ArticleCell reports2024
The HIF transcription network exerts innate antiviral activity in neurons and limits brain inflammation.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- IDH1-R132H enhances oncolytic HSV-1 therapy by facilitating viral entry and immune activation in glioma.Nature communications · 2026Article
- Metabolomic Profiles and Anti-Herpes Simplex Virus (Wild-Type and Drug-Resistant) Properties of Water-Based Extracts ofMolecules (Basel, Switzerland) · 2026Article
- NRF2 controls a diverse network of antiviral effectors with p62 acting as a central restriction factor effective across virus families.Redox biology · 2026Article
- Sex Differences in Metabolite-Immune Circuits of Neuroinflammation.Immunological reviews · 2026Review
- Article
- Temporally resolved single-cell RNA sequencing reveals protective and pathological responses during herpes simplex virus CNS infection.Journal of neuroinflammation · 2025Article
- A review of HSV pathogenesis, vaccine development, and advanced applications.Molecular biomedicine · 2024Review
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pattern recognition receptors (PRRs) induce host defense but can also induce exacerbated inflammatory responses. This raises the question of whether other mechanisms are also involved in early host defense. Using transcriptome analysis of disrupted transcripts in herpes simplex virus (HSV)-infected cells, we find that HSV infection disrupts the hypoxia-inducible factor (HIF) transcription network in neurons and epithelial cells. Importantly, HIF activation leads to control of HSV replication. Mechanistically, HIF activation induces autophagy, which is essential for antiviral activity. HSV-2 infection in vivo leads to hypoxia in CNS neurons, and mice with neuron-specific HIF1/2α deficiency exhibit elevated viral load and augmented PRR signaling and inflammatory gene expression in the CNS after HSV-2 infection. Data from human stem cell-derived neuron and microglia cultures show that HIF also exerts antiviral and inflammation-restricting activity in human CNS cells. Collectively, the HIF transcription factor system senses virus-induced hypoxic stress to induce cell-intrinsic antiviral responses and limit 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.