Experimental Vestibular Neuritis Induced by Herpes Simplex Virus

Hirata, Yoshinari; Sugita, Toshiaki; Gyo, Kiyofumi; Yanagihara, Naoaki

doi:10.3109/00016489309128079

Cited by 28 publications

(16 citation statements)

References 3 publications

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“…Although vestibular ganglia can be virally infected in murine models, with demonstrated vestibular hypofunction, these studies are limited by high animal mortality and difficulty in determining specific cellular triggers in response to infection. [21][22][23] The vast majority of relevant studies have focused on the reactivation of latent viruses, particularly on (the neurotrophic virus) herpes simplex virus type 1. Furuta et al studied 26 autopsied human vestibular ganglia and found herpes simplex virus type 1 DNA in 6 of 10 ganglia analysed by polymerase chain reaction.…”

Section: Discussionmentioning

confidence: 99%

Investigation of seasonal variability of vestibular neuronitis

2013

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Section: Discussionmentioning

confidence: 99%

Investigation of seasonal variability of vestibular neuronitis

2013

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“…We used 4-5-weekold male ICR mice (Korean Laboratory Animal Research Center) for this study. By using the method of Hirata et al [15], we scratched the earlobes of the mice with a needle and then inoculated them with 10 6 pfu/mL of HSV-1 (F strain). Virus inoculation was done 2 times 10 days apart, which was followed by 16 weeks of observation [16].…”

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confidence: 99%

Expression of Th2 Cytokines Decreases the Development of and Improves Behçet's Disease–Like Symptoms Induced by Herpes Simplex Virus in Mice

et al. 2001

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In the etiology of Behçet's disease (BD), viral infection has long been postulated as a contributing factor, and viral involvement has been demonstrated. However, viral infection alone is not sufficient to explain the pathogenesis of BD, and some evidence suggests that immunologic abnormalities are also important. To study the possible role of immune regulation in the development of BD-like symptoms induced by herpes simplex virus inoculation in ICR mice, macrophages were deleted by use of liposome-encapsulated clodronate (lip-Cl(2)MDP). Treatment with lip-Cl(2)MDP suppressed the development of BD-like symptoms, and this suppression was correlated with the induction of interleukin-4 expression in mouse spleens. When the Th2 adjuvant ovalbumin (OVA)-alum was injected into mice with BD-like symptoms, their cutaneous symptoms improved. Adoptive transfer with splenocytes from OVA-alum-injected mice also resulted in improvement. These findings suggest that up-regulated Th2 cytokine expression can attenuate the development of and improve some BD-like symptoms.

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“…Vestibular ganglia can be primarily infected with HSV1 in murine models, leading to peripheral vestibulopathy in these animals 5–7. These models are marked by high animal mortality and difficulties pursuant upon working with an in vivo model system in terms of determining cellular triggers and intracellular signaling mechanisms that lead to HSV1 reactivation.…”

Section: Introductionmentioning

confidence: 99%

Cultured vestibular ganglion neurons demonstrate latent HSV1 reactivation

et al. 2011

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Objectives/Hypothesis Vestibular neuritis is a common cause of both acute and chronic vestibular dysfunction. Multiple pathologies have been hypothesized to be the causative agent of vestibular neuritis; however, whether herpes simplex type I (HSV1) reactivation occurs within the vestibular ganglion has not been demonstrated previously by experimental evidence. We developed an in vitro system to study HSV1 infection of vestibular ganglion neurons (VGNs) using a cell culture model system. Study design basic science study. Results Lytic infection of cultured rat VGNs was observed following low viral multiplicity of infection (MOI). Inclusion of acyclovir suppressed lytic replication and allowed latency to be established. Upon removal of acyclovir, latent infection was confirmed with reverse-transcription polymerase chain reaction and by RNA fluorescent in situ hybridization for the latency-associated transcript (LAT). 29% cells in latently infected cultures were LAT positive. The lytic IPC27 transcript was not detected by reverse-transcription polymerase chain reaction (RT-PCR). Reactivation of HSV1 occurred at a high frequency in latently infected cultures following treatment with trichostatin A (TSA), a histone deactylase inhibitor. Conclusions VGNs can be both lytically and latently infected with HSV1. Furthermore, latently infected VGNs can be induced to reactivate using TSA. This demonstrates that reactivation of latent HSV1 infection in the vestibular ganglion can occur in a cell culture model, and suggests that reactivation of HSV1 infection a plausible etiologic mechanism of vestibular neuritis.

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Experimental Vestibular Neuritis Induced by Herpes Simplex Virus

Cited by 28 publications

References 3 publications

Investigation of seasonal variability of vestibular neuronitis

Investigation of seasonal variability of vestibular neuronitis

Expression of Th2 Cytokines Decreases the Development of and Improves Behçet's Disease–Like Symptoms Induced by Herpes Simplex Virus in Mice

Cultured vestibular ganglion neurons demonstrate latent HSV1 reactivation

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