ArticleNature communications2025
Viruses hijack FPN1 to disrupt iron withholding and suppress host defense.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- PEDV envelope protein promotes viral replication by remodeling host iron homeostasis via the TRIM28-KLF15-FPN axis.Journal of virology · 2026Article
- Ferritinophagy Rewires Carnitine-Dependent Lipid Metabolism to Inhibit PRRSV and IAV Replication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PEX19 restricts porcine deltacoronavirus replication through farnesylation-dependent and -independent mechanisms.Journal of virology · 2026Article
- STING Degradation by PRRSV Activates HKViruses · 2026Article
- Oyster Peptide-Ferrous Chelate Preparation Optimization Structural Characteristics and Enhanced Bioavailability.Foods (Basel, Switzerland) · 2026Article
- Protective Effect of Chinese Herbal Medicine on Cerebral Ischemia-Reperfusion Injury by Regulating Ferroptosis.Drug design, development and therapy · 2026Review
- Post-translational modifications in ferroptosis: mechanisms and therapeutic potential.International journal of biological sciences · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Viruses rely on intracellular materials, including iron, to complete their life cycles and iron withholding may limit viral infections. However, the mechanisms through which viruses disrupt host iron homeostasis and the impact of intracellular iron on the host's antiviral defense aren't well studied. Here we show that viral infections facilitate the polyubiquitination and degradation of ferroportin (FPN1, the only cellular iron exporter) by upregulating the host E3 ubiquitin ligase DTX3L, leading to an elevation in cellular iron levels. Excessive ferrous iron suppresses type I IFN responses and autophagy by promoting TBK1 hydroxylation and STING carbonylation in macrophages. FPN1 deficiency suppresses host antiviral defense and facilitates viral replication in vitro and in vivo, while DTX3L deficiency has the opposite effect. These results reveal that viruses hijack host FPN1 to disrupt iron withholding and achieve immune escape, and suggest that iron homeostasis maintained by FPN1 is required for the optimal activation of TBK1- and STING-dependent antiviral responses.
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Registered trials
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