Evidence map›Paper›PMID 41903474›Full record

ArticleEBioMedicine2026

Elevated body mass index is associated with delayed protective airway mucosal immune responses in mild SARS-CoV-2 infection.

Joe Fenn, Rhia Kundu, Janakan Sam Narean, Emily Conibear, Aleksandra Koycheva, Seran Hakki, Nieves Derqui, Sean Nevin, Mica Tolosa-Wright, Jakob Jonnerby and 10 more

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PubMed Full text at PMC Publisher
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Article in EBioMedicine, 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

20 authors.

Joe FennNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK. Electronic address: j.fenn@imperial.ac.uk.
Rhia KunduNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Janakan Sam NareanNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Emily ConibearNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Aleksandra KoychevaNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Seran HakkiNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Nieves DerquiNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; MRC Centre for Global Infectious Disease Analysis, School of Public Health, Imperial College London, UK.
Sean NevinNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Mica Tolosa-WrightNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Jakob JonnerbyNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Kieran MadonNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Samuel BaldwinNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Timesh D PillayNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Robert VarroNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Constanta LucaNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
Graham TaylorDepartment of Infectious Disease, Imperial College London, London.
Jake DunningPandemic Sciences Institute, University of Oxford, Oxford, UK.
John S TregoningDepartment of Infectious Disease, Imperial College London, London.
Ajit LalvaniNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK; National Heart and Lung Institute, Imperial College London, London, UK.
INSTINCT Study InvestigatorsNIHR Health Protection Research Unit in Respiratory Infections, Imperial College London, London, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSARS-CoV-2 viral load in the upper respiratory tract (URT) typically peaks and declines within days of infection, even in individuals without prior infection or vaccination. Although this implicates the URT innate immune response in effectively restricting viral replication, the nature of the protective responses and how they are affected by demographic factors is poorly defined.

methodsWe recruited 54 seronegative household contacts of recently diagnosed COVID-19 cases and prospectively collected URT samples during and after exposure. Among the 39 individuals who became infected, we quantified airway mucosal cytokine and chemokine responses and virus-specific nasal IgA using Meso Scale Discovery assays, and assessed associations with demographic factors, viral load, and symptoms.

findingsParticipants with higher BMI had higher URT viral loads and more marked symptoms. This was significantly associated with delayed induction of protective inflammatory mediators in the airway mucosa but not in blood. Induction of virus-specific nasal IgA at 1-week post-infection also correlated with lower viral load.

interpretationElevated BMI retards initial airway mucosal innate immune responses to infection, which may partially explain the pronounced adverse impact of higher BMI on clinical and virological outcomes in COVID-19.

fundingThis work is supported by the NIHR Health Protection Research Unit in Respiratory Infections, Imperial College London in partnership with the UK Health Security Agency (Grant number: NIHR200927; AL) and the Medical Research Council (Grant number: MR/X004058/1). Infrastructure support for this research was provided by the NIHR Imperial Biomedical Research Centre (BRC).

Indexed as

Body Mass IndexCOVID-19Immunity, MucosalRespiratory MucosaAdultAgedCytokinesFemaleHumansImmunity, InnateImmunoglobulin AMaleMiddle AgedPandemicsSARS-CoV-2Viral LoadCytokinesImmunoglobulin ABody mass indexCOVID-19CytokinesImmunoglobulin AMucosal immunity

Identifiers

PMID41903474
PMCPMC13058998

What OpenQuestion holds

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LicenceCC BY
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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.