Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Microglia integrated neural spheroids enable neuroinflammatory responses and correct network dysfunction induced by alpha-synuclein mutation.

Communications biology·2026
Same author

Adrenal metastases of differentiated thyroid cancer: clinicopathological characteristics and prognostic factors.

Frontiers in oncology·2026
Same author

The critical role of the endogenous immune compartment after CAR T cell therapy in recurrent GBM.

Cell·2026
Same author

Modeling Gliomas with Organoids: Classification, Fidelity, and Guidelines for Translational Neuro-Oncology.

Neuro-oncology·2026
Same author

Adult neurogenesis: New neurons, new opportunities.

Cell stem cell·2026
Same author

Author Correction: Leveraging deep single-soma RNA sequencing to explore the neural basis of human somatosensation.

Nature neuroscience·2026

Related Experiment Video

Updated: Nov 22, 2025

Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids
09:18

Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids

Published on: September 19, 2017

10.8K

Zika Virus-Induced Neuronal Apoptosis via Increased Mitochondrial Fragmentation.

Shu Yang1, Kirill Gorshkov1, Emily M Lee1

  • 1National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD, United States.

Frontiers in Microbiology
|January 11, 2021
PubMed
Summary

Zika virus (ZIKV) infection causes mitochondrial fragmentation and cell death in neural cells. Inhibiting mitochondrial fission may offer a therapeutic strategy for ZIKV-related neurodevelopmental disorders.

Keywords:
MFN2Zika virusapoptosismitochondrial fragmentationmitofusin

More Related Videos

Establishing Mouse Models for Zika Virus-induced Neurological Disorders Using Intracerebral Injection Strategies: Embryonic, Neonatal, and Adult
09:39

Establishing Mouse Models for Zika Virus-induced Neurological Disorders Using Intracerebral Injection Strategies: Embryonic, Neonatal, and Adult

Published on: April 26, 2018

8.9K
Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice
10:01

Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice

Published on: October 17, 2018

8.3K

Related Experiment Videos

Last Updated: Nov 22, 2025

Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids
09:18

Modelling Zika Virus Infection of the Developing Human Brain In Vitro Using Stem Cell Derived Cerebral Organoids

Published on: September 19, 2017

10.8K
Establishing Mouse Models for Zika Virus-induced Neurological Disorders Using Intracerebral Injection Strategies: Embryonic, Neonatal, and Adult
09:39

Establishing Mouse Models for Zika Virus-induced Neurological Disorders Using Intracerebral Injection Strategies: Embryonic, Neonatal, and Adult

Published on: April 26, 2018

8.9K
Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice
10:01

Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice

Published on: October 17, 2018

8.3K

Area of Science:

  • Neuroscience
  • Virology
  • Cell Biology

Background:

  • The 2015-2016 Zika virus (ZIKV) outbreak in the Americas was linked to increased neurodevelopmental abnormalities, notably fetal microcephaly.
  • ZIKV infection in pregnant women poses a significant threat to fetal neurodevelopment.

Purpose of the Study:

  • To investigate the impact of ZIKV infection on neuronal mitochondria.
  • To explore potential therapeutic strategies targeting mitochondrial dynamics for ZIKV-induced neuronal damage.

Main Methods:

  • Human neural stem cells and SNB-19 glioblastoma cells were infected with ZIKV.
  • Mitochondrial fragmentation, membrane potential, mitofusin 2 levels, and cell death were assessed.
  • The effect of mitochondrial division inhibitor 1 (Mdivi-1) on ZIKV-infected cells was evaluated.

Main Results:

  • ZIKV infection led to mitochondrial fragmentation and disrupted mitochondrial membrane potential in neural cells within 24 hours.
  • The severity of mitochondrial changes correlated with ZIKV protein expression.
  • ZIKV infection decreased mitofusin 2 levels, a key protein in mitochondrial fusion.
  • Mdivi-1 treatment ameliorated mitochondrial disruptions and reduced cell death in ZIKV-infected cells.

Conclusions:

  • Abnormal mitochondrial fragmentation is a key contributor to ZIKV-induced neuronal cell death.
  • Modulating mitochondrial dynamics, specifically the fission-fusion balance, presents a promising therapeutic avenue for ZIKV-related neurological conditions.
  • Targeting mitochondrial dysfunction could be crucial for developing drugs against ZIKV-mediated neuronal apoptosis.