ArticleBrain, behavior, and immunity2022
IL-1 reprogramming of adult neural stem cells limits neurocognitive recovery after viral encephalitis by maintaining a proinflammatory state.
Article in Brain, behavior, and immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- From viral epigenetic reprogramming to neuroinflammation: Mechanisms driving neurodegeneration.Journal of neurovirology · 2026Review
- TNF-α induces type I IFN signalling to suppress neurogenesis and recruit T cells.Nature communications · 2026Article
- The neuroimmune system and cognition.Nature immunology · 2026Review
- Unraveling Neurodevelopment: Synergistic Effects of Intrinsic Genetic Programs and Extrinsic Environmental Cues.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Modulation of adult hippocampal neurogenesis by interleukin 1 signaling.Neurobiology of sleep and circadian rhythms · 2025Article
- Emerging Insights into Brain Inflammation: Stem-Cell-Based Approaches for Regenerative Medicine.International journal of molecular sciences · 2025Review
- Neural stem cells fate under neuroinflammatory conditions and oxidative stress response.Frontiers in cellular neuroscience · 2025Review
- Underestimated virus impaired cognition-more evidence and more work to do.Frontiers in immunology · 2025Review
- West Nile Virus-Induced Expression of Senescent GeneBiomolecules · 2024Article
- Vaccination reduces central nervous system IL-1β and memory deficits after COVID-19 in mice.Nature immunology · 2024Article
- Molecular and Cellular Mechanisms Underlying Neurologic Manifestations of Mosquito-Borne Flavivirus Infections.Viruses · 2023Review
- Review
- Interleukins, Chemokines, and Tumor Necrosis Factor Superfamily Ligands in the Pathogenesis of West Nile Virus Infection.Viruses · 2023Review
- Article
- Mechanisms of coronavirus infectious disease 2019-related neurologic diseases.Current opinion in neurology · 2022Review
- Zika virus-induced TNF-α signaling dysregulates expression of neurologic genes associated with psychiatric disorders.Journal of neuroinflammation · 2022Article
- Glial Cells and Brain Diseases: Inflammasomes as Relevant Pathological Entities.Frontiers in cellular neuroscience · 2022Review
- COVID-19 induces neuroinflammation and loss of hippocampal neurogenesis.Research square · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Innate immune responses to emerging RNA viruses are increasingly recognized as having significant contributions to neurologic sequelae, especially memory disorders. Using a recovery model of West Nile virus (WNV) encephalitis, we show that, while macrophages deliver the antiviral and anti-neurogenic cytokine IL-1β during acute infection; viral recovery is associated with continued astrocyte inflammasome-mediated production of inflammatory levels of IL-1β, which is maintained by hippocampal astrogenesis via IL-1R1 signaling in neural stem cells (NSC). Accordingly, aberrant astrogenesis is prevented in the absence of IL-1 signaling in NSC, indicating that only newly generated astrocytes exert neurotoxic effects, preventing synapse repair and promoting spatial learning deficits. Ex vivo evaluation of IL-1β-treated adult hippocampal NSC revealed the upregulation of developmental differentiation pathways that derail adult neurogenesis in favor of astrogenesis, following viral infection. We conclude that NSC-specific IL-1 signaling within the hippocampus during viral encephalitis prevents synapse recovery and promotes spatial learning defects via altered fates of NSC progeny that maintain inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.