ArticleThe Journal of clinical investigation2025
A protective and heterosubtypic antibody lineage targeting the influenza A virus neuraminidase active site.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- What Antibody Repertoires See: Structural and Immunogenetic Insights Into Influenza A Virus Hemagglutinin Recognition.Immunological reviews · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
Influenza type A viruses (IAVs) remain an extraordinary burden to global public health and regularly circulate through human populations. This investigation describes the isolation of human mAbs from an individual with a substantial history of influenza exposure via vaccination and natural infection. From these mAbs, a clonally expanded B cell lineage was identified that recognizes the IAV neuraminidase (NA) glycoprotein and binds near the NA active site of H3N2 viruses to inhibit sialidase activity. Further characterization found that some somatically mutated members of this lineage exhibited cross-reactive binding to recombinant N1 and N9 antigens, suggesting that heterosubtypic reactivity was acquired through somatic mutation. Two candidate mAbs from this family - FluA-168 and FluA-173 - potently inhibited IAV replication in vitro and protected against lethality in vivo. The results of this study contribute to our understanding of cross-reactivity between IAV subtypes in response to diverse exposure patterns and identified 2 mAbs as potential therapeutic candidates for IAV infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.