Systems-level insights into age-dependent innate immune responses in influenza B infection
Microbiology Spectrum·
- DOI
- 10.1128/spectrum.02656-25
- PMID
- —
- PMCID
- —
- OpenAlex
- W7203755210
- Study type
- Journal article
- Publisher
- American Society for Microbiology
- Article type
- journal-article
- Integrity
- current
Why this research matters now
The authors frame the work as identifying potential therapeutic targets to improve outcomes of influenza B infection in elderly populations, highlighting age-dependent innate immune dysregulation as a relevant concern.
Structured evidence summary
Research question
The study investigates how aging alters innate immune responses during influenza B virus (IBV) infection, with a focus on age-related transcriptional and proteomic changes in the lung.
Study design
A preclinical mouse-model study comparing young adult and aged mice infected with the IBV strain Inf B/Phuket/3073/2013, combining bulk RNA sequencing, proteomics, and real-time PCR analyses of lung tissue.
Population and setting
Young adult and aged laboratory mice used in a controlled preclinical setting; no human subjects or geographic setting are described in the supplied evidence.
Main findings
Bulk RNA-seq identified 1,350 differentially expressed genes, of which 824 showed an aged-biased pattern and were upregulated in infected aged mice, with enrichment in innate immune signaling, apoptosis, cellular stress, and DNA damage pathways. Proteomics revealed differentially expressed proteins involved in viral entry, signaling, and interferon responses. PCR confirmed altered expression of TLRs, IRF7/IRF9, IFIT-2/IFIT-3, STAT-1, and type I/II interferons, with young mice showing coordinated antiviral activation while aged mice displayed delayed, dysregulated responses and excessive inflammation.
Public-health relevance
The authors frame the work as identifying potential therapeutic targets to improve outcomes of influenza B infection in elderly populations, highlighting age-dependent innate immune dysregulation as a relevant concern.
Important limitations
The summary is limited to the supplied single-article abstract and bibliographic metadata; explicit limitations (e.g., sample size, translational relevance of the murine model, or generalizability to human influenza B infection) are not stated in the provided text, and the original paper would be needed for decision-grade interpretation.
GIDS interpretation
From a discoverability standpoint, this peer-reviewed journal article is catalogued under the Influenza disease and Treatment topics; it contributes laboratory evidence on age-related innate immunity in influenza B and may aid reviewers contextualizing mechanistic literature, but it should not be interpreted as confirmation of any 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 5 auditable classifier relationships to diseases, places, topics, and study design.