ArticleVirologica Sinica2021
Influenza A Virus (H1N1) Infection Induces Glycolysis to Facilitate Viral Replication.
Article in Virologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 89 citations in OpenAlex.
- Lactylation in influenza a virus infection: Current evidence, knowledge gaps, and future perspectives.Virulence · 2026Review
- Influenza A deletion-containing viral genome production is altered by metabolites, metabolic signaling molecules, and cyanobacterial extracts.Applied and environmental microbiology · 2026Article
- Japanese encephalitis virus hijacks the host purine biosynthetic network to promote viral replication in neurons.PLoS pathogens · 2026Article
- Pestivirus bovine viral diarrhea virus infection induces ROS-HIF-1a axis-driven glycolytic reprogramming, which increases viral replication by impairing RIG-I-dependent type I interferon response.Journal of virology · 2026Article
- Host metabolic responses to SARS-CoV-2 and influenza viruses: parallels and contrasts.Metabolomics : Official journal of the Metabolomic Society · 2026Review
- Stress-induced OMA1-mediated cleavage of AIFM1 suppresses cell growth by controlling mitochondrial OXPHOS activity.The EMBO journal · 2026Article
- Curculigoside attenuates influenza virus-induced acute lung injury by modulating the Keap1/Nrf2 signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Viral-host interactions mediated by the mTOR signaling pathway.Cell insight · 2026Review
- Hypoxia: a critical pathophysiological driver in respiratory inflammatory diseases.Military Medical Research · 2026Review
- Research progress in the inhibitory mechanisms of traditional Chinese medicine therapies against influenza A.Frontiers in immunology · 2026Review
- Review
- Airway immunometabolic responses during pulmonary bacterial and viral infections.Cell reports · 2025Review
- The bittersweet link between glucose metabolism, cellular microenvironment and viral infection.Virulence · 2025Review
- Article
- Thapsigargin suppresses porcine hemagglutinating encephalomyelitis virus replication by disrupting host energy metabolism.Virologica Sinica · 2025Article
- Review
- Metabolic Hostile Takeover: How Influenza Virus Reprograms Cellular Metabolism for Replication.Viruses · 2025Review
- ARRDC4-mediated glycolysis enhances innate immunity to influenza A virus through fructose-1,6-bisphosphate.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Pyruvate kinase M2 modulates Japanese encephalitis virus replication in neuronal cells.The Journal of general virology · 2025Article
1 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
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses depend on host cellular metabolism to provide the energy and biosynthetic building blocks required for their replication. In this study, we observed that influenza A virus (H1N1), a single-stranded, negative-sense RNA virus with an eight-segmented genome, enhanced glycolysis both in mouse lung tissues and in human lung epithelial (A549) cells. In detail, the expression of hexokinase 2 (HK2), the first enzyme in glycolysis, was upregulated in H1N1-infected A549 cells, and the expression of pyruvate kinase M2 (PKM2) and pyruvate dehydrogenase kinase 3 (PDK3) was upregulated in H1N1-infected mouse lung tissues. Pharmacologically inhibiting the glycolytic pathway or targeting hypoxia-inducible factor 1 (HIF-1), the central transcriptional factor critical for glycolysis, significantly reduced H1N1 replication, revealing a requirement for glycolysis during H1N1 infection. In addition, pharmacologically enhancing the glycolytic pathway further promoted H1N1 replication. Furthermore, the change of H1N1 replication upon glycolysis inhibition or enhancement was independent of interferon signaling. Taken together, these findings suggest that influenza A virus induces the glycolytic pathway and thus facilitates efficient viral replication. This study raises the possibility that metabolic inhibitors, such as those that target glycolysis, could be used to treat influenza A virus infection in the future.
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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.