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Severe COVID-19

Disease

13 papers11 findings

  • Humans10
  • In silico2

Effects

4

NRP1

upin human cells1

1 study

  1. Severe COVID-19 increases NRP1 in human cells.

    “increased NRP1 abundance without corresponding changes in infection susceptibility”

    Cellssevere COVID-19 cases (<45 years)astrocytes

    Divergent responses to SARS-CoV-2 infection reveal brain resilience-associated astrocyte programs in centenarians

    Research SquareAug 12, 2026Preprint

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Cognitive function

downin humans1

1 study

  1. Severe COVID-19 impairs cognitive function in humans.

    “Cognitive decline primarily manifested in individuals with severe COVID-19 during the initial year of infection, after which the rate of decline decelerated.”

    Humans

    Tracking cognitive trajectories in older survivors of COVID-19 up to 2.5 years post-infection

    Nature agingJul 10, 2024

GrimAge

downin humans1

1 study

  1. Severe COVID-19 decreases GrimAge in humans (beta = -0.24, se = 0.07, P = 0.00122).

    “severe COVID-19 infection can slow the acceleration of the epigenetic clock "GrimAge" (beta = -0.24, se = 0.07, P = 0.00122)”

    Humansreverse Mendelian randomization

    Causal association of epigenetic aging and COVID-19 severity and susceptibility: A bidirectional Mendelian randomization study

    Frontiers in medicineSep 23, 2022

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Telomere length

downin humans1

1 study

  1. Severe COVID-19 decreases telomere length in humans (beta = -0.01; se = 0.01; P = 0.02779).

    “severe COVID-19 can cause telomere lengths to become shorter (beta = -0.01; se = 0.01; P = 0.02779).”

    Humansreverse Mendelian randomization

    Causal association of epigenetic aging and COVID-19 severity and susceptibility: A bidirectional Mendelian randomization study

    Frontiers in medicineSep 23, 2022

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Associations

7

Fraction of CD8+ cells classified as old-like

upin humans1

1 study

  1. Severe COVID-19 is associated with fraction of CD8+ cells classified as old-like in humans.

    “severe disease in younger adults was associated with a higher fraction of CD8+ cells classified as old-like by the pretrained model.”

    HumansCOVID-19 convalescent cohortCD8+ T cell

    Deep learning enables cross-species annotation and attribution of ageing states in haematopoietic stem and immune cells

    bioRxiv (Cold Spring Harbor Laboratory)Jul 26, 2026Preprint

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Biological age

upin humans1

1 study

  1. Severe COVID-19 is associated with biological age in humans.

    “They also had an acceleration of epigenetic age measured by DNA methylation.”

    Humansearly stage of SARS-CoV-2 infection

    Immunosenescence Profile Is Associated With Increased Susceptibility to Severe COVID-19

    Aging cellMay 19, 2025

Cellular senescence

upin humans1

1 study

  1. Severe COVID-19 is associated with cellular senescence in humans.

    “Patients who progressed to hospitalization displayed high frequencies of CD8+ and CD4+ T cells expressing exhaustion and senescence markers”

    Humansearly stage of SARS-CoV-2 infection

    Immunosenescence Profile Is Associated With Increased Susceptibility to Severe COVID-19

    Aging cellMay 19, 2025

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CD8+ stem cell-like memory T cells

downin humans1

1 study

  1. Severe COVID-19 is associated with CD8+ stem cell-like memory T cells in humans.

    “(ii) decreased early precursors CD8+ T stem cell-like memory cells (TSCM) and CD27+CD28+”

    HumansCOVID-19n = 104

    Increased levels of GM-CSF and CXCL10 and low CD8⁺ memory stem T Cell count are markers of immunosenescence and severe COVID-19 in older people

    Immunity & ageing : I & AMay 7, 2024

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Anti-platelet glycoprotein autoantibodies

upin humans1

1 study

  1. Anti-platelet glycoprotein autoantibodies raise the risk of severe COVID-19 in humans.

    “anti-cardiolipin and anti-platelet glycoprotein autoantibodies significantly increased the likelihood of developing a severe COVID-19 phenotype with aging”

    Humanswith aging

    Severe COVID-19 patients exhibit elevated levels of autoantibodies targeting cardiolipin and platelet glycoprotein with age: a systems biology approach

    npj agingAug 24, 2023

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Anti-cardiolipin autoantibody

upin humans1

1 study

  1. Anti-cardiolipin autoantibody raises the risk of severe COVID-19 in humans.

    “anti-cardiolipin and anti-platelet glycoprotein autoantibodies significantly increased the likelihood of developing a severe COVID-19 phenotype with aging”

    Humanswith aging

    Severe COVID-19 patients exhibit elevated levels of autoantibodies targeting cardiolipin and platelet glycoprotein with age: a systems biology approach

    npj agingAug 24, 2023

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Inflammation

upin humans1

1 study

  1. Inflammation raises the risk of severe COVID-19 in humans.

    “The chronic state of low-grade inflammation that accompanies aging (inflammaging) might predispose older adults to severe COVID-19.”

    Review

    Inflammaging at the Time of COVID-19

    Clinics in geriatric medicineMar 21, 2022

More on Inflammation

Funding

2 grants since 2022

National Institute of Allergy and Infectious DiseasesUS$446.9kJapan Society for the Promotion of ScienceJP¥4.7m

Latest

Nov 2025: 1Dec 2025: 3Jan 2026: 2Feb 2026: 1Mar 2026: 0Apr 2026: 2May 2026: 0Jun 2026: 2Jul 2026: 1Aug 2026: 0Sep 2026: 1Oct 2026: 215 in 12 months
Research Square

Small RNA linked to death in younger people with COVID-19

In patients under 55, higher levels of a gene-regulating RNA were associated with death, with a reported odds ratio of 6.00.In patients under 55, higher levels of a gene-regulating RNA were associated with death, with a reported odds ratio of 6.00.

Preprint: study in peopleMechanisms
Paper
Journal of Translational Medicine

Some T cell responses were weaker in older COVID-19 survivors

An observational study of COVID-19 survivors aged 18–59 and 60 or older found weaker responses after inactivated vaccines and subsequent Omicron infection in older…An observational study of COVID-19 survivors aged 18–59 and 60 or older found weaker responses after inactivated vaccines and subsequent Omicron infection in older adults.

Cohort studyImmune response
Paper

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