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Biomarkers

Study findings updated . AI-assisted evidence summary, not individual medical advice or a clinician endorsement.

THE SHORT VERSION

What’s worth knowing.

The key findings, what they mean, and the context that matters.

THE HEADLINE TAKEAWAYNone of 25 lab testsRoutine lab values did not differ between long COVID and full recovery

None of 25 routine lab tests could identify long COVID.

Among adults who had COVID-19, those with long COVID (a high score on the study's symptom index) had average routine lab results no different from infected people with a symptom score of zero. None of the 25 lab values studied worked as a useful marker of long COVID.

A normal routine lab panel cannot rule long COVID out, and standard blood work cannot confirm it either. People with real, lasting symptoms may still have normal results. Observational study of 10,094 adults at 83 sites, with labs taken about 6 months after infection; it could not tell whether lab differences were causes or results of infection.

See the evidence

NIH-funded RECOVER cohort comparing 25 standard lab tests in adults with and without prior infection and with or without long COVID symptoms.

From the study: “Among participants with prior infection, no meaningful differences in mean laboratory values were found between those with a PASC index of 12 or higher and those with a PASC index of zero.”

None of 25 lab tests

Erlandson KM et al. Differentiation of Prior SARS-CoV-2 Infection and Postacute Sequelae by Standard Clinical Laboratory Measurements in the RECOVER Cohort. Annals of internal medicine. 2024.

From the study: “Overall, no evidence was found that any of the 25 routine clinical laboratory values assessed in this study could serve as a clinically useful biomarker of PASC.”

None of 25 lab tests

Erlandson KM et al. Differentiation of Prior SARS-CoV-2 Infection and Postacute Sequelae by Standard Clinical Laboratory Measurements in the RECOVER Cohort. Annals of internal medicine. 2024.

02

In patients flagged by a suPAR blood test, anakinra improved recovery.

50% vs 27% recoveredFully recovered by day 28, anakinra vs placebo, in patients with high blood suPAR

In a randomized trial of 594 hospital patients whose blood suPAR (a protein whose early rise signals risk of worsening) flagged danger of respiratory failure, 50.4% given anakinra (sold as Kineret) had fully recovered by day 28 vs 26.5% on placebo. Deaths were 3.2% vs 6.9%.

A quick blood test picked out patients likely to worsen, and in that group an anti-inflammatory drug improved recovery, showing how a lab marker can help target treatment. Double-blind trial at 37 sites, December 2020 to March 2021, in patients at risk of respiratory failure rather than already critically ill; people with low suPAR were excluded.

See the evidence

Phase 3 double-blind trial (SAVE-MORE) randomizing 594 hospitalized COVID-19 patients with high suPAR to anakinra or placebo, December 2020 to March 2021.

From the study: “50.4% (204/405) of patients receiving anakinra had fully recovered with no viral RNA detected on day 28 compared to 26.5% (50/189) of patients receiving placebo”

50% vs 27% recovered

Kyriazopoulou E et al. Early treatment of COVID-19 with anakinra guided by soluble urokinase plasminogen receptor plasma levels: a double-blind, randomized controlled phase 3 trial. Nature medicine. 2021.

From the study: “3.2% (13/405) and 6.9% (13/189) of patients in the anakinra and placebo arms, respectively, died.”

50% vs 27% recovered

Kyriazopoulou E et al. Early treatment of COVID-19 with anakinra guided by soluble urokinase plasminogen receptor plasma levels: a double-blind, randomized controlled phase 3 trial. Nature medicine. 2021.

From the study: “594 patients with COVID-19 at risk of progressing to respiratory failure as identified by plasma suPAR”

50% vs 27% recovered

Kyriazopoulou E et al. Early treatment of COVID-19 with anakinra guided by soluble urokinase plasminogen receptor plasma levels: a double-blind, randomized controlled phase 3 trial. Nature medicine. 2021.

03

Infection was linked to Alzheimer's-type blood changes matching 4 years of aging.

Like 4 years of agingExtra fall in an Alzheimer's-linked blood ratio vs matched uninfected adults

In middle-aged and older adults with blood drawn before and during the pandemic, infected people had a bigger drop in the Aβ42:Aβ40 ratio (a blood sign linked to amyloid build-up in Alzheimer's disease) than matched people with no record of infection, equal to about 4 years of aging. Drops were larger after hospitalization: 5.5% versus 2.0% in those not hospitalized.

