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Zika Virus-Induced Neuronal Apoptosis via Increased Mitochondrial Fragmentation

  1. Author:
    Yang, Shu
    Gorshkov, Kirill
    Lee, Emily M
    Xu, Miao
    Cheng, Yu-Shan
    Sun, Nuo
    Soheilian,Ferri
    de Val, Natalia
    Ming, Guoli
    Song, Hongjun
    Tang, Hengli
    Zheng, Wei

  2. Author Address

    National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD, United States., Department of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, OH, United States., Electron Microscopy Laboratory, National Cancer Institute, Center for Cancer Research, Leidos Biomedical Research, Frederick National Laboratory, Frederick, MD, United States., Department of Neuroscience, Mahoney Institute for Neurosciences, University of Pennsylvania, Philadelphia, PA, United States., Department of Biological Science, Florida State University, Tallahassee, FL, United States.,
    1. Year: 2020
    2. Date: Dec 23
    3. Epub Date: 2020 12 23
  2. Journal: Frontiers in Microbiology
    1. 11
    2. Pages: 598203
  4. Type of Article: Article
  5. Article Number: 598203
  6. ISSN: 1664-302X
  1. Abstract:

    The 2015 to 2016 outbreak of Zika virus (ZIKV) infections in the Americas coincided with a dramatic increase in neurodevelopmental abnormalities, including fetal microcephaly, in newborns born to infected women. In this study, we observed mitochondrial fragmentation and disrupted mitochondrial membrane potential after 24 h of ZIKV infection in human neural stem cells and the SNB-19 glioblastoma cell line. The severity of these changes correlated with the amount of ZIKV proteins expressed in infected cells. ZIKV infection also decreased the levels of mitofusin 2, which modulates mitochondria fusion. Mitochondrial division inhibitor 1 (Mdivi-1), a small molecule inhibiting mitochondria fission, ameliorated mitochondria disruptions and reduced cell death in ZIKV-infected cells. Collectively, this study suggests that abnormal mitochondrial fragmentation contributes to ZIKV-induced neuronal cell death; rebalancing mitochondrial dynamics of fission-fusion could be a therapeutic strategy for drug development to treat ZIKV-mediated neuronal apoptosis. Copyright © 2020 Yang, Gorshkov, Lee, Xu, Cheng, Sun, Soheilian, de Val, Ming, Song, Tang and Zheng.

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  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.3389/fmicb.2020.598203
  3. PMID: 33424801
  4. PMCID: PMC7785723
  5. View record in Web of Science®
  6. WOS: 000604945500001

Library Notes

  1. Fiscal Year: FY2020-2021
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