Senescence genes in Long COVID: transcriptomic cohort findings
In this cohort abstract, senescence-associated genes were more enriched in early post-infection whole blood of people who later developed Long COVID symptoms than in those who did not. [1]
Automatic summary · not editorially reviewed
The key findings
In a cohort study, whole-blood samples taken after infection were compared against a 125-gene cellular-senescence set (SenMayo). [1]
SenMayo genes were significantly upregulated early after infection in 56 people who later developed Long COVID symptom phenotypes versus 104 who did not. [1]
The authors suggest senescence-associated genes may play a role in Long COVID development, with shared and unique patterns across phenotypes. [1]
The source at a glance
- Study type / format
- Cohort study; abstract of a transcriptomic gene-set enrichment analysis
- Population / context
- Cohort participants grouped by post-COVID-19 phenotypes, including people with and without Long COVID symptoms, cognitive impairment or persistent dyspnea.
- Summary based on
- Study abstract
- Original publication
- October 1, 2026
Senescence genes compared across Long COVID phenotypes
The researchers asked whether cellular senescence, described as cell-cycle arrest with release of inflammatory factors, may play a role in Long COVID. In a cohort study, participants were sorted into post-COVID-19 groups: symptom-based phenotypes from a machine-learning analysis (sensory, fatigue/difficulty thinking, difficulty breathing/exercise intolerance), cognitive impairment measured with the BRACE screening tool, and persistent dyspnea measured with a symptom scale known to correlate with a 6-minute walk test. Whole-blood samples taken after infection were analysed for gene activity, comparing 47,125 reference genes against a 125-gene cellular-senescence set (SenMayo).
Supporting source [1]
Higher enrichment in those who later developed symptoms
SenMayo genes were significantly upregulated in the early period after infection in three comparisons: 56 people who later developed Long COVID symptom phenotypes versus 104 who did not (enrichment score 6.04, P = .001); 32 with long-term cognitive impairment versus 40 without, measured by BRACE (2.58, P = .032); and 26 with persistent dyspnea versus 53 without, measured by the validated dyspnea instrument (6.29, P = .001). ETS2 was upregulated across all impairment-related phenotypes, while other SenMayo genes varied by phenotype.
Supporting source [1]
Abstract-only gene-activity associations, not causes
The authors conclude that senescence-associated genes may play a role in Long COVID development, with shared and unique transcriptomic patterns across phenotypes. These are associations in gene activity from whole blood, not evidence that senescence causes Long COVID or that altering it would help. Only the abstract was reviewed; the full text was not reviewed, so design details, follow-up and how the early post-infection period was defined are not available here.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. These are gene-activity associations, not causal evidence, and the abstract does not define the early post-infection period or follow-up.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Epsi NJ, Richard SA, Morris MJ, Lindholm DA, Ganesan A, Colombo RE, Mende K, Jones MU, Malloy AMW, Rubin LH, Agan BK, Tribble DR, Burgess TH, Dalgard C, Puskarich MA, Pollett SD. · europepmc.org · October 1, 2026