Evidence map›Paper›PMID 40262853›Full record

ArticleLife science alliance2025

Human iPS cell-derived respiratory organoids as a model for respiratory syncytial virus infection.

Rina Hashimoto, Yukio Watanabe, Abeer Keshta, Masaya Sugiyama, Yuki Kitai, Ai Hirabayashi, Naoko Yasuhara, Shiho Morimoto, Ayaka Sakamoto, Yasufumi Matsumura and 6 more

Abstract read
In one paragraph

Article in Life science alliance, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

16 authors.

Rina HashimotoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.
Yukio WatanabeCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.
Abeer KeshtaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.ORCID 0009-0003-3497-2748
Masaya SugiyamaDepartment of Viral Pathogenesis and Controls, National Center for Global Health and Medicine, Ichikawa, Japan.
Yuki KitaiDepartment of Microbiology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Ai HirabayashiLaboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Naoko YasuharaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.
Shiho MorimotoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.
Ayaka SakamotoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.
Yasufumi MatsumuraDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0001-8595-8944
Hidekazu NishimuraVirus Research Center, Clinical Research Division, Sendai Medical Center, National Hospital Organization, Sendai, Japan.
Takeshi NodaLaboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Takuya YamamotoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan.ORCID 0000-0002-0022-3947
Miki NagaoDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-8886-6145
Makoto TakedaDepartment of Microbiology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Kazuo TakayamaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan kazuo.takayama@cira.kyoto-u.ac.jp.ORCID 0000-0002-1132-2457

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory syncytial virus (RSV) is a seasonal respiratory pathogen that primarily affects young children, potentially causing severe lower respiratory tract disease. Despite the high disease burden, understanding of RSV pathophysiology remains limited. To address this, advanced RSV infection models are needed. Whereas HEp-2 cells are widely used because of their high susceptibility to RSV, they do not accurately reflect the host response of the human respiratory tract. In this study, we evaluated human-induced pluripotent stem cell-derived respiratory organoids, which contain respiratory epithelial cells, immune cells, fibroblasts, and vascular endothelial cells, for their potential to model RSV infection and support pharmaceutical research. RSV-infected organoids exhibited high viral genome and protein expression, epithelial layer destruction, and increased collagen accumulation. Pro-inflammatory cytokine levels in culture supernatants also increased post-infection. Furthermore, RSV infection was significantly inhibited by monoclonal antibodies (nirsevimab, palivizumab, suptavumab, or clesrovimab), although ribavirin showed limited efficacy. These findings highlight the utility of respiratory organoids for RSV research.

Indexed as

Induced Pluripotent Stem CellsOrganoidsRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsAntibodies, MonoclonalAntiviral AgentsCytokinesEpithelial CellsHumansRespiratory Syncytial VirusesAntibodies, MonoclonalAntiviral AgentsCytokines

Identifiers

PMID40262853
PMCPMC12015132

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.