Detection of Varicella-Zoster Virus DNA in Human Geniculate Ganglia by Polymerase Chain Reaction

Furuta, Yasushi; Takasu, Toshiyuki; Fukuda, Satoshi; Sato‐Matsumura, Kazuko C.; Inuyama, Yukio; Hondo, Ryo; Nagashima, Kazuo

doi:10.1093/infdis/166.5.1157

Cited by 90 publications

(49 citation statements)

References 10 publications

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“…The cell bodies of the sensory fibers are in the geniculate ganglion, and some afferent fibers supply the mucous membranes of the oropharynx and the skin of the external auditory meatus and around the ear. VZV reactivation in the geniculate ganglia and subsequent inflammation of the facial nerve in the temporal bone are suspected to cause facial palsy (2,8), while VZV migrates from the geniculate ganglia into the skin around the ear or into the oropharynx via the sensory fibers, where it replicates and produces zoster in RHS. In the present study, VZV DNA tended to be detectable in saliva from RHS patients who had zoster in the oropharyngeal epithelium, and the saliva from these patients contained a high copy number of the viral DNA.…”

Section: Discussionmentioning

confidence: 99%

Quantitation of Varicella-Zoster Virus DNA in Patients with Ramsay Hunt Syndrome and Zoster Sine Herpete

Furuta¹,

Ohtani²,

Sawa

et al. 2001

J Clin Microbiol

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Varicella-zoster virus (VZV) reactivation causes facial nerve palsy in Ramsay Hunt syndrome (RHS) and zoster sine herpete (ZSH) with and without zoster rash, respectively. In the present study, we analyzed the VZV DNA copy number in saliva samples from 25 patients with RHS and 31 patients with ZSH using a TaqMan PCR assay to determine differences in the viral load between the two diseases. VZV copy number in saliva peaked near the day of the appearance of zoster in patients with RHS. Consequently, VZV DNA was less frequently detected in patients with RHS who exhibited facial palsy several days after the appearance of zoster. These findings suggest that the VZV load in saliva samples reflects the kinetics of viral reactivation in patients with RHS. In addition, VZV DNA was equally detected in saliva from patients with RHS and ZSH, and there was no significant difference in the highest viral copy number between patients with RHS and those with ZSH. The VZV load does not appear to reflect a major difference between RHS and ZSH.Ramsay Hunt syndrome (RHS) is a varicella-zoster virus (VZV)-associated neurological disease, characterized by zoster around the ears or in the oropharynx and by acute peripheral facial palsy. In addition, RHS is frequently complicated by a disorder of the eighth cranial nerve. Facial palsy and zoster do not always appear simultaneously, and some patients with RHS exhibit facial palsy several days before or after the onset of zoster. VZV also causes acute peripheral facial palsy with the absence of skin lesions; such cases are termed zoster sine herpete (ZSH) and are usually diagnosed using serological assays (11) or PCR (3, 12, 13). Although VZV reactivation causes facial nerve disorder in both RHS and ZSH, no study has analyzed the difference in virological background between these two diseases. One hypothesis to explain the presence or absence of mucocutaneous lesions (zoster) is that the VZV load is higher in RHS than in ZSH.Only a few studies have investigated the VZV load in patients with varicella and zoster. Studies using a TaqMan-based PCR assay have reported that the viral copy number of peripheral blood mononuclear cells (PBMCs) in patients with varicella was higher than that in patients with zoster (6, 10). However, in these studies, VZV DNA was detected in PBMCs from only 20% of patients with zoster. In addition, it has been demonstrated that VZV DNA was not detected in PBMCs from patients with ZSH (3). Judging from these reports, an analysis of PBMCs does not provide a useful measure of the VZV load in facial palsy patients.Since it has been reported that VZV DNA is detectable in saliva samples from 58 to 59% of patients with RHS and ZSH (4), we employed a TaqMan PCR assay of DNAs from saliva samples for quantitation of VZV DNA and initially analyzed whether the viral copy number in saliva reflects the kinetics of VZV reactivation. We then compared the viral load between RHS and ZSH. MATERIALS AND METHODSPatient samples. Twenty-five patients with RHS and 31 patients with ZSH wer...

