Zika virus infection causes widespread damage to the inner ear

Area of Science:

• Virology
• Neuroscience
• Otolaryngology

Background:

• Zika virus (ZIKV) is linked to neurological issues, including microcephaly in newborns.
• Hearing loss is an emerging comorbidity of ZIKV infection in both prenatal and adult cases.
• Previous studies showed diminished hearing in prenatal ZIKV infection mouse models without cellular damage.

Purpose of the Study:

• To investigate the effects of ZIKV on inner ear cellular integrity and protein expression in adult mice.
• To identify molecular and morphological damage in the cochlea and vestibular organs following ZIKV infection.

Main Methods:

• Infection of type I interferon receptor null (Ifnar1-/-) mice at 5-6 weeks of age with ZIKV.
• Detection of ZIKV antigens in cochlear tissues using immunohistochemistry.
• Analysis of gene expression changes related to cell damage, fluid transport, immune response, and gaseous transmitters.
• Morphological examination of cochlear and vestibular structures.

Main Results:

• ZIKV antigens were found in multiple cochlear cell types, including the cochlear epithelium, lateral wall, spiral limbus, and spiral ganglion.
• ZIKV infection altered the expression of genes involved in cell damage (S100B), fluid transport (AQP1), gaseous transmission (eNOs), and immune response (F4/80).
• Morphological analysis revealed compromised cochlear structures and damage in vestibular end organs, with a graded distribution of damage along the cochlear tonotopic axis.

Conclusions:

• ZIKV infection induces molecular and morphological damage to the inner ear in adult mice.
• The findings provide the first evidence of ZIKV-induced inner ear damage in adults.
• These cellular consequences offer potential mechanisms for hearing loss observed in human ZIKV infections.