The American journal of otology · 1998
The etiology of idiopathic sudden sensorineural hearing loss. Experimental herpes simplex virus infection of the inner ear.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Stokroos R J, Albers F W, Schirm J
Аннотация
HYPOTHESIS: Experimentally induced herpes simplex virus type 1 (HSV-1) labyrinthitis provides a suitable model for idiopathic sudden sensorineural hearing loss (ISSHL).
BACKGROUND: Viral labyrinthitis has been postulated to play a role in the pathophysiology of ISSHL. Circumstantial evidence is pointing at members of the herpes virus family. Experimental viral labyrinthitis elicited by various virus families leaves a virus-specific pattern of cochlear damage. Herpes viruses provide the best matching pattern in the distribution of cochlear damage when compared with ISSHL postmortem cochlear histopathology.
METHODS: Herpetic viral labyrinthitis was induced in guinea pigs using perilymphatic inoculation with HSV-1. A control group was inoculated with the culture medium only. Infection was confirmed by the measurement of HSV antibodies. Hearing was monitored. Cochlear damage was evaluated by light and electron microscopy.
RESULTS: In all HSV-1 inoculated animals, rapid loss of hearing occurred. Seroconversion took place, but no systemic manifestations of herpetic infection were observed. The control group showed no cochlear or systemic symptoms. When comparing cochlear histopathology in ISSHL to experimental viral HSV-1 labyrinthitis, strong similarities were found: degeneration of the stria vascularis, destruction of the organ of Corti, loosening of the tectorial membrane, and inflammatory changes in neural structures.
CONCLUSIONS: Based on clinical and histopathologic characteristics, experimental HSV-1 labyrinthitis provides a suitable model of ISSHL.
BACKGROUND: Viral labyrinthitis has been postulated to play a role in the pathophysiology of ISSHL. Circumstantial evidence is pointing at members of the herpes virus family. Experimental viral labyrinthitis elicited by various virus families leaves a virus-specific pattern of cochlear damage. Herpes viruses provide the best matching pattern in the distribution of cochlear damage when compared with ISSHL postmortem cochlear histopathology.
METHODS: Herpetic viral labyrinthitis was induced in guinea pigs using perilymphatic inoculation with HSV-1. A control group was inoculated with the culture medium only. Infection was confirmed by the measurement of HSV antibodies. Hearing was monitored. Cochlear damage was evaluated by light and electron microscopy.
RESULTS: In all HSV-1 inoculated animals, rapid loss of hearing occurred. Seroconversion took place, but no systemic manifestations of herpetic infection were observed. The control group showed no cochlear or systemic symptoms. When comparing cochlear histopathology in ISSHL to experimental viral HSV-1 labyrinthitis, strong similarities were found: degeneration of the stria vascularis, destruction of the organ of Corti, loosening of the tectorial membrane, and inflammatory changes in neural structures.
CONCLUSIONS: Based on clinical and histopathologic characteristics, experimental HSV-1 labyrinthitis provides a suitable model of ISSHL.