Evidence map›Paper›PMID 41758737›Full record

ArticleJournal of innate immunity2026

Respiratory Syncytial Virus Nonstructural Protein 1 Inhibits Production of Cytokines and Chemokines by Differentiated Primary Nasal Epithelial Cells Cultured at Air-Liquid Interface.

Rosanne W Koutstaal, Amadeo Munoz Garcia, Nadine Ebert, Manon F Licheri, Anke J Lakerveld, Hendrik-Jan Hamstra, Anne T Gelderloos, Jørgen de Jonge, Cécile A C M van Els, Volker Thiel and 2 more

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In one paragraph

Article in Journal of innate immunity, 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 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Rosanne W KoutstaalCenter for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Amadeo Munoz GarciaCenter for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Nadine EbertInstitute of Virology and Immunology (IVI), Bern, Switzerland.
Manon F LicheriInstitute for Infectious Diseases, University of Bern, Bern, Switzerland.
Anke J LakerveldCenter for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Hendrik-Jan HamstraCenter for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Anne T GelderloosCenter for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Jørgen de JongeCenter for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Cécile A C M van ElsCenter for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands.
Volker ThielInstitute of Virology and Immunology (IVI), Bern, Switzerland.
Ronald DijkmanInstitute for Infectious Diseases, University of Bern, Bern, Switzerland.
Puck B van KasterenCenter for Infectious Disease Control, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands, puck.van.kasteren@rivm.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionRespiratory syncytial virus (RSV) is a major cause of severe respiratory infections in children and older adults. Currently, approved vaccines target only the viral fusion protein, but live-attenuated vaccines - e.g., through inactivation of nonstructural protein 1 (NS1) - likely induce a broader immune response. NS1 inhibits the immune response by repressing interferon production, but this has mostly been shown in immortalized cell lines, which do not necessarily represent the in vivo situation.

methodsHere, we assessed the effect of NS1 mutations on replication and host responses in physiologically relevant differentiated primary human nasal epithelial cells (HNEC) cultured at air-liquid interface (ALI). Using yeast-based reverse genetics, NS1-inactivating mutations were introduced.

resultsIn differentiated HNECs, NS1 mutants showed delayed replication compared to wild-type (WT) virus. Bulk RNA sequencing early after infection revealed stronger antiviral signatures in HNEC infected with NS1 mutants compared to WT, characterized by upregulation of interferons and chemokines. Cytokine analysis confirmed these results. Finally, an indirect immune cell migration assay revealed that both WT and NS1-mutant viruses induce migration of mainly neutrophils.

conclusionThis study shows that RSV NS1 supports viral replication not only via inhibition of the production of interferons, but also by reducing early chemokine production and secretion by epithelial cells. Together, our data highlight the suitability of the ALI transwell model for preclinical assessment of live-attenuated vaccine candidates.

Indexed as

Epithelial CellsNasal MucosaRespiratory Syncytial Virus, HumanRespiratory Syncytial Virus InfectionsViral Nonstructural ProteinsCell DifferentiationCells, CulturedChemokinesCytokinesHumansMutationVirus ReplicationChemokinesCytokinesViral Nonstructural ProteinsHost responseImmune evasionIn vitro preclinical modelRespiratory syncytial virusReverse genetics

Identifiers

PMID41758737
PMCPMC13175544

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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.