It raises the possibility that COVID-19, especially severe illness, could add to future Alzheimer's risk in older adults, a question that needs long-term follow-up. Observational matched study in the UK of mostly mild cases (only 20 hospitalized); it cannot prove infection caused the change, and a blood marker is not a dementia diagnosis.

See the evidence

Matched case-control study of 1,252 UK Biobank adults aged 46–80 at a pre-pandemic visit, with blood retested in 2021–2022.

From the study: “We observed a mean additional reduction in plasma Aβ42:Aβ40 ratio after SARS-CoV-2 infection equivalent to 4 years of aging”

Like 4 years of aging

Duff EP et al. Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection. Nature medicine. 2025.

From the study: “cases who were hospitalized with COVID-19 showed over twice the magnitude of reduction relative to non-hospitalized cases (5.5% versus 2.0%)”

Like 4 years of aging

Duff EP et al. Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection. Nature medicine. 2025.

04

In mostly immune adults, virus peaked around the fourth symptom day.

Peak on the fourth dayMedian nasal viral load in mostly immune adults with new COVID-19 symptoms

Among 348 adults testing positive, 91.1% had been vaccinated, infected before, or both. Their virus levels kept rising after symptoms began and peaked around the fourth day. Rapid antigen tests would catch an estimated 30.0%-60.0% of infections on the first day of symptoms but 80.0%-93.3% on the fourth day.

A negative rapid test on the first day of symptoms is weak reassurance. In today's highly immune population, a test a few days into symptoms is more likely to catch an infection. Day-by-day test accuracy was estimated from lab viral-load cutoffs, not from actual home tests, in one state's symptomatic adults.

See the evidence

Study of 348 symptomatic adults who tested PCR-positive at testing sites in Georgia, US, from April 2022 to April 2023, when Omicron dominated.

From the study: “Ag RDT sensitivity estimates were 30.0%-60.0% on the first day, 59.2%-74.8% on the third day, and 80.0%-93.3% on the fourth day of symptoms.”

Peak on the fourth day

Frediani JK et al. The New Normal: Delayed Peak SARS-CoV-2 Viral Loads Relative to Symptom Onset and Implications for COVID-19 Testing Programs. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2024.

From the study: “In a highly immune adult population, median SARS-CoV-2 viral loads peaked around the fourth day of symptoms.”

Peak on the fourth day

Frediani JK et al. The New Normal: Delayed Peak SARS-CoV-2 Viral Loads Relative to Symptom Onset and Implications for COVID-19 Testing Programs. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2024.

From the study: “Of 348 newly-diagnosed SARS-CoV-2 PCR-positive individuals (65.5% women, median 39.2 years), 317/348 (91.1%) had a history of vaccination, natural infection, or both.”

Peak on the fourth day

Frediani JK et al. The New Normal: Delayed Peak SARS-CoV-2 Viral Loads Relative to Symptom Onset and Implications for COVID-19 Testing Programs. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2024.

05

Virus protein in blood did not distinguish long COVID from recovery.

No long-COVID signalFree spike and nucleocapsid in blood did not differ with vs without long COVID

Researchers measured free spike and nucleocapsid (pieces of the virus) in blood from 200 people, 112 with post-COVID condition (long COVID), for up to 18 months after infection. Low levels lingered in some people, but neither protein differed between those with long COVID and controls, who had recovered or gave blood before the pandemic.

A blood test for leftover spike protein is not ready to diagnose long COVID, and these results argue against lingering virus protein in blood being the main driver for most patients. Observational study of only 200 people; it also showed that one lab method (DTT treatment) creates false spike signals, a reason to read such tests cautiously.

See the evidence

Longitudinal study in the ORCHESTRA project measuring virus proteins in 576 blood samples from 200 people, taken during infection and at 3, 6, 12 and 18 months.

From the study: “we quantified free spike and nucleocapsid in 200 participants (112 PCC, 58 non-PCC, and 30 prepandemic controls)”

No long-COVID signal

Coppens L et al. Longitudinal assessment of SARS-CoV-2 spike and nucleocapsid antigenemia in the ORCHESTRA post-COVID cohort. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2026.

From the study: “Low-level antigen persisted in a subset of participants up to 18 months; however, neither free spike nor nucleocapsid differed between PCC and controls”

No long-COVID signal

Coppens L et al. Longitudinal assessment of SARS-CoV-2 spike and nucleocapsid antigenemia in the ORCHESTRA post-COVID cohort. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2026.

