The Implication of Viruses in Idiopathic Sudden Hearing Loss: Primary Infection or Reactivation of Latent Viruses?

Veltri, Robert W.; Wilson, William R.; Sprinkle, Philip M.; Rodman, Susan M.; Kavesh, Debra A.

doi:10.1177/019459988108900129

Cited by 88 publications

(44 citation statements)

References 12 publications

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“…We demonstrated that there is an association between VZV, CVB5 and influenza B and inner ear diseases, especially among patients with SSHL, in line with some previous works. Our results are in line with Veltri et al [77] , who investigated 77 patients with SSHL and seroconversion reactions [77] . After testing 15 different viruses, they observed an incidence of 65% for significant seroconversions to one or more of them.…”

Section: Comments On the Resultssupporting

confidence: 93%

Do Viruses Cause Inner Ear Disturbances?

Pyykkö

Zou

2008

ORL

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The association of viral infection to inner ear disease is controversial. Experiments on animals show that several viruses are capable of causing hearing loss, if applied into the perilymph. Some of these have specific affinity to the cellular type of the inner ear, as sensory epithelia and cochlear nerve. Some viruses as adenoviruses and Coxsackie virus B have specific CAR receptors that are identified in different cell types, whereas other act by attaching onto nonspecific cellular surface receptors. Some viruses such as varicella zoster virus (VZV) do not cause disease in rodents. We assessed 273 patients with clinical, serological, neuro-otologic and endoscopic evaluations. Of the 273 patients, 43 served as control subjects. The patients either had Ménière’s disease (n = 158), recurrent vertigo of unknown etiology (n = 56), or hearing loss (n = 17). Antibodies against neurotropic and common viruses were evaluated. VZV, influenza B, CBV5 and RSV titers were significantly elevated in patients with inner ear disease when compared with the control group. In analyzing the internal relationship, VZV and influenza B were intercorrelated. We did not find a correlation between hearing loss and viral titers. In conclusion, VZV, Coxsackie virus B5 and influenza B virus may be the main causes of inner ear disorder. The spiral and Scarpa’s ganglion are potential sites harboring viral DNA for possible latent infection.

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Section: Comments On the Resultssupporting

confidence: 93%

Do Viruses Cause Inner Ear Disturbances?

Pyykkö

Zou

2008

ORL

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“…However, viral etiology has been a popular causative theory in recent years. The proposed viral hypothesis includes direct viral invasion of the fluid and soft tissues of the cochlea (cochleitis) or SGNs (neuritis), reactivation of a latent virus within a spiral ganglion, and an indirect immune-mediated mechanism [6,7]. Viral etiology of ISSHL has received a variety of support from temporal bone analysis and clinical characteristics.…”

Section: Discussionmentioning

confidence: 99%

“…A few kinds of viruses, such as mumps, measles, and rubella, have been shown to be associated with ISSHL by sensitive serological techniques, such as polymerase chain reaction (PCR) and immunoglobulin titers [7,8,9]. However, the decline of the incidence of these virus infections due to worldwide immunization against them has not decreased the incidence of ISSHL [10].…”

Section: Introductionmentioning

confidence: 99%

A Cell Culture Model of Latent and Lytic Herpes Simplex Virus Type 1 Infection in Spiral Ganglion

Liu¹,

Li²

2015

ORL

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Purpose of the Study: Reactivation of latent herpes simplex virus type 1 (HSV-1) in spiral ganglion neurons (SGNs) is supposed to be one of the causes of idiopathic sudden sensorineural hearing loss. This study aims to establish a cell culture model of latent and lytic HSV-1 infection in spiral ganglia. Procedures: In the presence of acyclovir, primary cultures of SGNs were latently infected with HSV-1 expressing green fluorescent protein. Four days later, these cells were treated with trichostatin A (TSA), a known chemical reactivator of HSV-1. TCID₅₀ was used to measure the titers of virus in cultures on Vero cells. RNA from cultures was detected for the presence of transcripts of ICP27 and latency-associated transcript (LAT) using reverse transcription polymerase chain reaction. Results: There is no detectable infectious HSV-1 in latently infected cultures, whereas they could be observed in both lytically infected and latently infected/TSA-treated cultures. LAT was the only detectable transcript during latent infection, whereas lytic ICP27 transcript was detected in lytically infected and latently infected/TSA-treated cultures. Conclusion: Cultured SGNs can be both latently and lytically infected with HSV-1. Furthermore, latently infected SGNs can be reactivated using TSA, yielding infectious virus.

