What this means
This review explains how aging can weaken quick antiviral signals and keep inflammation running. It is a summary of earlier work, so it does not test any new treatment.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- A review of earlier research, no new people or animals
- Kind of research
- A summary of earlier studies
The science
- Original title
- Remodeling of innate antiviral immunity in aging.
- Authors
- Zhang X, Yang Q
- Journal
- Cell insight
- Published
- Oct 13, 2026
- Study type
- Review
- PMID
- 42866291 ↗
Abstract
Aging increases susceptibility to severe viral infection, weakens vaccine responses, promotes chronic inflammatory disease, and alters tumor immune surveillance. These outcomes reflect not a simple loss of immune activity, but age-associated remodeling of the amplitude, kinetics, and resolution of innate immune responses. In aged tissues, nucleic acid-sensing pathways often display elevated basal inflammatory or antiviral-like signaling, whereas inducible type I interferon (IFN) and interferon-stimulated gene (ISG) responses to infection or vaccination are delayed, blunted, or poorly resolved. This review summarizes the innate antiviral signaling pathways and discusses how aging and cellular senescence narrow the range between basal and inducible responses. We emphasize senescent cells as sources of senescence-associated secretory phenotype (SASP) factors that suppress neighboring-cell antiviral IFN responses and amplify inflammatory tissue damage, and discuss strategies to restore inducible IFN competence while limiting chronic basal activation in older adults, to improve vaccine efficacy and treat aging-associated infectious diseases.
Zhang X, Yang Q Remodeling of innate antiviral immunity in aging. Cell insight. 2026. doi:10.1016/j.cellin.2026.100362. PMID: 42866291. https://pubmed.ncbi.nlm.nih.gov/42866291/