Evidence map›Paper›PMID 40501971›Full record

ArticlebioRxiv : the preprint server for biology2025

COVID-19 induces persistent transcriptional changes in adipose tissue that are not associated with Long COVID.

Soneida DeLine-Caballero, Kalani Ratnasiri, Heping Chen, Seynt Jiro Sahagun, Uma M Mangalanathan, Trisha R Barnard, Nicole Turk, Jasmine Yang, Natesh Saini, Ekrem M Ayhan and 13 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. 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

23 authors.

Soneida DeLine-CaballeroDivision of Infectious Disease, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Kalani RatnasiriDivision of Infectious Disease, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0001-5953-0004
Heping ChenDivision of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Seynt Jiro SahagunMaineHealth Institute for Research, Scarborough, ME 04074.
Uma M MangalanathanDivision of Infectious Disease, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Trisha R BarnardDivision of Infectious Disease, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Nicole TurkDivision of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Jasmine YangDivision of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Natesh SainiDivision of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Ekrem M AyhanDivision of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Hasiyet MemetiminDivision of Endocrinology, Department of Internal Medicine, University of Kentucky College of Medicine, Lexington, KY 40506.
Brian S FinlinDivision of Endocrinology, Department of Internal Medicine, University of Kentucky College of Medicine, Lexington, KY 40506.
Zachary LeichtDivision of Endocrinology, Department of Internal Medicine, University of Kentucky College of Medicine, Lexington, KY 40506.
Phillip A KernDivision of Endocrinology, Department of Internal Medicine, University of Kentucky College of Medicine, Lexington, KY 40506.
Ivette EmeryMaineHealth Institute for Research, Scarborough, ME 04074.
Brooke M LeemanDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Gregory E EdelsteinDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Samantha CostaMaineHealth Institute for Research, Scarborough, ME 04074.
Alina ChoiDivision of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Jonathan Z LiDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Clifford RosenMaineHealth Institute for Research, Scarborough, ME 04074.
Tracey McLaughlinDivision of Endocrinology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.
Catherine A BlishDivision of Infectious Disease, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305.

Funding

OTA-21-015A Post-Acute Sequelae of SARS-CoV-2 Infection Initiative: NYU Langone Health Clinical Science Core, Data Resource Core, and PASC Biorepository CoreOT2HL161847 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI GROSS, RACHEL SHARON, HORWITZ, LEORA · 2021 to 2025
$651.0M
Understanding Factors Influencing COVID-19 Testing and Vaccination in Immigrant Low-income and Homeless Populations and Testing Targeted InterventionsU54GM115516 · NIGMS · MAINEHEALTH · PI Robert A Koza · 2017 to 2026
$51.6M
Kentucky Center for Clinical and Translational ScienceUL1TR001998 · NCATS · UNIVERSITY OF KENTUCKY · PI HARTMANN, KATHERINE E, KERN, PHILIP A · 2016 to 2025
$34.2M
Stanford Center for Clinical and Translational Research and EducationUM1TR004921 · NCATS · STANFORD UNIVERSITY · PI MANISHA DESAI, DEAN W FELSHER · 2024 to 2026
$30.1M
NCATS NIH HHS UL1 TR001998NCATS NIH HHS UM1 TR004921NHLBI NIH HHS OT2 HL161847NIGMS NIH HHS U54 GM115516
6 · The paper itself

Abstract

Long COVID is a heterogeneous condition characterized by a wide range of symptoms that persist for 90 days or more following SARS-CoV-2 infection. Now more than five years out from the onset of the SARS-CoV-2 pandemic, the mechanisms driving Long COVID are just beginning to be elucidated. Adipose tissue has been proposed as a potential reservoir for viral persistence and tissue dysfunction contributing to symptomology seen in Long COVID. To test this hypothesis, we analyzed subcutaneous adipose tissue (SAT) from two cohorts: participants with subacute COVID-19 (28-89 days post-infection) compared to pre-pandemic controls, and participants with Long COVID compared to those with those classified as "indeterminate" based on the RECOVER-Adult Long COVID Research Index (12-47 months post-infection). We found no evidence of persistent SARS-CoV-2 RNA in adipose tissue in any participant. SAT from participants with subacute COVID-19 displayed significant transcriptional remodeling, including depleted immune activation pathways and upregulated Hox genes and integrin interactions, suggesting resident immune cell exhaustion and perturbations in tissue function. However, no consistent changes in gene expression were observed between Long COVID samples and samples from indeterminant participants. Thus, SAT may contribute to inflammatory dysregulation following COVID-19, but does not appear to play a clear role in Long COVID pathophysiology. Further research is needed to clarify the role of adipose tissue in COVID-19 recovery.

Indexed as

Long COVIDRNA SequencingSARS-CoV-2Subacute COVID-19Subcutaneous Adipose TissueTranscriptome

Identifiers

PMID40501971
PMCPMC12154766

What OpenQuestion holds

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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.