Virus induced cochlear inflammation alters stria vascularis function and auditory development

Human cytomegalovirus (HCMV) is the most common viral infection acquired in utero and a leading cause of sensorineural hearing loss (SNHL). In previous studies utilizing a murine model of SNHL that follows congenital CMV infection (cCMV), virus-induced cochlear inflammation has been shown to result in SNHL that develops in the absence of histopathology in the sensory neuroepithelium but is associated with the dysregulation of a number of deafness related genes (DRG). In this study, virus-induced cochlear inflammation was shown to dysregulate the expression of multiple DRG that have been shown to contribute to ion and metabolite transport within stria vacularis (SV).

In addition, cochlear inflammation in virus-infected mice resulted in the loss of barrier functions of the SV that have also been linked to SNHL. Decreased expression of these DRG in infected animals was associated with SNHL that was similar to that observed in genetically engineered murine models with deletion of these DRG. Together, these results argue that virus-induced inflammation can lead to dysregulation of host genes associated with barrier and ion transport function of the SV, thus providing further insight into potential mechanisms of SNHL that follow virus infections during early auditory development.

The authors would like to thank Dr. Veronica Sanchez for assistance in reviewing the data from these studies. This study was supported by grants from the NIH, NIDCD: (R01DC015980 to WJB and R01DC021649 to KH) and NIAID (5R01AI089956 to WJB).

Department of Microbiology, Heersink School of Medicine, UAB, Birmingham, Ala, USA Department of Otolaryngology, Washington University, St. Louis, Mo, USA Department of Pediatrics, Microbiology, and Neurobiology, Heersink School of Medicine, UAB, Birmingham, Ala, USA The authors declare no competing interests. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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