Evidence map›Paper›PMID 40444468›Full record

ArticlemBio2025

A rotavirus VP4 or VP7 monoreassortant panel identifies genotypes that are less susceptible to neutralization by systemic antibodies induced by vaccination or natural infection.

Tomohiro Kotaki, Yuta Kanai, Kristen M Ogden, Megumi Onishi, Kattareeya Kumthip, Pattara Khamrin, Patcharaporn Boonyos, Pornkamol Phoosangwalthong, Phakapun Singchai, Tipsuda Luechakham and 8 more

Abstract read
In one paragraph

Article in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Frontiers in immunology · 2026
    Article
  7. 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

18 authors.

Tomohiro KotakiDepartment of Virology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.ORCID 0000-0003-0284-8278
Yuta KanaiDepartment of Virology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.
Kristen M OgdenDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.ORCID 0000-0002-2670-4335
Megumi OnishiDepartment of Virology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.
Kattareeya KumthipDepartment of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.ORCID 0000-0001-7028-7607
Pattara KhamrinDepartment of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Patcharaporn BoonyosThailand-Japan Research Collaboration Center on Emerging and Re-emerging Infections, Nonthaburi, Thailand.ORCID 0000-0003-0981-103X
Pornkamol PhoosangwalthongThailand-Japan Research Collaboration Center on Emerging and Re-emerging Infections, Nonthaburi, Thailand.
Phakapun SingchaiDepartment of Medical Sciences, Ministry of Public Health, Nonthaburi, Thailand.
Tipsuda LuechakhamDepartment of Medical Sciences, Ministry of Public Health, Nonthaburi, Thailand.
Shohei MinamiDepartment of Virology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.ORCID 0000-0002-3999-348X
Zelin ChenDepartment of Virology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.
Katsuhisa HiraiDepartment of Virology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.
Ratana TacharoenmuangDepartment of Medical Sciences, Ministry of Public Health, Nonthaburi, Thailand.
Hiroto MizushimaThailand-Japan Research Collaboration Center on Emerging and Re-emerging Infections, Nonthaburi, Thailand.
Hiroshi UshijimaDepartment of Pathology and Microbiology, Nihon University School of Medicine, Tokyo, Japan.
Niwat ManeekarnDepartment of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.ORCID 0000-0001-5665-3332
Takeshi KobayashiDepartment of Virology, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.ORCID 0000-0002-5532-207X

Funding

Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MARY Kay WASHINGTON · 2002 to 2026
$29.9M
BIKEN FoundationJapan Agency for Medical Research and Development JP22gm1610008, JP22wm0125010, JP223fa627002, JP23fk0108668, JP20wm0225006Japan Society for the Promotion of Science 21H02739, 24K02285, 22K07100, 22H03117Moonshot Research and Development Program JPMJMS2025NIDDK NIH HHS P30 DK058404
6 · The paper itself

Abstract

Rotavirus infections remain a significant cause of morbidity and mortality in infants. The viral surface proteins VP4 and VP7 are each classified into multiple genotypes (P[1]-P[58] for VP4 and G1-G42 for VP7), which differ in their susceptibility to neutralizing antibodies; however, detailed analyses of these differences remain limited. This study investigates the susceptibility of diverse VP4 and VP7 genotypes to neutralizing antibodies induced by vaccination or natural infection. A reverse genetics system based on the human rotavirus Odelia strain (G4P[8]) was used to create monoreassortant viruses by replacing the VP4 or VP7 genes with those from clinical isolates (obtained in Thailand) or prototype strains. We generated 11 VP4 and 19 VP7 reassortants, covering 7 and 17 genotypes, respectively. Neutralization tests using the monoreassortant viruses, immune sera, and MA104 cells indicate that the VP7 genotype, rather than the VP4 genotype, primarily influences susceptibility to neutralization. Furthermore, genotypes G2, bat-like G3, G11, G12, G25, and G33 were significantly less susceptible to sera from naturally infected Thai individuals, highlighting the importance of monitoring these genotypes. To identify the protein region responsible for susceptibility to neutralization, we generated chimeric viruses by exchanging the domains of high- and low-susceptibility VP7 genotypes and found that Domain I appears to play a substantial role in determining susceptibility. Thus, we identified multiple rotavirus genotypes with reduced susceptibility to neutralization, as well as the region primarily responsible for this reduction. These findings may help to predict possible future rotavirus outbreaks in humans and facilitate the development of effective rotavirus vaccines.IMPORTANCERotavirus, the leading cause of severe acute gastroenteritis in infants, is responsible for approximately 128,500 infant deaths globally each year. The virus's surface proteins are highly diverse, comprising approximately 100 genotypes. This diversity affects susceptibility to neutralizing antibodies and the efficacy of vaccines. Here, we found that certain genotypes are highly resistant to serum neutralizing antibodies induced by vaccination and natural infections. Furthermore, we identified a specific region in the viral outer capsid protein that plays a significant role in determining susceptibility to neutralization. These findings may be important for predicting outbreak-causing strains and for developing more effective vaccines, ultimately contributing to the prevention of future outbreaks and improving global infant health.

Indexed as

Antibodies, NeutralizingAntibodies, ViralAntigens, ViralCapsid ProteinsGenotypeRotavirusRotavirus InfectionsRotavirus VaccinesHumansNeutralization TestsReassortant VirusesReverse GeneticsThailandVaccinationAntibodies, NeutralizingAntibodies, ViralAntigens, ViralCapsid ProteinsRotavirus VaccinesVP4 protein, RotavirusVP7 protein, Rotavirusgenotypeneutralization susceptibilityreverse geneticsrotavirusvaccineVP4VP7

Identifiers

PMID40444468
PMCPMC12239578

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.