ReviewCell insight2026
Remodeling of innate antiviral immunity in aging.
Review in Cell insight, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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0 citing papers in PubMed.
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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