06

By the third quarter of 2022, 96.4% aged 16+ had antibodies.

96.4% had antibodiesAges 16 and older, July–September 2022, from infection, vaccination or both

In a nationwide blood donor cohort, an estimated 96.4% of people aged 16 and older had COVID-19 antibodies by the third quarter of 2022. Spike (S) antibodies come from both infection and vaccination; only nucleocapsid (N) antibodies come from infection. Hybrid immunity, from both infection and vaccination, was lowest in people aged 65 and older: 36.9%.

A positive spike antibody result mostly reflects vaccination or past infection, which nearly everyone has. Only a nucleocapsid antibody test points specifically to past infection. Based on US blood donors weighted to resemble the population; donors may not represent everyone, and the study did not account for boosters or waning immunity.

See the evidence

CDC analysis of repeat donations from 72,748 people in a nationwide US blood donor cohort, tested for antibodies from April 2021 to September 2022.

From the study: “By the third quarter of 2022, an estimated 96.4% of persons aged ≥16 years in a longitudinal blood donor cohort had SARS-CoV-2 antibodies from previous infection or vaccination”

96.4% had antibodies

Jones JM et al. Estimates of SARS-CoV-2 Seroprevalence and Incidence of Primary SARS-CoV-2 Infections Among Blood Donors, by COVID-19 Vaccination Status - United States, April 2021-September 2022. MMWR. Morbidity and mortality weekly report. 2023.

From the study: “Both SARS-CoV-2 infection and COVID-19 vaccination result in production of anti-S antibodies, whereas anti-N antibodies only result from infection.”

96.4% had antibodies

Jones JM et al. Estimates of SARS-CoV-2 Seroprevalence and Incidence of Primary SARS-CoV-2 Infections Among Blood Donors, by COVID-19 Vaccination Status - United States, April 2021-September 2022. MMWR. Morbidity and mortality weekly report. 2023.

From the study: “Prevalence of hybrid immunity was lowest among persons aged ≥65 years (36.9%), the group with the highest risk for severe disease if infected”

96.4% had antibodies

Jones JM et al. Estimates of SARS-CoV-2 Seroprevalence and Incidence of Primary SARS-CoV-2 Infections Among Blood Donors, by COVID-19 Vaccination Status - United States, April 2021-September 2022. MMWR. Morbidity and mortality weekly report. 2023.

07

Sewage testing forecast COVID-19 hospital admissions weeks in advance.

Up to 4 weeks' warningSewage virus levels predicted weekly new COVID-19 hospital admissions by county

Using weekly sewage virus measurements from 159 counties in 45 states, covering nearly 100 million people, computer models accurately predicted each county's weekly new COVID-19 hospital admissions, with a preparation window of 1-4 weeks.

Sewage testing does not depend on people getting tested, so it can warn hospitals of a coming surge in time to plan staff and beds. Retrospective modeling study from June 2021 to January 2023; models needed periodic updating, and accuracy may vary by county.

See the evidence

Modeling study linking weekly sewage virus data to hospital admission records in 159 US counties across 45 states, June 2021 to January 2023.

From the study: “WBE-based models accurately predicted the county-level weekly new admissions, allowing a preparation window of 1-4 weeks.”

Up to 4 weeks' warning

Li X et al. Wastewater-based epidemiology predicts COVID-19-induced weekly new hospital admissions in over 150 USA counties. Nature communications. 2023.

From the study: “to predict COVID-19-induced weekly new hospitalizations in 159 counties across 45 states in the United States of America (USA), covering a population of nearly 100 million”

Up to 4 weeks' warning

Li X et al. Wastewater-based epidemiology predicts COVID-19-induced weekly new hospital admissions in over 150 USA counties. Nature communications. 2023.

08

Long COVID patients had lower cortisol more than a year after infection.

More than a year laterLower blood cortisol, a key stress hormone, in long COVID vs comparison groups

In a study of 275 people, those with long COVID, mostly after mild infections, had lower blood cortisol (a hormone central to the body's stress response) than comparison groups, which included uninfected people and people who recovered. They also had higher antibody levels against other viruses, especially Epstein-Barr virus, a common virus that stays dormant in the body.

It shows long COVID comes with measurable changes in the blood, not just reported symptoms. These are leads for future tests, not a proven way to diagnose it. Small snapshot study at two hospitals; it cannot show whether low cortisol causes symptoms, and the blood signs are research leads, not a validated test.

