Evidence map›Paper›PMID 41639986›Full record

ArticleThe Journal of infectious diseases2026

Genomic Evolution of Influenza A Virus During the 2024-2025 Season, the Johns Hopkins Health System: Antigenic Drift Reduces Serum Neutralization.

David Villafuerte, Amary Fall, Elgin Akin, Anne P Werner, Matthew Pinsley, Yee Vue, Omar Abdullah, Ting Xuan Zhuang, Julie M Norton, Richard E Rothman and 5 more

Abstract read
In one paragraph

Article in The Journal of infectious diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

David VillafuerteDepartment of Pathology, Division of Medical Microbiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0009-0006-7159-7889
Amary FallDepartment of Pathology, Division of Medical Microbiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Elgin AkinW.Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.
Anne P WernerW.Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.ORCID 0000-0003-2322-6830
Matthew PinsleyW.Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.ORCID 0009-0007-6588-8812
Yee VueW.Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.ORCID 0000-0002-6489-2007
Omar AbdullahDepartment of Pathology, Division of Medical Microbiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Ting Xuan ZhuangDepartment of Pathology, Division of Medical Microbiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0009-0001-7044-7751
Julie M NortonDepartment of Pathology, Division of Medical Microbiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Richard E RothmanDepartment of Emergency Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Katherine Z J FenstermacherDepartment of Emergency Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
C Paul MorrisIntegrated Research Facility, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, USA.ORCID 0000-0002-6403-5048
Eili KleinDepartment of Emergency Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-1304-5289
Andrew PekoszW.Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.ORCID 0000-0003-3248-1761
Heba H MostafaDepartment of Pathology, Division of Medical Microbiology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.

Funding

NIAID Centers of Excellence for Influenza Research and Response: Universal Influenza Vaccine Research Activities75N93021C00045 · NIAID · JOHNS HOPKINS UNIVERSITY · PI PEKOSZ, ANDREW · 2021 to 2025
$23.3M
Training: Molecular & Cellular Bases of Infectious DiseasesT32AI007417 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Arturo Casadevall · 1994 to 2026
$11.9M
Johns Hopkins Center of Excellence in Influenza Research and Response 5T32AI007417-25Johns Hopkins Center of Excellence in Influenza Research and Response HHS 75N93021C000045NHLBI NIH HHSNIAID NIH HHS T32 AI007417NIBIB NIH HHSNIH HHS 75N93021C00045US Department of Health and Human Services
6 · The paper itself

Abstract

backgroundSeasonal influenza causes significant global morbidity, mortality, and economic burden. Ongoing viral evolution can lead to vaccine mismatch and the emergence of antiviral resistance, highlighting the importance of genomic surveillance. The 2024-2025 influenza season was characterized by high incidence and increased hospitalizations.

methodsWe analyzed influenza A virus (IAV) genomes and clinical characteristics from the 2024-2025 season. Whole-genome sequencing was performed on 648 influenza A-positive clinical specimens collected between October 2024 and April 2025.

resultsHemagglutinin (HA) sequences were recovered from 74.23% (481/648) of samples and used for subtyping and phylogenetic analysis. A(H1N1)pdm09 and A(H3N2) viruses cocirculated, representing 55.5% and 44.5% of cases, respectively. Among A(H1N1)pdm09 viruses, the HA1 substitution T120A, located near the Sa antigenic site, increased more than 2-fold compared with the prior season. Circulating A(H3N2) viruses belonged to multiple HA subclades and exhibited distinct amino acid substitutions at key antigenic sites. Neutralization assays using sera from individuals vaccinated with the 2024-2025 seasonal influenza vaccine demonstrated reduced neutralization of 3 dominant A(H1N1)pdm09 isolates and 2 A(H3N2) isolates compared with vaccine strains, consistent with antigenic drift. In addition, the neuraminidase substitution S247N, previously associated with reduced oseltamivir susceptibility, was detected in 13.9% of A(H1N1)pdm09 samples.

conclusionsThese findings demonstrate ongoing antigenic drift and the presence of antiviral resistance-associated mutations during the 2024-2025 influenza season, underscoring the need for continued genomic surveillance to guide vaccine and antiviral strategies.

Indexed as

Antibodies, NeutralizingAntigenic Drift and ShiftEvolution, MolecularGenome, ViralInfluenza A virusInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H3N2 SubtypeInfluenza, HumanAdolescentAdultAntibodies, ViralChildDrug Resistance, ViralFemaleGenetic DriftHemagglutinin Glycoproteins, Influenza VirusAntibodies, NeutralizingAntibodies, ViralHemagglutinin Glycoproteins, Influenza VirusIAVinfluenzasequencingviral genomic surveillance

Identifiers

PMID41639986
PMCPMC13271379

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LicenceCC BY-NC-ND
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Registered trials

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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.