Demyelination Associated with HSV-1-Induced Facial Paralysis

Wakisaka, Hiroyuki; Hato, Naohito; Honda, Nobumitsu; Takahashi, Hirotaka; Kisaki, Hisanobu; Murakami, Shingo; Gyo, Kiyofumi; Mominoki, Katsumi; Kobayashi, Naoto; Matsuda, Seiji

doi:10.1006/exnr.2002.8035

Cited by 18 publications

(14 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies, however, report an increased risk of MS in HSV-1 infected individuals without the DRB1*15 allele [23]; raising the possibility that this virus may play a role in the development of MS in individuals with a specific genotype. HSV-1 can also induce CNS demyelination in mice with the nature of the demyelinating lesions reported to be dependent on virus strain [24-31], route of infection [32], and mouse strain [33,34]. The mechanisms mediating the mouse strain effect are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

The effect of mouse strain on herpes simplex virus type 1 (HSV-1) infection of the central nervous system (CNS)

2012

View full text Add to dashboard Cite

BackgroundMice infected with HSV-1 can develop lethal encephalitis or virus induced CNS demyelination. Multiple factors affect outcome including route of infection, virus and mouse strain. When infected with a sub-lethal dose of HSV-1 strain 2 via the oral mucosa, susceptible SJL/J, A/J, and PL/J mice develop demyelinating lesions throughout the brain. In contrast, lesions are restricted to the brainstem (BST) in moderately resistant BALB/c mice and are absent in resistant BL/6 mice. The reasons for the strain differences are unknown.MethodsIn this study, we combine histology, immunohistochemistry, and in-situ hybridization to investigate the relationship between virus and the development of lesions during the early stage (< 24 days PI) of demyelination in different strains of mice.ResultsInitially, viral DNA and antigen positive cells appear sequentially in non-contiguous areas throughout the brains of BALB/c, SJL/J, A/J, and PL/J mice but are restricted to an area of the BST of BL/6 mice. In SJL/J, A/J, and PL/J mice, this is followed by the development of 'focal' areas of virus infected neuronal and non-neuronal cells throughout the brain. The 'focal' areas follow a hierarchical order and co-localize with developing demyelinating lesions. When antigen is cleared, viral DNA positive cells can remain in areas of demyelination; consistent with a latent infection. In contrast, 'focal' areas are restricted to the BST of BALB/c mice and do not occur in BL/6 mice.ConclusionsThe results of this study indicate that susceptible mouse strains, infected with HSV-1 via the oral mucosa, develop CNS demyelination during the first 24 days PI in several stages. These include: the initial spread of virus and infection of cells in non-contiguous areas throughout the brain, the development of 'focal' areas of virus infected neuronal and non-neuronal cells, the co-localization of 'focal' areas with developing demyelinating lesions, and latent infection in a number of the lesions. In contrast, the limited demyelination that develops in BALB/c and the lack of demyelination in BL/6 mice correlates with the limited or lack of 'focal' areas of virus infected neuronal and non-neuronal cells in these two strains.

show abstract

Section: Introductionmentioning

confidence: 99%

The effect of mouse strain on herpes simplex virus type 1 (HSV-1) infection of the central nervous system (CNS)

2012

View full text Add to dashboard Cite

show abstract

“…Quantitative PCR showed an increase in HSV-1 DNA copies in the intra-temporal facial nerve from 24 to 72 h, and suggested that HSV-1 infection occurred in the facial nerve, although we did not detect HSV-1 antigens (data not shown). Previously, experimental HSV-1-induced facial palsy has been studied using Balb/c mice and the KOS strain of HSV-1 [6][7][8], and the facial palsy in the mice was transient and improved naturally. The facial palsy in the current study did not improve and the ENoG value was 33%.…”

Section: Discussionmentioning

confidence: 99%

“…Kumagami et al induced complete facial palsy by injecting HSV-1 into the stylomastoid foramen of the facial nerve of rabbits [9]. In the animal disease model, no improvement of the facial palsy was noticed 223 days after [6][7][8]. In that model, the initial HSV-1 infection occurred in the skin and HSV-1 spread to the descending root and geniculate ganglion.…”

Section: Discussionmentioning

confidence: 99%

“…The neuroinvasiveness of HSV-1 is affected by the host strain and HSV-1 strain [14,15], so we modified the animal disease model of Sugita et al and induced more severe facial palsy using Wister rats and the KOS strain of HSV-1 [6][7][8]. In the Wister rats, the facial palsy did not improve naturally, and facial palsy was more severe than that in the mouse model.…”

Section: Discussionmentioning

confidence: 99%

“…Sugita et al successfully introduced acute and transient facial palsy by inoculating HSV-1 onto the auricles of Balb/c mice [6]. In their animal disease model, HSV-1 infected and spread transaxonally to the descending root, geniculate ganglion and facial nucleus, induced demyelination in the descending root, and caused transient facial palsy [7]. This model is useful for elucidating the mechanism underlying the disease [7,8].…”

mentioning

confidence: 99%

See 2 more Smart Citations

Facial paralysis induced by ear inoculation of herpes simplex virus in rat

et al. 2017

Self Cite

View full text Add to dashboard Cite

Role of Nitric Oxide in the Onset of Facial Nerve Palsy by HSV-1 Infection

Hato

Kohno

Yamada

et al. 2013

JAMA Otolaryngol Head Neck Surg

Self Cite

View full text Add to dashboard Cite

These findings suggest that NO produced by inducible NO synthase in the facial nerve plays an important role in the onset of facial palsy caused by HSV-1 infection, which is considered a causative virus of Bell palsy. Hato and colleagues elucidate the role of nitric oxide in HSV-1–related facial nerve paralysis in mice and evaluate the role of edaravone, a free radical scavenger, in preventing the paralysis.

show abstract

Demyelination Associated with HSV-1-Induced Facial Paralysis

Cited by 18 publications

References 19 publications

The effect of mouse strain on herpes simplex virus type 1 (HSV-1) infection of the central nervous system (CNS)

The effect of mouse strain on herpes simplex virus type 1 (HSV-1) infection of the central nervous system (CNS)

Facial paralysis induced by ear inoculation of herpes simplex virus in rat

Role of Nitric Oxide in the Onset of Facial Nerve Palsy by HSV-1 Infection

Contact Info

Product

Resources

About