ArticleiScience2025
Dual role of HO-1 in mediating antiviral immune responses and mitigating excessive inflammatory damage during influenza virus infection.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- E3 Ubiquitin Ligase UBR5 Aggravates Cardiac Hypertrophy Via Inhibiting Nrf2/HO-1 Pathway.Cardiovascular drugs and therapy · 2026Article
- Verapamil HCl demonstrates antiviral activity against porcine reproductive and respiratory syndrome virus by regulating CaMicrobiology spectrum · 2026Article
- Seneca Valley virus 3C protease targets the Nrf2/HO-1 pathway to antagonize its antiviral activity.Journal of virology · 2026Article
- The Dual Role of Nrf2 Signaling in Virus Infections: Antiviral Guardian or Proviral Accomplice?Pathogens (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) remains a global health threat, with severe cases causing high morbidity and mortality. Type I interferons (IFN-α/β) are crucial for early innate immunity to IAV but can drive immunopathology. This study investigates the role of heme oxygenase-1 (HO-1), a stress-responsive protein with anti-inflammatory properties, in modulating the immune response to IAV. Lung-tropic adeno-associated virus (AAV)-mediated HO-1 overexpression reduces lung damage by limiting immune cells infiltration, including plasmacytoid dendritic cells and classical monocytes, while promoting regulatory T cells (Tregs) and nonclassical monocytes. Additionally, HO-1 increases macrophage populations, enhancing antiviral responses via IFN pathways. Consistent with this, HO-1 knockout mice experience more severe infections, and HO-1 recruit inhibited IAV replication and alleviated pulmonary inflammation. In addition, compared with wide-type, the catalytically inactive mutation (H25A) impairs HO-1's anti-inflammatory function. These findings underscore HO-1's critical role in balancing antiviral immunity and inflammation, positioning it as a potential therapeutic target for severe influenza.
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Registered trials
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