ArticleJournal of neuroinflammation2016
Fast type I interferon response protects astrocytes from flavivirus infection and virus-induced cytopathic effects.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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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.
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Who cites it
99 citing papers in PubMed, 140 citations in OpenAlex.
- SIRT1 remodels astrocyte metabolism and promotes viral replication during neurotropic orthoflavivirus infection.bioRxiv : the preprint server for biology · 2026Article
- Beyond the neuron: the role of glial cells in viral neuropathogenesis.Journal of virology · 2026Review
- Integrative proteomics and lipidomics reveals dual roles for lipid droplets in the host cell antiviral response.Nature communications · 2026Article
- Integrative modelling of innate immune response dynamics during virus infection.PLoS computational biology · 2026Article
- Type I and III interferon responses restrict infection by tick-borne orthoflaviviruses through IFI6.Journal of virology · 2026Article
- Transcriptomic insights into the neuropathogenic and immune response alterations in mouse neurons challenged with west nile and japanese encephalitis viruses.Virology journal · 2026Article
- Role of innate immune and inflammatory signaling in West Nile virus tropism and neuronal and glial cell death.Scientific reports · 2025Article
- Spatial gene expression analysis reveals pathological niches in Japanese encephalitis virus neuroinvasion.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Influence of the pre-membrane and envelope proteins on structure, pathogenicity, and tropism of tick-borne encephalitis virus.Journal of virology · 2025Article
- The activation of complement C5a-C5aR1 axis in astrocytes facilitates the neuropathogenesis due to EV-A71 infection by upregulating CXCL1.Journal of virology · 2025Article
- Phenazine biosynthesis-like domain-containing protein (PBLD) and Cedrelone promote antiviral immune response by activating NF-ĸB.Nature communications · 2025Article
- Neural and endothelial cell-derived extracellular vesicles mediate Zika virus genome dissemination and productive infection in vivo.PloS one · 2025Article
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- Transcriptional Response to Tick-Borne Flavivirus Infection in Neurons, Astrocytes and Microglia In Vivo and In Vitro.Viruses · 2024Article
- The Flavivirus Non-Structural Protein 5 (NS5): Structure, Functions, and Targeting for Development of Vaccines and Therapeutics.Vaccines · 2024Review
- Role of inflammatory cytokine burst in neuro-invasion of Japanese Encephalitis virus infection: an immunotherapeutic approaches.Journal of neurovirology · 2024Review
- Understanding the link between neurotropic viruses, BBB permeability, and MS pathogenesis.Journal of neurovirology · 2024Review
- Brain-wide circuit-specific targeting of astrocytes.Cell reports methods · 2023Article
- Astrocytes in human central nervous system diseases: a frontier for new therapies.Signal transduction and targeted therapy · 2023Review
- Astrocytes evoke a robust IRF7-independent type I interferon response upon neurotropic viral infection.Journal of neuroinflammation · 2023Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeurotropic flaviviruses such as tick-borne encephalitis virus (TBEV), Japanese encephalitis virus (JEV), West Nile virus (WNV), and Zika virus (ZIKV) are causative agents of severe brain-related diseases including meningitis, encephalitis, and microcephaly. We have previously shown that local type I interferon response within the central nervous system (CNS) is involved in the protection of mice against tick-borne flavivirus infection. However, the cells responsible for mounting this protective response are not defined.
methodsPrimary astrocytes were isolated from wild-type (WT) and interferon alpha receptor knock out (IFNAR
resultsHere, we show that astrocytes control viral replication of different TBEV strains, JEV, WNV, and ZIKV. In contrast to fibroblast, astrocytes mount a rapid interferon response and restrict viral spread. Furthermore, basal expression levels of key interferon-stimulated genes are high in astrocytes compared to mouse embryonic fibroblasts. Bioinformatic analysis of RNA-sequencing data reveals that astrocytes have established a basal antiviral state which contributes to the rapid viral recognition and upregulation of interferons. The most highly upregulated pathways in neighboring cells were linked to type I interferon response and innate immunity. The restriction in viral growth was dependent on interferon signaling, since loss of the interferon receptor, or its blockade in wild-type cells, resulted in high viral replication and virus-induced cytopathic effects. Astrocyte supernatant from TBEV-infected cells can restrict TBEV growth in astrocytes already 6 h post infection, the effect on neurons is highly reinforced, and astrocyte supernatant from 3 h post infection is already protective.
conclusionsThese findings suggest that the combination of an intrinsic constitutive antiviral response and the fast induction of type I IFN production by astrocytes play an important role in self-protection of astrocytes and suppression of flavivirus replication in the CNS.
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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.