Telomeres and COVID‐19
Open accessAbstract
The medical, public health, and scientific communities are grappling with monumental imperatives to contain COVID‐19, develop effective vaccines, identify efficacious treatments for the infection and its complications, and find biomarkers that detect patients at risk of severe disease. The focus of this communication is on a potential biomarker, short telomere length (TL), that might serve to identify patients more likely to die from the SARS‐CoV‐2 infection, regardless of age. The common thread linking these patients is lymphopenia, which largely reflects a decline in the numbers of CD4/CD8 T cells but not B cells. These findings are consistent with data that lymphocyte TL dynamics impose a limit on T‐cell proliferation. They suggest that T‐cell lymphopoiesis might stall in individuals with short TL who are infected with SARS‐CoV‐2.
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COVID-19 disease severity correlates with patient age and leukocyte telomere length, and tDDR activation induced by telomere shortening increases ACE2 expression on human lung cells.
“Disease severity has been correlated with patient age and leukocyte telomere length71, which is consistent with a recent finding that tDDR activation induced by telomere shortening increases the expression of ACE2, the SARS-CoV-2 receptor on human lung cells72.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [71]
The “Major features of COVID-19” section reports worse outcomes among older people and proposes that their comparatively short telomeres may help explain those outcomes. The Abstract describes short telomere length as a potential risk marker, not an established patient-level correlation with disease severity. The ACE2 finding is attached to citation 72, so it is not assessed against this paper. (LLM, conf=0.88)
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References 66 · Cited by 73
- Authors
- Aviv, A.
- Affiliations
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- Aviv, Abraham
- ORCID
- Aviv, Abraham
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2020-05-19
- Volume
- 34
- Issue
- 6
- Pages
- 7247-7252
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC7276714
- OpenAlex
- W3025637034
- Cited by
- 73
- References
- 66
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 9 · 2023: 10 · 2022: 12 · 2021: 21 · 2020: 13
- FWCI
- 8.42
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The FASEB Journal (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01 HL134840)
- National Institute on Aging (U01AG066529)
- Norges Forskningsråd (ES562296)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Keywords
- telomere length, short telomeres, COVID-19 pandemic, SARS-CoV-2, lymphopenia, CD4+ T cells, CD8+ T cells, T cell proliferation, severe COVID-19
- MeSH terms
- Betacoronavirus, COVID-19, SARS-CoV-2, Bone Marrow, Cell Division, Hematopoietic Stem Cells, Humans, Lymphocyte Activation, Lymphopenia, Models, Biological, Pneumonia, Viral, Prognosis, Risk, Biomarkers, T-Lymphocyte Subsets, Telomere, Coronavirus Infections, Disease Progression, Lymphocyte Count, Lymphopoiesis, Pandemics, Telomere Shortening
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