Auditory and vestibular defects induced by experimental labyrinthitis following herpes simplex virus in mice

Abstract

Conclusion. Our herpes simplex virus (HSV) labyrinthitis mouse model suggests that HSV infection induces vestibular neuritis and sudden deafness. Objective: Viral labyrinthitis has been postulated to play a role in vestibular neuritis and sudden deafness. We established a mouse model to investigate the pathogenesis of HSV-induced labyrinthitis. The relationship between HSV infection and apoptosis in the labyrinth was assessed. Methods: HSV types 1 and 2 were inoculated into the middle ear of mice, and the function of the cochlear and vestibular nerves was assessed. Histopathological changes were examined with hematoxylin and eosin staining. Anti-HSV immunohistochemistry staining and TUNEL staining were done to investigate the relationship between HSV-infected cells and apoptotic cells. Results: Hearing loss and vestibular dysfunction were observed in all mice after inoculation of HSV type 1 or 2. In the cochlear duct, columnar epithelial cells in the stria vascularis were infected with HSV, but only a portion of the infected cells underwent apoptosis. In contrast, many uninfected cells in the spiral organ of Corti were apoptotic. Vestibular dysfunction was observed when vestibular ganglion cells were largely infected, but not apoptotic. These findings recapitulate sudden deafness and vestibular neuritis described in patients.

Keywords::

• Apoptosis
• inner ear
• auditory dysfunction
• vestibular dysfunction

Acknowledgments

This work was supported by a Grant-in-Aid for Scientific Research of Priority Areas from the Ministry of Education, Culture, Sports, Sciences, and Technology of Japan.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.