ArticleVirologica Sinica2024
HIF-1α promotes virus replication and cytokine storm in H1N1 virus-induced severe pneumonia through cellular metabolic reprogramming.
Article in Virologica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 27 citations in OpenAlex.
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- Topical Glycolysis Inhibition Restores MAVS-Associated Antiviral Signaling in Herpes Simplex Keratitis.Investigative ophthalmology & visual science · 2026Article
- ENO1 interacts with PKM to promote HBV-related hepatocellular carcinoma progression and HBV replication.Journal of translational medicine · 2026Article
- Triptolide exerts antiviral effects and alleviates influenza A‑induced pneumonia by inhibiting the overactivation of absent in melanoma 2 signaling in immune cells.International journal of molecular medicine · 2026Article
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- Human Influenza Virus Infection: A Focus on Key Host Determinants Linked to Clinical Disease Severity.Viruses · 2026Review
- Beyond a metabolite: lactate and lactylation in lung diseases.Respiratory research · 2026Review
- Beyond Viral Restriction: The Metabolic Dimensions of Interferon-Stimulated Genes in Antiviral Immunity.Viruses · 2026Review
- Hypoxia: a critical pathophysiological driver in respiratory inflammatory diseases.Military Medical Research · 2026Review
- Identification of poly(I:C) interacted proteins and their regulation in transcription level against bacterial infection in zebrafish.Frontiers in immunology · 2026Article
- SARS-CoV-2 infection in hiPSC-derived neurons is cathepsin-dependent and causes differential accumulation of HIF1ɑ and phosphorylated tau.Molecular therapy. Nucleic acids · 2025Article
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- Metabolic Hostile Takeover: How Influenza Virus Reprograms Cellular Metabolism for Replication.Viruses · 2025Review
- Attenuate host susceptibility to respiratory virus invasion by inhibiting interactions between host proteins SLC16A3 and AP1G1.Microbiology spectrum · 2025Article
- Study on the Mechanism of RuHaoDaShi Granules in Treating H1N1 Viral Pneumonia Based on Network Pharmacology and Experimental Validation.Pathogens (Basel, Switzerland) · 2025Article
- Article
- CypA inhibits respiratory syncytial virus (RSV) replication by suppressing glycolysis through the downregulation of PKM2 expression.Journal of virology · 2025Article
- Metabolic Reprogramming in Respiratory Viral Infections: A Focus on SARS-CoV-2, Influenza, and Respiratory Syncytial Virus.Biomolecules · 2025Review
- The Role of Lactylation in Virus-Host Interactions.International journal of molecular sciences · 2025Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mortality of patients with severe pneumonia caused by H1N1 infection is closely related to viral replication and cytokine storm. However, the specific mechanisms triggering virus replication and cytokine storm are still not fully elucidated. Here, we identified hypoxia inducible factor-1α (HIF-1α) as one of the major host molecules that facilitates H1N1 virus replication followed by cytokine storm in alveolar epithelial cells. Specifically, HIF-1α protein expression is upregulated after H1N1 infection. Deficiency of HIF-1α attenuates pulmonary injury, viral replication and cytokine storm in vivo. In addition, viral replication and cytokine storm were inhibited after HIF-1α knockdown in vitro. Mechanistically, the invasion of H1N1 virus into alveolar epithelial cells leads to a shift in glucose metabolism to glycolysis, with rapid production of ATP and lactate. Inhibition of glycolysis significantly suppresses viral replication and inflammatory responses. Further analysis revealed that H1N1-induced HIF-1α can promote the expression of hexokinase 2 (HK2), the key enzyme of glycolysis, and then not only provide energy for the rapid replication of H1N1 virus but also produce lactate, which reduces the accumulation of the MAVS/RIG-I complex and inhibits IFN-α/β production. In conclusion, this study demonstrated that the upregulation of HIF-1α by H1N1 infection augments viral replication and cytokine storm by cellular metabolic reprogramming toward glycolysis mainly through upregulation of HK2, providing a theoretical basis for finding potential targets for the treatment of severe pneumonia caused by H1N1 infection.
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