ArticleJournal of virology2026
Type I interferon signaling is required for resistance to primary influenza virus infection and vaccine-induced long-term immunity.
Article in Journal of virology, 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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10 authors.
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Abstract
Type I interferons (IFNs) are critical for early antiviral defense, yet their role in shaping vaccine-induced immunity remains incompletely understood. Here, we investigated the impact of type I IFN receptor (IFNαβR) deficiency on immune responses to influenza virus infection and vaccination in IFNαβR-deficient (AB6) mice. AB6 mice exhibited profound susceptibility to influenza virus infection, characterized by accelerated weight loss, elevated lung viral loads, and severe histopathology. Despite inducing short-term IgG antibodies and protection against weight loss after H5 hemagglutinin virus-like particle (H5 VLP) vaccination, AB6 mice were less effective in controlling lung viral loads and inflammation after lethal influenza virus infection, compared to the wild-type (B6) mice. IFNαβR deficiency dysregulated chemokines and numerous innate immune cells, particularly neutrophils, contributing to lung pathology after H5 VLP vaccination and influenza virus infection. AB6 mice exhibited a faster kinetics of waning IgG antibodies and lower efficacy of long-term protection after vaccination than wild-type B6 mice.IMPORTANCEType I interferons (IFNs) are essential mediators of antiviral defense, but their contribution to vaccine-induced immunity remains unclear. This study reveals that type I IFN receptor signaling is dispensable for the initial antibody induction but is critical for sustaining long-term humoral immunity and balanced immune regulation after influenza vaccination and infection. Loss of IFNαβR signaling leads to impaired viral control, excessive neutrophil-driven inflammation, and disrupted immune cell homeostasis. These findings highlight type I IFN signaling as a key integrator of innate and adaptive immune responses required for adequate and durable antiviral protection.
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