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Section: Discussionmentioning

confidence: 99%

Quantitation of Varicella-Zoster Virus DNA in Patients with Ramsay Hunt Syndrome and Zoster Sine Herpete

Furuta¹,

Ohtani²,

Sawa

et al. 2001

J Clin Microbiol

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“…This is demonstrated by the reactivation of VZV in these individuals as herpes zoster and by the presence of VZV DNA and proteins in ganglia recovered at autopsy (2,3,5,9,10,12,13,15,16,19,20,(22)(23)(24)26). Different laboratories have ascribed the site of latency to either neurons (12-14, 18, 22) or perineuronal satellite cells (5,26); some laboratories suggest that neurons are the primary site of latency together with a smaller proportion of satellite cells containing the VZV genome (16,20).…”

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confidence: 99%

Varicella-Zoster Virus DNA in Cells Isolated from Human Trigeminal Ganglia

Levin

Cai

Manchak

et al. 2003

J Virol

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To determine the type of cell(s) that contain latent varicella-zoster virus (VZV) DNA, we prepared pure populations of neurons and satellite cells from trigeminal ganglia of 18 humans who had previously had a VZV infection. VZV DNA was present in 34 of 2,226 neurons (1.5%) and in none of 20,700 satellite cells. There was an average of 4.7 (range of 2 to 9) copies of VZV DNA per latently infected neuron. Latent VZV DNA was primarily present in large neurons, whereas the size distribution of herpes simplex virus DNA was markedly different.Varicella-zoster virus (VZV) is present in a latent form in sensory ganglia of humans who have had a primary infection (varicella) with VZV (11). This is demonstrated by the reactivation of VZV in these individuals as herpes zoster and by the presence of VZV DNA and proteins in ganglia recovered at autopsy (2,3,5,9,10,12,13,15,16,19,20,(22)(23)(24)26). Different laboratories have ascribed the site of latency to either neurons (12-14, 18, 22) or perineuronal satellite cells (5, 26); some laboratories suggest that neurons are the primary site of latency together with a smaller proportion of satellite cells containing the VZV genome (16,20). The primary aim of the experiments described here was to determine the type of cell in trigeminal ganglia that harbors latent VZV and also to obtain data on the proportion of these cells that contain latent VZV. One reason why the site of VZV latency has remained an open question is that neurons and satellite-supporting cells are tightly associated in ganglia and the in situ methods used to locate VZV DNA did not clearly resolve the source of the hybridization signal. This resolution was easier for latent HSV because a strong hybridization signal to HSV facilitated its localization to the nucleus of the neuron. In contrast, the hybridization signal from VZV DNA is considerably weaker and dispersed over both nucleus and cytoplasm. While the hybridization methodology has improved, these considerations remain (21, 30). To reduce the ambiguities inherent in the in situ methods, we developed a procedure to separate cell types prior to analysis. The separation procedure has been verified with a study of HSV (1). This report presents data on the cellular localization of latent VZV, the frequency of latency, and the number of viral genomes present in latent cells.

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“…In patients of RHS, VZV reactivation occurs in the geniculate ganglion and the subsequent neuritis may result in facial nerve palsy [9]. On the other hand, in cases of lower cranial polyneuropathy caused by VZV infection, as in this case, inflammation may occur in the nuclei of the affected nerves.…”

Section: Discussionmentioning

confidence: 88%

Varicella Zoster Virus Infection of the Pharynx and Larynx without Vocal Cord Palsy

Kim¹,

Shim²

2018

Korean J Otorhinolaryngol-Head Neck Surg

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We report a patient with significant weakness of the left soft palate, paralysis of the left vocal cord, and left facial nerve palsy. Although the patient showed no herpetic eruption in the pharyngolaryngeal mucosa and auricle skin, reactivation of varicella zoster virus (VZV) was confirmed by serological examination. She was diagnosed with zoster sine herpete. After treatment with antiviral drugs and corticosteroids, her neurological disorder improved completely. When we encounter a patient with associated laryngeal paralysis, we should consider the possibility of reactivation of VZV even when no typical herpetic eruption is observed.

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Detection of Varicella-Zoster Virus DNA in Human Geniculate Ganglia by Polymerase Chain Reaction

Cited by 90 publications

References 10 publications

Quantitation of Varicella-Zoster Virus DNA in Patients with Ramsay Hunt Syndrome and Zoster Sine Herpete

Quantitation of Varicella-Zoster Virus DNA in Patients with Ramsay Hunt Syndrome and Zoster Sine Herpete

Varicella-Zoster Virus DNA in Cells Isolated from Human Trigeminal Ganglia

Varicella Zoster Virus Infection of the Pharynx and Larynx without Vocal Cord Palsy

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