Embryonic and Neonatal Mouse Cochleae Are Susceptible to Zika Virus Infection
Autor: | Nabilah H. Sammudin, Donna M. Fekete, Vidhya Munnamalai, Caryl A. Young, Richard J. Kuhn, Ankita Thawani |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Cochlear Diseases
Cellular differentiation cochlea Biology Antibodies Viral Microbiology hair cell Article Zika virus Embryo Culture Techniques Mice Organ Culture Techniques Virology Proto-Oncogene Proteins medicine otorhinolaryngologic diseases Animals Progenitor cell Cochlea ZIKV Fetus Cell Death Zika Virus Infection Receptor Protein-Tyrosine Kinases biology.organism_classification Embryonic stem cell Antibodies Neutralizing Axl Receptor Tyrosine Kinase QR1-502 Flavivirus Disease Models Animal Infectious Diseases medicine.anatomical_structure hearing Hair cell Disease Susceptibility |
Zdroj: | Viruses Volume 13 Issue 9 Department of Biological Sciences Faculty Publications Viruses, Vol 13, Iss 1823, p 1823 (2021) |
ISSN: | 1999-4915 |
DOI: | 10.3390/v13091823 |
Popis: | Congenital Zika Syndrome (CZS) is caused by vertical transmission of Zika virus (ZIKV) to the gestating human fetus. A subset of CZS microcephalic infants present with reduced otoacoustic emissions this test screens for hearing loss originating in the cochlea. This observation leads to the question of whether mammalian cochlear tissues are susceptible to infection by ZIKV during development. To address this question using a mouse model, the sensory cochlea was explanted at proliferative, newly post-mitotic or maturing stages. ZIKV was added for the first 24 h and organs cultured for up to 6 days to allow for cell differentiation. Results showed that ZIKV can robustly infect proliferating sensory progenitors, as well as post-mitotic hair cells and supporting cells. Virus neutralization using ZIKV-117 antibody blocked cochlear infection. AXL is a cell surface molecule known to enhance the attachment of flavivirus to host cells. While Axl mRNA is widely expressed in embryonic cochlear tissues susceptible to ZIKV infection, it is selectively downregulated in the post-mitotic sensory organ by E15.5, even though these cells remain infectible. These findings may offer insights into which target cells could potentially contribute to hearing loss resulting from fetal exposure to ZIKV in humans. |
Databáze: | OpenAIRE |
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