RELMα establishes a permissive environment for influenza virus infection through direct effects on lung epithelial cells
Journal of Virology·
- DOI
- 10.1128/jvi.02225-25
- PMID
- 42461031
- PMCID
- —
- OpenAlex
- W7168992054
- Study type
- Journal article
- Publisher
- American Society for Microbiology
- Article type
- journal-article
- Integrity
- current
Why this research matters now
The findings identify RELMα as a host factor associated with influenza A virus growth in epithelial cells and suggest that epithelial-cell pathways could be investigated as potential therapeutic targets. The supplied evidence is preclinical and does not establish effectiveness, safety, or relevance in humans.
Structured evidence summary
Research question
The study examined whether RELMα contributes to an influenza A virus-permissive state in lung epithelial cells and whether this factor could represent a target for limiting viral replication.
Study design
The study used influenza-infected mice, whole-body and club cell-specific Retnla-deficient mouse models, cultured murine lung epithelial cells, RELMα treatment, and transcriptomic analysis.
Population and setting
The experimental setting involved mice infected with influenza A virus strain A/California/04/2009 (H1N1), along with murine lung epithelial cell lines and EpCAM-positive epithelial cells.
Main findings
Influenza infection was associated with increased RELMα secretion by infected lung epithelial cells. Mice lacking RELMα had less infectious virus in epithelial cells, while the measured lung immune response was unchanged; RELMα exposure increased infection in cultured murine epithelial cells and was associated with metabolic transcriptional changes.
Public-health relevance
The findings identify RELMα as a host factor associated with influenza A virus growth in epithelial cells and suggest that epithelial-cell pathways could be investigated as potential therapeutic targets. The supplied evidence is preclinical and does not establish effectiveness, safety, or relevance in humans.
Important limitations
The supplied evidence describes mouse and cultured-cell experiments, so its applicability to human infection and clinical treatment is not established. The summary is limited to the supplied single-article abstract and metadata; the original paper would be required for decision-grade assessment of methods, effect estimates, statistical details, and study limitations.
GIDS interpretation
The article is discoverable in the supplied metadata under influenza and treatment-related topics. It provides experimental context about a possible host mechanism in influenza infection, but it does not confirm or characterize a live surveillance signal.
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 6 auditable classifier relationships to diseases, places, topics, and study design.