Bell's palsy associated with herpes simplex gingivostomatitis

Nasatzky, E.; Katz, Joseph

doi:10.1016/s1079-2104(98)90174-3

Cited by 9 publications

(4 citation statements)

References 43 publications

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“…An association between HSV and Bell’s palsy has been proposed (176). It has been postulated that reactivation of HSV, in the geniculate ganglion, may result in a lower motor nerve palsy of the facial nerve.…”

Section: Other Diseases Associated With Hsv‐1 Infectionmentioning

confidence: 99%

Herpes Simplex Virus Type 1 infection: overview on relevant clinico‐pathological features*

Arduino

Porter

2007

J Oral Pathology Medicine

332

256

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Herpes Simplex Virus Type 1 (HSV-1) is a nuclear replicating enveloped virus, usually acquired through direct contact with infected lesions or body fluids (typically saliva). The prevalence of HSV-1 infection increases progressively from childhood, the seroprevalence being inversely related to socioeconomic background. Primary HSV-1 infections in children are either asymptomatic or following an incubation period of about 1 week gives rise to mucocutaneous vesicular eruptions. Herpetic gingivostomatitis typically affects the tongue, lips, gingival, buccal mucosa and the hard and soft palate. Most primary oro-facial HSV infection is caused by HSV-1, infection by HSV-2 is increasingly common. Recurrent infections, which occur at variable intervals, typically give rise to vesiculo-ulcerative lesions at mucocutaneous junctions particularly the lips (herpes labialis). Recurrent HSV-1 infection within the mouth is uncommon in otherwise healthy patients, although in immunocompromised patients, recurrent infection can be more extensive and/or aggressive. The diagnosis of common herpetic infection can usually be based upon the clinical history and presenting features. Confirmatory laboratory diagnosis is, however, required when patients are, or may be, immunocompromised.

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Section: Other Diseases Associated With Hsv‐1 Infectionmentioning

confidence: 99%

Herpes Simplex Virus Type 1 infection: overview on relevant clinico‐pathological features*

Arduino

Porter

2007

J Oral Pathology Medicine

332

256

View full text Add to dashboard Cite

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“…Bogger‐Goren [93] reported a case of acute epiglottitis in a child aged 16 months that was caused by HSV, and involvement of the peripheral nervous system or the spinal cord may also be complications resulting from PHGS. Nasatzky and Katz [94] reported a case of Bell's palsy associated with HSV gingivostomatitis. It has been postulated that Bell's palsy results from the replication of HSV in geniculate ganglia, and that axonal spread and multiplication of the reactivated virus leads to inflammation, demyelination and palsy, which usually resolve within 6–8 weeks, although sequelae may occur in some patients.…”

Section: Complications and Recurrent Infectionsmentioning

confidence: 99%

Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis

Kolokotronis

Doumas²

2006

Clinical Microbiology and Infection

117

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Primary herpetic gingivostomatitis (PHGS) represents the clinically apparent pattern of primary herpes simplex virus (HSV) infection, since the vast majority of other primary infections are symptomless. PHGS is caused predominantly by HSV-1 and affects mainly children. Prodromal symptoms, such as fever, anorexia, irritability, malaise and headache, may occur in advance of disease. The disease presents as numerous pin-head vesicles, which rupture rapidly to form painful irregular ulcerations covered by yellow-grey membranes. Sub-mandibular lymphadenitis, halitosis and refusal to drink are usual concomitant findings. Following resolution of the lesions, the virus travels through the nerve endings to the nerve cells serving the affected area, whereupon it enters a latent state. When the host becomes stressed, the virus replicates and migrates in skin, mucosae and, in rare instances, the central nervous system. A range of morbidities, or even mortality, may then occur, i.e., recurrent HSV infections, which are directly or indirectly associated with PHGS. These pathological entities range from the innocuous herpes labialis to life-threatening meningoencephalitis.

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“…All of the in vivo animal studies elicit an acute facial palsy following lytic (primary) HSV1 infection. These studies more closely resemble HSV1-related BP in pediatric patients, who develop their facial palsy in the setting of a primary HSV1 infection (39,40). However, they are less relevant to cases of BP and DFP in adults, who have experienced primary HSV1 infection many years prior to onset of facial palsy (17).…”

Section: Discussionmentioning

confidence: 67%

A Cell Culture Model of Facial Palsy Resulting From Reactivation of Latent Herpes Simplex Type 1

Kuhn¹,

Nayak²,

Camarena³

et al. 2012

Otology &Amp; Neurotology

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Hypothesis Reactivation of herpesvirus type 1 (HSV1) in geniculate ganglion neurons (GGN) is an etiologic mechanism of Bell’s palsy (BP) and delayed facial palsy (DFP) following otologic surgery. Background Several clinical studies, including temporal bone studies, antibody, titers, and intraoperative studies suggest that reactivation of HSV1 from latently infected GGNs may lead to both BP and DFP. However, it is difficult to study these processes in humans or live animals. Methods Primary cultures of GGNs were latently infected with Patton strain HSV1 expressing a green fluorescent protein-late lytic gene chimera. Four days later these cultures were treated with trichostatin A (TSA), a known chemical reactivator of HSV1 in other neurons. Cultures were monitored daily by fluorescent microscopy. Titers of media from lytic, latent, and latent/TSA treated GGN cultures were obtained using plaque assays on Vero cells. RNA was harvested from latently infected GGN cultures and examined for the presence of viral transcripts using reverse-transcription polymerase chain reaction. Results Latently infected GGN cultures displayed latency-associated transcript only, while lytically-infected and reactivated latent cultures produced other viral transcripts. GGN cultures displayed a reactivation rate of 65% after treatment with TSA. Media from latently infected cultures contained no infectious HSV1, while infectious virus was seen in both lytically and latently/TSA treated culture media. Conclusions We have shown that cultured GGNs can be latently infected with HSV1, and HSV1 in these latently infected neurons can be reactivated using TSA, yielding infectious virus. These results have implications for the etiology of both BP and DFP.

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Bell's palsy associated with herpes simplex gingivostomatitis

Cited by 9 publications

References 43 publications

Herpes Simplex Virus Type 1 infection: overview on relevant clinico‐pathological features*

Herpes Simplex Virus Type 1 infection: overview on relevant clinico‐pathological features*

Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis

A Cell Culture Model of Facial Palsy Resulting From Reactivation of Latent Herpes Simplex Type 1

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