Hypoxia-inducible factor 1-alpha inhibition mitigates inflammatory responses induced by H9N2 avian influenza virus.
Microbiology spectrum·
- DOI
- 10.1128/spectrum.02680-25
- PMID
- 42641155
- PMCID
- —
- OpenAlex
- —
- Study type
- Journal article
- Publisher
- Publisher unavailable
- Article type
- journal-article
- Integrity
- current
Why this research matters now
The authors frame the work as relevant to mitigating inflammation and lung damage associated with influenza virus infection, positioning Sotetsuflavone as a candidate HIF-1α-targeted therapeutic against influenza-associated immunopathology.
Structured evidence summary
Research question
The study investigates how hypoxia-inducible factor 1-alpha contributes to H9N2 avian influenza virus pathogenesis and inflammatory responses, and whether the natural flavonoid Sotetsuflavone can modulate these responses via HIF-1α inhibition.
Study design
A preclinical experimental study combining molecular docking and surface plasmon resonance binding assays, in vitro infection experiments in HD11 cells, and in vivo experiments in H9N2-infected mice.
Population and setting
Laboratory-based models: HD11 cells infected with H9N2 AIV and mice infected with H9N2 AIV; no human or field-population data are described.
Main findings
HIF-1α was reported to worsen H9N2-induced inflammation through effects on mitochondrial function. Sotetsuflavone showed binding affinity for HIF-1α in docking and SPR assays, reduced IL-1β, IL-6, and TNF-α production in infected HD11 cells, and in mice reduced pulmonary inflammation while increasing expression of type II alveolar epithelial markers Abca3 and Sftpb.
Public-health relevance
The authors frame the work as relevant to mitigating inflammation and lung damage associated with influenza virus infection, positioning Sotetsuflavone as a candidate HIF-1α-targeted therapeutic against influenza-associated immunopathology.
Important limitations
The abstract does not list explicit limitations. This summary is restricted to the supplied single-article abstract and metadata, and decision-grade interpretation would require review of the full original paper, including its experimental controls, dosing, and statistical reporting.
GIDS interpretation
The paper is discoverable through influenza and treatment-related classifiers; it provides mechanistic and preclinical pharmacological context that could be relevant to anti-inflammatory host-directed strategies for influenza. No connection to any live surveillance signal is established by the supplied evidence.
Related GIDS surveillance
Literature context does not validate, explain, or change a surveillance signal. Exact and contextual relationships are shown separately.
Evidence relationships
This article has 7 auditable classifier relationships to diseases, places, topics, and study design.