients who have had VN, it could also be a sequel of viral labyrinthitis.

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Section: Introductionmentioning

confidence: 99%

HSV-1 Not Only in Human Vestibular Ganglia but Also in the Vestibular Labyrinth

et al. 2001

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“…A viral etiology of VN is supported by studies showing inflammatory degeneration of the vestibular nerves and the presence of herpes simplex virus 1 (HSV-1) DNA as well as latency-associated transcript (LAT) in the vestibular ganglia (VG) (6)(7)(8)(9). After primary infection, usually occurring via the oral mucosa of the mouth, HSV-1 infects the trigeminal ganglion (TG) and can reach the geniculate ganglion (GG) via the lingual nerve.…”

mentioning

confidence: 99%

“…Reactivation can occur during different diseases such as herpes labialis (TG) and, in rarer cases, Bell's palsy (GG), sudden hearing loss, or vestibular neuritis (VG). Such a reactivation of HSV-1 from the VG has been proposed to cause vestibular neuritis, although final confirmation is still lacking (6)(7)(8)10).…”

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confidence: 99%

Differential Involvement during Latent Herpes Simplex Virus 1 Infection of the Superior and Inferior Divisions of the Vestibular Ganglia: Implications for Vestibular Neuritis

Himmelein

Lindemann

Sinicina

et al. 2017

J Virol

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Controversy still surrounds both the etiology and pathophysiology of vestibular neuritis (VN). Especially uncertain is why the superior vestibular nerve (SVN) is more frequently affected than the inferior vestibular nerve (IVN), which is partially or totally spared. To address this question, we developed an improved method for preparing human vestibular ganglia (VG) and nerve. Subsequently, macro-and microanatomical as well as PCR studies were performed on 38 human ganglia from 38 individuals. The SVN was 2.4 mm longer than the IVN, and in 65% of the cases, the IVN ran in two separate bony canals, which was not the case for the SVN. Anastomoses between the facial and cochlear nerves were more common for the SVN (14/38 and 9/38, respectively) than for the IVN (7/38 and 2/38, respectively). Using reverse transcription-quantitative PCR (RT-qPCR), we found only a few latently herpes simplex virus 1 (HSV-1)-infected VG (18.4%). In cases of two separate neuronal fields, infected neurons were located in the superior part only. In summary, these PCR and micro-and macroanatomical studies provide possible explanations for the high frequency of SVN infection in vestibular neuritis.IMPORTANCE Vestibular neuritis is known to affect the superior part of the vestibular nerve more frequently than the inferior part. The reason for this clinical phenomenon remains unclear. Anatomical differences may play a role, or if latent HSV-1 infection is assumed, the etiology may be due to the different distribution of the infection. To shed further light on this subject, we conducted different macro-and microanatomical studies. We also assessed the presence of HSV-1 in VG and in different sections of the VG. Our findings add new information on the macro-and microanatomy of the VG as well as the pathophysiology of vestibular neuritis. We also show that latent HSV-1 infection of VG neurons is less frequent than previously reported.KEYWORDS HSV-1 latency, human, vestibular ganglia, vestibular neuritis V estibular neuritis (VN) is a common cause of an "acute unilateral vestibulopathy." The main clinical symptoms of VN are acute onset of prolonged severe spinning vertigo with spontaneous horizontal torsional nystagmus toward the unaffected ear, postural imbalance, and nausea (1). Its annual incidence is reported to be 3.5 to 15.5 per population of 100,000 (2, 3). It is the third most common cause of peripheral vestibular

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“…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].…”

Section: Etiology and Pathogenesis Of Pvp: The Evidence So Farmentioning

confidence: 97%