ArticleImmunity, inflammation and disease2026
Somatic Hypermutations Enhance Neutralization Breadth of IGHV3-53/3-66 Public Antibodies Against SARS-CoV-2 Variants.
Takeo Kuwata, Kyo Okazaki, Hiroshi Morioka, Yu Kaku, Mikiko Shimizu, Yoshimi Maruyama, Ahmed K Hamdy, Genotype to Phenotype Japan (G2P‐Japan) Consortium, Tateki Suzuki, Takao Hashiguchi and 2 more
Abstract read
In one paragraphArticle in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from itWhat 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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
12 authors.
Takeo KuwataCollaborative Research Program With the Chemo-Sero-Therapeutic Research Institute for Anti-Viral Agents and Hematological Diseases, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0001-7793-6585 Kyo OkazakiDepartment of Analytical and Biophysical Chemistry, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Hiroshi MoriokaDepartment of Analytical and Biophysical Chemistry, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
Mikiko ShimizuCollaborative Research Program With the Chemo-Sero-Therapeutic Research Institute for Anti-Viral Agents and Hematological Diseases, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Yoshimi MaruyamaCollaborative Research Program With the Chemo-Sero-Therapeutic Research Institute for Anti-Viral Agents and Hematological Diseases, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.
Ahmed K HamdyCollaborative Research Program With the Chemo-Sero-Therapeutic Research Institute for Anti-Viral Agents and Hematological Diseases, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-1830-9132 Genotype to Phenotype Japan (G2P‐Japan) Consortium
Tateki SuzukiLaboratory of Medical Virology, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Takao HashiguchiLaboratory of Medical Virology, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Kei SatoDepartment of Microbiology and Immunology, Division of Systems Virology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Shuzo MatsushitaCollaborative Research Program With the Chemo-Sero-Therapeutic Research Institute for Anti-Viral Agents and Hematological Diseases, Joint Research Center for Human Retrovirus Infection, Kumamoto University, Kumamoto, Japan.ORCID https://orcid.org/0000-0002-9649-8821 Funding
Japan Agency for Medical Research and Development JP223fa627009Japan Agency for Medical Research and Development JP23ym0126048Japan Agency for Medical Research and Development JP25jf0126002Japan Society for Promotion of Science (Core-to-Core Program)
6 · The paper itselfAbstract
objectiveSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continuously evolves to evade antibodies elicited by prior infection or vaccination. Most IGHV3-53/3-66 public antibodies potently neutralize the prototype strain, but show limited activity against recent variants. However, some acquire broad neutralizing activity through accumulation of somatic hypermutations. We assessed whether non-broadly neutralizing IGHV3-53/3-66 antibodies could mature into broadly neutralizing antibodies.
methodsA series of mutant antibodies was constructed based on the IGHV3-53/3-66 antibodies, 9-105 and K4-66. Neutralizing and binding activities were compared with the original antibodies.
resultsIntroducing six mutations frequently observed in broadly neutralizing antibodies markedly improved the neutralization and binding of 9-105 against Omicron variants. Introducing Y66F into K4-66 enhanced neutralization of variants including BA.4/5 and JN.1.
conclusionThese findings show that mutations within the IGHV3-53/3-66 gene can enhance antibody breadth and potency, suggesting the potential of vaccine strategies to promote the maturation of these widely prevalent public antibodies.
Indexed as
Antibodies, NeutralizingAntibodies, ViralCOVID-19SARS-CoV-2Somatic Hypermutation, ImmunoglobulinAnimalsHumansMutationNeutralization TestsSpike Glycoprotein, CoronavirusAntibodies, NeutralizingAntibodies, ViralSpike Glycoprotein, Coronavirusneutralizing antibodypublic antibodySARS‐CoV‐2variant
Identifiers
PMID42747156
PMCPMC13580150
What OpenQuestion holds
Textmetadata
Read underepoch 390