See the evidence

Cross-sectional study of 275 people at Mount Sinai and Yale New Haven hospitals; samples were taken on average more than a year after a mostly mild infection.

From the study: “Here 275 individuals with or without long COVID were enrolled in a cross-sectional study”

More than a year later

Klein J et al. Distinguishing features of long COVID identified through immune profiling. Nature. 2023.

From the study: “the current finding of persistently lower cortisol levels in those with LC more than a year after acute infection warrants further investigations”

More than a year later

Klein J et al. Distinguishing features of long COVID identified through immune profiling. Nature. 2023.

From the study: “higher antibody responses directed against non-SARS-CoV-2 viral pathogens were observed among individuals with long COVID, particularly Epstein-Barr virus”

More than a year later

Klein J et al. Distinguishing features of long COVID identified through immune profiling. Nature. 2023.

Study-specific findings. Different populations, treatments and follow-up periods can produce different results.

Read all 4 study explanationsThe complete approved explanations, with study-specific limits and original results.
THE RESEARCH, AS IT ARRIVES

Latest studies.

The newest findings added to this collection.
The learning from each, already distilled.

  1. STUDY 01Findings added
    TL;DR

    CORIS classified illness severity at hospital admission

    CORIS distinguished severe or critical COVID-19 from non-severe illness at hospital admission better than a lymphocyte-subset model and a routine-laboratory model in its internal validation set.

    This single-centre study used internal data splitting, without external validation. The model was not intended to diagnose infection or predict later deterioration, survival or blood-clot events.

    Study details & original results

    Zhang, Yihe et al.. Integrating Anti-SARS-CoV-2 Spike Protein IgG, IL-6, and NK Cell Percentage with Routine Laboratory Markers for COVID-19 Severity Assessment: Development and Validation of the CORIS Nomogram.. Diagnostics (Basel, Switzerland). 2026.

    Internal split-sample performance of the age, LDH, anti-spike IgG, IL-6, and NK-cell percentage CORIS nomogram for distinguishing severe/critical from non-severe COVID-19 at hospital admission; it was not intended for diagnosis or prediction of post-admission deterioration, survival, or thrombotic events.

    AUC 0.914 (training); AUC 0.918 (validation)
    95% CI: 0.884-0.940 (training); 0.868-0.960 (validation)

    In the internal validation set, CORIS admission-severity discrimination was compared with a lymphocyte subset-based model and a routine laboratory parameter-based model.

    Comparator AUC 0.811 (DeLong p < 0.001) and AUC 0.839 (DeLong p = 0.003), versus CORIS AUC 0.918
    CORIS 95% CI: 0.868-0.960; comparator CIs not reported

    Citation in Biomarkers
  2. STUDY 02Findings added
    TL;DR

    Routine laboratory tests did not distinguish long COVID symptom patterns

    Routine laboratory measures did not distinguish age-independent symptom patterns in a single-centre long COVID cohort. Routine values also did not usefully predict clinical improvement.

    Symptom groups used self-reported organ-system domains. There was no comparison group without long COVID, and routine panels may miss relevant markers; these findings do not establish that symptoms have no biological basis.

    Study details & original results

    Oberhauser, Viola et al.. Routine laboratory data are decoupled from symptom phenotype and prognosis in Long COVID: within-cohort variation is dominated by age.. Clinical chemistry and laboratory medicine. 2026.

    Differences in routine analytes across three age-independent Long COVID symptom phenotypes

    0/89 analytes

    Equivalence of routine laboratory values across Long COVID symptom phenotypes

    86/89 within ±0.5 SD; 63/70 within the reference change value

    Prediction of clinical improvement from routine laboratory analytes in Long COVID

    AUC 0.46

    Citation in Biomarkers
  3. STUDY 03Findings added
    TL;DR

    Exploratory marker analyses did not establish a treatment-selection rule

    An exploratory anakinra-versus-control analysis reported treatment-superiority estimates by ferritin and low or high suPAR in critically ill COVID-19. The clinical outcome behind these estimates is not available in this summary.

    Both suPAR intervals included no difference. Ferritin probabilities were not estimates of differences in treatment effect between marker groups. This exploratory intensive-care analysis does not establish a biomarker-guided benefit.