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“…Wilson [2] hatte bei 7,4% (n = 122) eine Serokonversion für anti-HSV-1-Antikörper und bei 5,0% der Patienten für anti-VZV-Antikörper nachgewiesen. Damit korrespondierend fanden auch Veltri et al [22] bei 8% (n = 77) einen Anstieg von anti-HSV-Antikörpern.…”

Section: Diskussionunclassified

Herpesviren bei akuter Innenohr-schwerhörigkeit und «Vestibularisausfall»: klinische und serologische Befunde

Walther

Hentschel

Oehme

et al. 2002

Otorhinolaryngol Nova

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Ziel: In der vorliegenden Studie erfolgte die statistische Evaluierung klinischer Befunde auf der Grundlage der spezifischen Prävalenzen von IgG-, IgM- und IgA-Antikörpern gegen Herpes-simplex-Viren (HSV) und Varicella-zoster-Viren (VZV) in Serum bei Patienten mit akuter Innenohrschwerhörigkeit und akutem isoliertem peripherem Vestibularisausfall. Patienten und Methoden: Untersucht wurden Patienten mit akuter Innenohrschwerhörigkeit (HSV: n = 150, VZV: n = 104) und Vestibularisausfall (HSV: n = 60, VZV: n = 45), die sich zwischen 1996 und 2000 in stationärer Behandlung an der Universitäts-HNO-Klinik Jena befunden hatten. Die Seroprävalenzen wurden mittels ELISA (Dade Behring Enzygnost^®-anti-HSV und -anti-VZV) ermittelt. Anamnestische Angaben und klinische Befunde von seropositiven wurden denen von seronegativen Patienten gegenübergestellt und statistisch analysiert. Ergebnisse: Der Grossteil (87,3%) der Patienten mit einem «Hörsturz» hatten erhöhte IgG-Titer gegen HSV, 9,3% waren gleichzeitig IgM-positiv. Die IgG-Prävalenz für VZV betrug 98,1%. Gut 4,8% waren IgM-positiv, 24% hatten eine erhöhte IgA-Konzentration, 2,9% waren IgM- und IgA-positiv. Bei Patienten mit Vestibularisausfall waren 90% HSV-IgG-positiv und 3,3% gleichzeitig IgM-positiv. Bei 100% war das VZV-IgG erhöht; 15,6% waren VZV-IgA-positiv, darunter 2 auch IgM-positiv. Die Altersverteilung der Patienten mit serologischem Hinweis auf eine HSV- oder VZV-Reaktivierung war zweigipfelig. Patienten mit eine «Hörsturz» mit möglicher HSV-Reaktivierung zeigten signifikant öfter Rezidiverkrankungen (36 versus 12%) sowie Ohrschmerz und Ohrdruck (21 versus 7%). Bei anti-VZV-IgA-positiven Erkrankten mit Vestibularisausfall lag häufiger eine Rezidiverkrankung (14 versus 5%) sowie ein vollständiger Erregbarkeitsausfall in der kalorischen Prüfung (71 versus 45%) vor. Schlussfolgerungen: Das Vorliegen einer Rezidiverkrankung und Ohrdruck bei akuter Innenohrschwerhörigkeit können Hinweise für eine HSV-Reaktivierung sein, Kopfschmerzen und ein Rezidivereignis bei Vestibularisausfall können für eine VZV-Reaktivierung sprechen.

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The Implication of Viruses in Idiopathic Sudden Hearing Loss: Primary Infection or Reactivation of Latent Viruses?

Cited by 88 publications

References 12 publications

Do Viruses Cause Inner Ear Disturbances?

Do Viruses Cause Inner Ear Disturbances?

A Cell Culture Model of Latent and Lytic Herpes Simplex Virus Type 1 Infection in Spiral Ganglion

Herpesviren bei akuter Innenohr-schwerhörigkeit und «Vestibularisausfall»: klinische und serologische Befunde

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