ArticlePLoS neglected tropical diseases2021
Inhibition of innate immune response ameliorates Zika virus-induced neurogenesis deficit in human neural stem cells.
Article in PLoS neglected tropical diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Comparison of human cerebral organoids infected with wild-type Zika versus attenuated DN-2 virus strains uncovers differences in host immune responses.Cell communication and signaling : CCS · 2025Article
- Intrauterine Zika Virus Infection: An Overview of the Current Findings.Journal of personalized medicine · 2025Review
- Antiviral and immunomodulatory effects of ouabain against congenital Zika syndrome model.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Role of microglia in brain development after viral infection.Frontiers in cell and developmental biology · 2024Review
- Pathogenesis of Zika Virus Infection.Annual review of pathology · 2023Review
- Vav Proteins in Development of the Brain: A Potential Relationship to the Pathogenesis of Congenital Zika Syndrome?Viruses · 2022Review
- Zika Virus: A New Therapeutic Candidate for Glioblastoma Treatment.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Global Zika virus (ZIKV) outbreaks and their strong link to microcephaly have raised major public health concerns. ZIKV has been reported to affect the innate immune responses in neural stem/progenitor cells (NS/PCs). However, it is unclear how these immune factors affect neurogenesis. In this study, we used Asian-American lineage ZIKV strain PRVABC59 to infect primary human NS/PCs originally derived from fetal brains. We found that ZIKV overactivated key molecules in the innate immune pathways to impair neurogenesis in a cell stage-dependent manner. Inhibiting the overactivated innate immune responses ameliorated ZIKV-induced neurogenesis reduction. This study thus suggests that orchestrating the host innate immune responses in NS/PCs after ZIKV infection could be promising therapeutic approach to attenuate ZIKV-associated neuropathology.
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Registered trials
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