ArticlePLoS pathogens2022
TNFα-induced metabolic reprogramming drives an intrinsic anti-viral state.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
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- UDP-Glucose-6-Dehydrogenase Mediated O-GlcNAcylation of Tight Junction Protein 1 Suppresses Metastasis in Renal Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- Correlates of protection against African swine fever virus identified by a systems immunology approach.eLife · 2026Article
- HCMV infection depends on EGLN1-mediated mitochondrial activation to increase dNTP pools for viral DNA replication.Cell reports · 2026Article
- Reprogramming of host energy metabolism mediated by the TNF-iNOS-HIF-1α axis plays a key role in host resistance tobioRxiv : the preprint server for biology · 2026Article
- A crucial role of the malate aspartate shuttle in metabolic reprogramming in TNF-induced SIRS.Frontiers in immunology · 2025Article
- A UL26-PIAS1 complex antagonizes anti-viral gene expression during Human Cytomegalovirus infection.PLoS pathogens · 2024Article
- The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication.bioRxiv : the preprint server for biology · 2024Article
- Pattern-Recognition Receptors and Immunometabolic Reprogramming: What We Know and What to Explore.Journal of innate immunity · 2024Review
- Metabolic transcriptomics dictate responses of cone photoreceptors to retinitis pigmentosa.Cell reports · 2023Article
- Application of spatial transcriptomics analysis using the Visium system for the mouse nasal cavity after intranasal vaccination.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cytokines induce an anti-viral state, yet many of the functional determinants responsible for limiting viral infection are poorly understood. Here, we find that TNFα induces significant metabolic remodeling that is critical for its anti-viral activity. Our data demonstrate that TNFα activates glycolysis through the induction of hexokinase 2 (HK2), the isoform predominantly expressed in muscle. Further, we show that glycolysis is broadly important for TNFα-mediated anti-viral defense, as its inhibition attenuates TNFα's ability to limit the replication of evolutionarily divergent viruses. TNFα was also found to modulate the metabolism of UDP-sugars, which are essential precursor substrates for glycosylation. Our data indicate that TNFα increases the concentration of UDP-glucose, as well as the glucose-derived labeling of UDP-glucose and UDP-N-acetyl-glucosamine in a glycolytically-dependent manner. Glycolysis was also necessary for the TNFα-mediated accumulation of several glycosylated anti-viral proteins. Consistent with the importance of glucose-driven glycosylation, glycosyl-transferase inhibition attenuated TNFα's ability to promote the anti-viral cell state. Collectively, our data indicate that cytokine-mediated metabolic remodeling is an essential component of the anti-viral response.
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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.