Background: Sensorineural hearing loss (SNHL) is the most common consequence of congenital cytomegalovirus (CMV) infection, and could result in neurological abnormalities and intellectual and developmental disabilities.
Purpose: To explore the mechanism of murine CMV (MCMV)-induced SNHL in neonatal mice model.
Research design: A repeated measures design was used.
Study sample: Total 72 neonatal BALB/C mice (36 males and 36 females) were randomly divided into two groups.
Data collection and analysis: MCMV suspension (50% tissue culture infective dose = 10(4.15) IU/0.1 ml, 15 μl) or physiological saline was intracranially injected into neonatal mice in the experimental or control group, respectively. Auditory brainstem response (ABR) was measured at three weeks postinjection. At 1, 3, 5, 7, 14, and 21 days postinjection, MCMV-DNA polymerase chain reaction analysis was performed to detect MCMV infection in cochlea, followed by terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling analysis and immunohistochemistry staining.
Results: Extended latency, decreased amplitude, and increased threshold of ABR wave I were observed in the experimental group. Polymerase chain reaction test was positive from 3 to 21 days postinjection in the experimental group and negative at each time point in the control group. The average apoptosis index was higher in the experimental group than that in the control group from 3 to 21 days postinjection (p < 0.01). In addition, compared with the control group, B-cell lymphoma 2 and B-cell lymphoma 2-associated protein ratio was decreased in the experimental group (p < 0.01).
Conclusion: Spiral ganglion neuron apoptosis was an important component of the mechanism of SNHL in MCMV-infected mice.
American Academy of Audiology.