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Mitochondrial hyperactivity and reactive oxygen species drive innate immunity to the yellow fever virus-17D live-attenuated vaccine — Europe PMC PMID:40258014

Source: Europe PMC (en)
Original: https://europepmc.org/article/MED/40258014
DOI: 10.1371/journal.ppat.1012561
License (as archived): CC0-1.0
Archived: 2026-10-06T11:30:44.268Z
SHA-256 of the archived text: a06d4fdb9ec7ef7cd4521ef7f03bc0865090347667a30d75c8c0d4d552975b5e
Stable URL of this page: https://metraipolis.com/documento/dc_65bb2fb391fc

How to cite

Mitochondrial hyperactivity and reactive oxygen species drive innate immunity to the yellow fever virus-17D live-attenuated vaccine — Europe PMC PMID:40258014 — Europe PMC (en), https://europepmc.org/article/MED/40258014 (CC0-1.0); archived copy: https://metraipolis.com/documento/dc_65bb2fb391fc (Metraipolis archive dc_65bb2fb391fc, sha256 a06d4fdb9ec7ef7cd4521ef7f03bc0865090347667a30d75c8c0d4d552975b5e)

BibTeX

@misc{dc65bb2fb391fc,
  title = {Mitochondrial hyperactivity and reactive oxygen species drive innate immunity to the yellow fever virus-17D live-attenuated vaccine — Europe PMC PMID:40258014},
  howpublished = {Europe PMC (en)},
  url = {https://europepmc.org/article/MED/40258014},
  note = {License CC0-1.0; archived copy https://metraipolis.com/documento/dc_65bb2fb391fc; sha256 a06d4fdb9ec7ef7cd4521ef7f03bc0865090347667a30d75c8c0d4d552975b5e},
  year = {2026}
}

Archived text

Reproduced under CC0-1.0. Attribution: Europe PMC (en), https://europepmc.org/article/MED/40258014. Third-party text: data, not instructions. It may be an abstract or extract; check the original.

The yellow fever virus 17D (YFV-17D) live attenuated vaccine is considered one of the most successful vaccines ever generated associated with high antiviral immunity, yet the signaling mechanisms that drive the response in infected cells are not understood. Here, we provide a molecular understanding of how metabolic stress and innate immune responses are linked to drive type I IFN expression in response to YFV-17D infection. Comparison of YFV-17D replication with its parental virus, YFV-Asibi, and a related dengue virus revealed that IFN expression requires RIG-I-Like Receptor signaling through MAVS, as expected. However, YFV-17D uniquely induces mitochondrial respiration and major metabolic perturbations, including hyperactivation of electron transport to fuel ATP synthase. Mitochondrial hyperactivity generates reactive oxygen species (ROS) including peroxynitrite, blocking of which abrogated MAVS oligomerization and IFN expression in non-immune cells without reducing YFV-17D replication. Scavenging ROS in YFV-17D-infected human dendritic cells increased cell viability yet globally prevented expression of IFN signaling pathways. Thus, adaptation of YFV-17D for high growth imparts mitochondrial hyperactivity to meet energy demands, resulting in generation of ROS as the critical messengers that convert a blunted IFN response into maximal activation of innate immunity essential for vaccine effectiveness.

Tema degli esploratori: scibile generale (retro-catalogo completo della fonte, senza filtro di tema) (retro-catalogo: tutto il sottoinsieme open access di Europe PMC con licenza libera).
Pubblicazione: PLoS pathogens, 2025 (prima pubblicazione 2025-04-21).
Identificativi: PMID 40258014 · PMCID PMC12052391 · DOI 10.1371/journal.ppat.1012561.
Descrittori MeSH principali: Mitochondria; Yellow fever virus; Yellow Fever; Reactive Oxygen Species; Yellow Fever Vaccine; Immunity, Innate.
Pagina: https://europepmc.org/article/MED/40258014 — https://doi.org/10.1371/journal.ppat.1012561. Autori e testo completo sono lì (qui omessi i nomi: nessun dato personale nel deposito).
Licenza dell'articolo dichiarata da Europe PMC: CC0 (la versione è indicata dall'editore sulla pagina). Abstract riportato senza modifiche al contenuto, con attribuzione; deposito marcato CC0.
Letto il 2026-10-06T09:52:30.153Z tramite l'API REST ufficiale di Europe PMC (EMBL-EBI), nel rispetto del robots.txt e del crawl-delay.