Evidence map›Paper›PMID 41761254›Full record

ArticleClinical epigenetics2026

Genome-wide DNA methylation profiling in COVID-19 positive patients reveals alterations in pathways linked to neurological dysfunction.

Saima Zameer, Ehraz Anis, Qiong Sha, Martha L Escobar Galvis, Sanam Khan, Jennifer A Steiner, Milda Milčiūtė, Ieva Kerševičiūtė, Migle Gabrielaite, Juozas Gordevicius and 5 more

Abstract read
In one paragraph

Article in Clinical epigenetics, 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

15 authors.

Saima ZameerDepartment of Neurodegenerative Science, Van Andel Institute, 333 Bostwick Ave NE, Grand Rapids, MI, 49503, USA.
Ehraz AnisDepartment of Neurodegenerative Science, Van Andel Institute, 333 Bostwick Ave NE, Grand Rapids, MI, 49503, USA.
Qiong ShaDepartment of Neurodegenerative Science, Van Andel Institute, 333 Bostwick Ave NE, Grand Rapids, MI, 49503, USA.
Martha L Escobar GalvisResearch Development, Van Andel Institute, Grand Rapids, MI, USA.
Sanam KhanDepartment of Neurodegenerative Science, Van Andel Institute, 333 Bostwick Ave NE, Grand Rapids, MI, 49503, USA.
Jennifer A SteinerDepartment of Neurodegenerative Science, Van Andel Institute, 333 Bostwick Ave NE, Grand Rapids, MI, 49503, USA.
Milda MilčiūtėVugene LLC, Grand Rapids, MI, USA.
Ieva KerševičiūtėVugene LLC, Grand Rapids, MI, USA.
Migle GabrielaiteVugene LLC, Grand Rapids, MI, USA.
Juozas GordeviciusVugene LLC, Grand Rapids, MI, USA.
Andrew PospisilikDepartment of Epigenetics, Van Andel Institute, Grand Rapids, MI, USA.
Nazia SaiyedMetabolomics Department, Corewell Health Research Institute, Royal Oak, MI, USA.
Stewart F GrahamMetabolomics Department, Corewell Health Research Institute, Royal Oak, MI, USA.
Patrik BrundinRoche Pharma Research and Early Development (pRED), Neuroscience and Rare Disorders, F.Hoffmann La-Roche AG, Basel, Switzerland.
Lena BrundinDepartment of Neurodegenerative Science, Van Andel Institute, 333 Bostwick Ave NE, Grand Rapids, MI, 49503, USA. Lena.Brundin@vai.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible RNA betacoronavirus, causing coronavirus disease-19 (COVID-19). Infection with SARS-CoV-2 can result in a broad spectrum of clinical outcomes, ranging from asymptomatic or mild to a severe, deadly illness. Emerging evidence suggests SARS-CoV-2 affects host gene regulation through epigenetic mechanisms, such as DNA methylation, potentially contributing to immune dysregulation and post-acute sequelae, including neurological and psychiatric disorders. However, the extent and functional relevance of these epigenetic changes remain uncertain. METHODS AND

resultsWe employed whole-genome methylation sequencing (WGMS) to profile DNA methylation in peripheral blood from SARS-CoV-2-positive patients across a spectrum of symptom severity, ranging from asymptomatic to severe (n = 101), in comparison to SARS-CoV-2-negative individuals (n = 105). We observed a widespread hypomethylation in the genomes of infected individuals, which was more pronounced in severe cases. Notably, we identified differentially methylated genes in patients with mild (19 genes), moderate (19 genes), and severe (35 genes) symptoms. These genes included those involved in canonical immune responses as well as known to be linked to neurodegenerative diseases. Subsequent pathway enrichment analysis further supported the significant association between the differentially methylated genes and those implicated in Alzheimer's and Parkinson's disease, as well as neuropsychiatric conditions, suggesting potential epigenetic links between acute SARS-CoV-2 infection and long-term neurological outcomes. Our WGMS comprehensively mapped severity-stratified genome-wide DNA methylation changes in COVID-19 patients.

conclusionOur findings underscore the potential importance of epigenetic regulation in the acute responses to SARS-CoV-2 infection and highlight an overlap with epigenetic mechanisms relevant for neuropsychiatric disease processes.

Indexed as

COVID-19DNA MethylationNervous System DiseasesAdultAgedEpigenesis, GeneticFemaleGenome-Wide Association StudyHumansMaleMiddle AgedSARS-CoV-2Severity of Illness IndexWhole Genome SequencingCOVID-19DNA methylationEpigenomeNeurodegeneration

Identifiers

PMID41761254
PMCPMC13049855

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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.