Viral infections are assumed to play an important etiologic role in sudden deafness but most evidence so far has been circumstantial. Correlating the cochlear locations and symptomes of sudden deafness, it is assumed that lesions of stria vascularis, primary neurons and tectorial membrane are able to accout for sudden onset and reversibility of the perceptive deafness.
The survey of the previous reports on the experimental viral labyrinthitis suggests that paramyxoviruses such as mumps and Sendai viruses are the candidate of etiologic agents because of selective involvement of stria vascularis in a rather localized segment of the cochlea.
Serological studies of the patients revealed that seroconversion was most frequent in 5 viral infections, e. g. mumps, rubeola, varicella-zoster, CMV and influenza B.
In addition to primary viral infection, reactivation of herpes virus family is deemed as another possibility of sudden deafness.
Detection of HSV-1 and varicella-zoster virus DNA or RNA in the human spiral ganglia appears a supportive evidence for reactivation of those viruses.