    Study details & original results

    Boyle, Andrew J et al.. Evaluating plasma ferritin and suPAR as treatable traits for critically ill patients with COVID-19 treated with anakinra: an exploratory analysis of the immune modulation domain of the REMAP-CAP randomised clinical trial.. Critical care (London, England). 2026.

    Exploratory estimate of anakinra being superior to control among critically ill COVID-19 patients with high baseline suPAR (≥6 ng/mL).

    OR 0.88; 38.6% posterior probability of benefit
    95% CrI: 0.39-2.00

    Exploratory estimate of anakinra being superior to control among critically ill COVID-19 patients with low baseline suPAR (<6 ng/mL).

    OR 2.28; 94.8% posterior probability of benefit
    95% CrI: 0.85-6.06

    Exploratory posterior probabilities that anakinra was superior to control across increasing ferritin terciles in critically ill COVID-19 patients; these are not interaction estimates.

    64%, 71%, and 21% across increasing ferritin terciles, versus 53% without ferritin adjustment

    Citation in Biomarkers
  4. STUDY 04Findings added
    TL;DR

    Blood mitochondrial DNA measurements were associated with disease occurrence and severity

    A systematic review linked elevated cell-free mitochondrial DNA in blood with COVID-19 development; levels were also associated with disease severity.

    Comparison groups and measurement units are not available in this summary, so mean-difference magnitudes are omitted. The associations do not establish an individual diagnostic test, prognosis or causal mechanism.

    Study details & original results

    Souza, Felipe C DE et al.. Evaluating the Relationship Between Plasma Cell-Free Mitochondrial DNA (cf-mtDNA) Levels and COVID-19 Severity: A Systematic Review and Meta-Analysis.. Anais da Academia Brasileira de Ciencias. 2026.

    Association between elevated cf-mtDNA levels and the development of COVID-19

    MD 0.70; p<0.001
    95% CI: 0.39-1.01

    Association between cf-mtDNA levels and COVID-19 disease severity

    MD 1.08; p=0.004
    95% CI: 0.35-1.82

    Citation in Biomarkers
4 of 4 study updates

Dates show when findings were added here, not when papers were published. Study populations and comparisons differ.

WHEN YOU WANT TO GO DEEPER
See all 10 findingsOriginal results, comparisons and study details.
4 of 4 source groupsFindings stay together with their study.
SOURCE 042 findings

Zhang, Yihe et al.. Integrating Anti-SARS-CoV-2 Spike Protein IgG, IL-6, and NK Cell Percentage with Routine Laboratory Markers for COVID-19 Severity Assessment: Development and Validation of the CORIS Nomogram.. Diagnostics (Basel, Switzerland). 2026.

Internal split-sample performance of the age, LDH, anti-spike IgG, IL-6, and NK-cell percentage CORIS nomogram for distinguishing severe/critical from non-severe COVID-19 at hospital admission; it was not intended for diagnosis or prediction of post-admission deterioration, survival, or thrombotic events.

Added
AUC 0.914 (training); AUC 0.918 (validation)95% CI: 0.884-0.940 (training); 0.868-0.960 (validation)Source [4]

In the internal validation set, CORIS admission-severity discrimination was compared with a lymphocyte subset-based model and a routine laboratory parameter-based model.

Added
Comparator AUC 0.811 (DeLong p < 0.001) and AUC 0.839 (DeLong p = 0.003), versus CORIS AUC 0.918CORIS 95% CI: 0.868-0.960; comparator CIs not reportedSource [4]
SOURCE 033 findings

Oberhauser, Viola et al.. Routine laboratory data are decoupled from symptom phenotype and prognosis in Long COVID: within-cohort variation is dominated by age.. Clinical chemistry and laboratory medicine. 2026.

Differences in routine analytes across three age-independent Long COVID symptom phenotypes

Added
0/89 analytesSource [3]

Equivalence of routine laboratory values across Long COVID symptom phenotypes

Added
86/89 within ±0.5 SD; 63/70 within the reference change valueSource [3]
All 3 findings from this source

Prediction of clinical improvement from routine laboratory analytes in Long COVID

Added
AUC 0.46Source [3]
SOURCE 023 findings

Boyle, Andrew J et al.. Evaluating plasma ferritin and suPAR as treatable traits for critically ill patients with COVID-19 treated with anakinra: an exploratory analysis of the immune modulation domain of the REMAP-CAP randomised clinical trial.. Critical care (London, England). 2026.

Exploratory posterior probabilities that anakinra was superior to control across increasing ferritin terciles in critically ill COVID-19 patients; these are not interaction estimates.

