ArticleThe Journal of experimental medicine2024
Fetal MAVS and type I IFN signaling pathways control ZIKV infection in the placenta and maternal decidua.
Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Tunneling nanotubes contribute to Zika virus pathogenesis at the maternal-fetal interfacemBio · 2026Article
- SLC3A2 promotes early-stage of Zika virus infection in human placental cells and astrocytes.Infectious diseases & immunity · 2026Article
- A dual-pronged host-directed therapeutic targeting cyclophilin A and pathogenic interferon response abrogates virus-triggered pregnancy pathologies.Nature communications · 2026Article
- Type I interferon controls vertical transmission and fetoplacental infection of Oropouche virus.iScience · 2026Article
- Vertical Transmission of Zika Virus: The Immune-Pathophysiological Interface of the Placenta.Journal of immunology research · 2026Review
- Interplay between flaviviruses and the interferon response: mechanisms of immune evasion and therapeutic implications.Frontiers in pharmacology · 2026Review
- Innate immune responses to pathogens at the maternal-fetal interface.Nature reviews. Immunology · 2025Review
- Harnessing the microbiota-gut-brain axis to prevent and treat pediatric neurodevelopmental disorders: translational insights and strategies.Journal of translational medicine · 2025Review
- Zika virus-induced fetal demise is triggered by strain- and dose-specific RLR-driven activation of the interferon response in the decidua, placenta, and fetus inJournal of virology · 2025Article
- Eastern equine encephalitis virus: Pathogenesis, immune response, and clinical manifestations.Infectious medicine · 2025Review
- Harnessing cellular immunity for next-generation vaccines against respiratory viruses: mechanisms, platforms, and optimization strategies.Frontiers in immunology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
The contribution of placental immune responses to congenital Zika virus (ZIKV) syndrome remains poorly understood. Here, we leveraged a mouse model of ZIKV infection to identify mechanisms of innate immune restriction exclusively in the fetal compartment of the placenta. ZIKV principally infected mononuclear trophoblasts in the junctional zone, which was limited by mitochondrial antiviral-signaling protein (MAVS) and type I interferon (IFN) signaling mechanisms. Single nuclear RNA sequencing revealed MAVS-dependent expression of IFN-stimulated genes (ISGs) in spongiotrophoblasts but not in other placental cells that use alternate pathways to induce ISGs. ZIKV infection of Ifnar1-/- or Mavs-/- placentas was associated with greater infection of the adjacent immunocompetent decidua, and heterozygous Mavs+/- or Ifnar1+/- dams carrying immunodeficient fetuses sustained greater maternal viremia and tissue infection than dams carrying wild-type fetuses. Thus, MAVS-IFN signaling in the fetus restricts ZIKV infection in junctional zone trophoblasts, which modulates dissemination and outcome for both the fetus and the pregnant mother.
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