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Updated: Jan 20, 2026
Virus-Mediated Gene Transfer Into the Mouse Dorsal Cochlear Nucleus for Light-Induced Auditory Stimulation
Published on: August 29, 2025
Virus-induced cochlear inflammation in newborn mice alters auditory function
Cathy Yea Won Sung1, Maria C Seleme2, Shelby Payne3
1Department of Microbiology and.
Abstract:
Although human cytomegalovirus (HCMV) is a known cause of sensorineural hearing loss in infants with congenital HCMV (cCMV) infections, mechanisms that contribute to sensorineural hearing loss (SNHL) in infants with cCMV infection are not well defined. Using a murine model of CMV infection during auditory development, we have shown that peripheral infection of newborn mice with murine CMV (MCMV) results in focal infection of the cochlea and virus-induced cochlear inflammation. Approximately 50%-60% of infected mice exhibited increased auditory brainstem response (ABR) thresholds across a range of sound frequencies. Histological analyses of the cochlea in MCMV-infected mice with elevated ABR thresholds revealed preservation of hair cell (HC) number and morphology in the organ of Corti. In contrast, the number of spiral ganglion neurons (SGN), synapses, and neurites connecting the cochlear HC and SGN nerve terminals were decreased. Decreasing cochlear inflammation by corticosteroid treatment of MCMV-infected mice resulted in preservation of SGN and improved auditory function. These findings show that virus-induced cochlear inflammation during early auditory development, rather than direct virus-mediated damage, could contribute to histopathology in the cochlea and altered auditory function without significant loss of HCs in the sensory epithelium.
Insights
Congenital cytomegalovirus (CMV) infection can cause hearing loss. In mice, CMV-induced cochlear inflammation, not direct viral damage, led to sensorineural hearing loss by damaging spiral ganglion neurons.
Area of Science:
- Otolaryngology
- Virology
- Neuroscience
Background:
- Human cytomegalovirus (HCMV) is a leading cause of congenital sensorineural hearing loss (SNHL).
- Mechanisms underlying SNHL in congenital HCMV (cCMV) infections remain unclear.
- Murine cytomegalovirus (MCMV) models offer insights into auditory development and CMV-induced hearing impairment.
Purpose of the Study:
- To investigate the mechanisms of sensorineural hearing loss (SNHL) in a murine model of congenital cytomegalovirus (CMV) infection.
- To determine the role of cochlear inflammation and direct viral damage in auditory dysfunction.
- To assess the impact of inflammation on cochlear structures like hair cells and spiral ganglion neurons.
Main Methods:
- Utilized a murine model of MCMV infection during the critical period of auditory development.
- Assessed auditory function using auditory brainstem response (ABR) threshold measurements.
- Performed histological analyses of cochlear tissues to evaluate hair cell (HC) and spiral ganglion neuron (SGN) integrity.
- Investigated the therapeutic effect of corticosteroid treatment on cochlear inflammation and auditory function.
Main Results:
- MCMV infection led to focal cochlear inflammation and SNHL in 50%-60% of infected mice.
- Histological analysis revealed preserved hair cells but decreased spiral ganglion neurons, synapses, and neurites.
- Corticosteroid treatment reduced cochlear inflammation, preserved SGNs, and improved auditory function.
- These findings indicate inflammation, not direct viral damage, is a key factor in MCMV-induced SNHL.
Conclusions:
- Virus-induced cochlear inflammation during early auditory development contributes significantly to SNHL in congenital CMV infections.
- Damage to spiral ganglion neurons and their connections, rather than hair cell loss, is a primary pathology.
- Targeting cochlear inflammation may be a therapeutic strategy to prevent or mitigate hearing loss in infants with cCMV.
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