Added
64%, 71%, and 21% across increasing ferritin terciles, versus 53% without ferritin adjustmentSource [2]

Exploratory estimate of anakinra being superior to control among critically ill COVID-19 patients with low baseline suPAR (<6 ng/mL).

Added
OR 2.28; 94.8% posterior probability of benefit95% CrI: 0.85-6.06Source [2]
All 3 findings from this source

Exploratory estimate of anakinra being superior to control among critically ill COVID-19 patients with high baseline suPAR (≥6 ng/mL).

Added
OR 0.88; 38.6% posterior probability of benefit95% CrI: 0.39-2.00Source [2]
SOURCE 012 findings

Souza, Felipe C DE et al.. Evaluating the Relationship Between Plasma Cell-Free Mitochondrial DNA (cf-mtDNA) Levels and COVID-19 Severity: A Systematic Review and Meta-Analysis.. Anais da Academia Brasileira de Ciencias. 2026.

Association between elevated cf-mtDNA levels and the development of COVID-19

Added
MD 0.70; p<0.00195% CI: 0.39-1.01Source [1]

Association between cf-mtDNA levels and COVID-19 disease severity

Added
MD 1.08; p=0.00495% CI: 0.35-1.82Source [1]
Browse the 12 original sourcesThe complete bibliography behind this monitor.
  1. [1]

    Souza, Felipe C DE et al.. Evaluating the Relationship Between Plasma Cell-Free Mitochondrial DNA (cf-mtDNA) Levels and COVID-19 Severity: A Systematic Review and Meta-Analysis.. Anais da Academia Brasileira de Ciencias. 2026.

    Open original source in a new tab
  2. [2]

    Boyle, Andrew J et al.. Evaluating plasma ferritin and suPAR as treatable traits for critically ill patients with COVID-19 treated with anakinra: an exploratory analysis of the immune modulation domain of the REMAP-CAP randomised clinical trial.. Critical care (London, England). 2026.

    Open original source in a new tab
  3. [3]

    Oberhauser, Viola et al.. Routine laboratory data are decoupled from symptom phenotype and prognosis in Long COVID: within-cohort variation is dominated by age.. Clinical chemistry and laboratory medicine. 2026.

    Open original source in a new tab
  4. [4]

    Zhang, Yihe et al.. Integrating Anti-SARS-CoV-2 Spike Protein IgG, IL-6, and NK Cell Percentage with Routine Laboratory Markers for COVID-19 Severity Assessment: Development and Validation of the CORIS Nomogram.. Diagnostics (Basel, Switzerland). 2026.

    Open original source in a new tab
  5. [5]

    Erlandson KM et al. Differentiation of Prior SARS-CoV-2 Infection and Postacute Sequelae by Standard Clinical Laboratory Measurements in the RECOVER Cohort. Annals of internal medicine. 2024.

    Open original source in a new tab
  6. [6]

    Kyriazopoulou E et al. Early treatment of COVID-19 with anakinra guided by soluble urokinase plasminogen receptor plasma levels: a double-blind, randomized controlled phase 3 trial. Nature medicine. 2021.

    Open original source in a new tab
  7. [7]

    Duff EP et al. Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection. Nature medicine. 2025.

    Open original source in a new tab
  8. [8]

    Frediani JK et al. The New Normal: Delayed Peak SARS-CoV-2 Viral Loads Relative to Symptom Onset and Implications for COVID-19 Testing Programs. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2024.

    Open original source in a new tab
  9. [9]

    Coppens L et al. Longitudinal assessment of SARS-CoV-2 spike and nucleocapsid antigenemia in the ORCHESTRA post-COVID cohort. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2026.

    Open original source in a new tab
  10. [10]

    Jones JM et al. Estimates of SARS-CoV-2 Seroprevalence and Incidence of Primary SARS-CoV-2 Infections Among Blood Donors, by COVID-19 Vaccination Status - United States, April 2021-September 2022. MMWR. Morbidity and mortality weekly report. 2023.

    Open original source in a new tab
  11. [11]

    Li X et al. Wastewater-based epidemiology predicts COVID-19-induced weekly new hospital admissions in over 150 USA counties. Nature communications. 2023.

    Open original source in a new tab
  12. [12]

    Klein J et al. Distinguishing features of long COVID identified through immune profiling. Nature. 2023.

    Open original source in a new tab

About this collection.

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