Covid19NCT04892797
Understanding Immunology and Patient Outcomes of COVID-19 in Hospitalized Patients
An observational study of Covid19, run by University of Vermont at 1 site in United States.
Trial summary
The adaptive immune response, consisting of antiviral T and B cells, is critical for providing protection against viruses such as SARS-CoV-2, both during an active infection and later following a subsequent exposure. They can both also potentially contribute to pathogenesis if they are overstimulated. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Covid19
- What is being tested?
- Covid-19+ observational
- How many people
- 16 participants
- Where
- 1 siteUnited States
- Study dates
- 3 Feb 2021to 30 Jun 2023
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: This study will enroll patients hospitalized at the University of Vermont Medical Center who have a positive test result for COVID-19. These patients are expected to have a greater acuity of illness and burden of disease based on the fact that they require inpatient care. Enrolling hospitalized patients ensures a greater opportunity to collect serial biological specimens over the course of the illness due to the proximity of the patient to medical and research staff and UVM laboratories.
Who may be able to join
- Adult (≥18 years old) at the time of consent
- Positive COVID-19 PCR test result
Who cannot join
- Expected death or withdrawal of life-sustaining treatments within 3 days
- Hemoglobin ≤7.0 at the time of consent
- Unable to provide consent and no legally authorized representative (LAR) identified or reached by phone
- Pregnant
- Incarcerated
- Physician declines patient enrollment (attending physician or study physician)
- Patient or LAR do not consent to participate in the study
Trial locations and contacts
1 site in 1 country.
About this study
Official title: Understanding Immunology and Patient Outcomes of COVID-19: A 1-Year Longitudinal Follow-Up Study of Hospitalized Patients
The adaptive immune response, consisting of antiviral T and B cells, is critical for providing protection against viruses such as SARS-CoV-2, both during an active infection and later following a subsequent exposure. They can both also potentially contribute to pathogenesis if they are overstimulated. Despite these advances in knowledge, there are still significant gaps in understanding of what constitutes a protective or immunopathologic immune response and its durability.
Significant knowledge gaps also remain pertaining to the early recognition of COVID patients with increased risk of clinical deterioration who require continued hospitalization and the use of more intensive treatments designed to improve outcomes. Data from non-COVID patients with MI show that platelet surface expression of FcγRIIa, the low-affinity receptor for the Fc fragment of immunoglobulin (Ig) G, identifies patients at high and low risk of subsequent cardiovascular events. Platelet expression of FcγRIIa is increased by interferon γ20 that is significantly elevated in severe COVID-19 infections. The high prevalence of arterial thrombosis among COVID-19 patients and the central role of thrombosis in respiratory failure support the hypothesis that elevated platelet expression of FcγRIIa will identify COVID patients at increased risk of thrombotic complications and clinical deterioration.
Read more
In addition to the potential role of platelet activation in thrombosis associated with COIVD-19, the endothelium may also play a significant role. The investigators hypothesize that elevated EMPs in plasma will identify patients at high risk of thrombosis and clinical deterioration.
To begin to address the knowledge gaps above and obtain preliminary data for future large grant submission, the investigators propose a small, prospective, single-center cohort study that will enroll patients hospitalized for COVID-19 infection and exhibiting a range of disease severity. Biosamples will be obtained and used to study T and B cells, antibody repertoire, and durability of protective immunity, and also to quantify platelet expression of FcγRIIa and circulating EMPs, as described in the protocol.
Read the detailed description
Since December 2019, the novel coronavirus (SARS-CoV-2) and associated COVID-19 illness has spread worldwide. Globally, there are >86 million infections and over 1.8 million confirmed deaths, with the pandemic continuing at record levels throughout the USA. While new data on COVID-19 are emerging daily, several knowledge gaps remain, including understanding of the adaptive immune response to infection, the propensity for infected patients to experience thrombotic events, and identification of biomarkers that might predict clinical deterioration.
The adaptive immune response, consisting of antiviral T and B cells, is critical for providing protection against viruses such as SARS-CoV-2, both during an active infection and later following a subsequent exposure. They can both also potentially contribute to pathogenesis if they are overstimulated. Much has been learned about the T and B cell responses to SARS-CoV-2 since the beginning of the COVID-19 pandemic. The most comprehensive study to date shows that most individuals make a balanced T and B cell response that persists for at least 8 months. Despite these advances in knowledge, there are still significant gaps in understanding of what constitutes a protective or immunopathologic immune response and their durability.
Significant knowledge gaps also remain pertaining to the early recognition of COVID patients with increased risk of clinical deterioration who require continued hospitalization and the use of more intensive treatments designed to improve outcomes. In addition, the identification of low risk patients who can be discharged from the hospital would reduce the use of potentially scarce medical resources, particularly during a surge. Among patients with thrombosis, 49% required critical care and 43% died. Data from non-COVID patients with MI show that platelet surface expression of FcγRIIa, the low-affinity receptor for the Fc fragment of immunoglobulin (Ig) G, identifies patients at high and low risk of subsequent cardiovascular events. Platelet expression of FcγRIIa is increased by interferon γ20 that is significantly elevated in severe COVID-19 infections. Because FcγRIIa amplifies platelet activation, greater expression of FcγRIIa on the surface of the platelet increases platelet reactivity. The high prevalence of arterial thrombosis among COVID-19 patients and the central role of thrombosis in respiratory failure support the hypothesis that elevated platelet expression of FcγRIIa will identify COVID patients at increased risk of thrombotic complications and clinical deterioration.
In addition to the potential role of platelet activation in thrombosis associated with COIVD-19, the endothelium may also play a significant role. The endothelium is a key site of entry for COVID-19 infection and endothelial injury contributes to thrombotic events that increase morbidity and mortality. Endothelial microparticles (EMPs), submicron membranous vesicles indicating endothelial activation and injury, are released by the endothelium into blood and reflect the competency of endothelial function by identifying endothelial activation and injury, which promote thrombosis. Circulating EMPs can be quantified with the use of flow cytometry. The investigators hypothesize that elevated EMPs in plasma will identify patients at high risk of thrombosis and clinical deterioration.
To begin to address the knowledge gaps above and obtain preliminary data for future large grant submission, the investigators propose a small, prospective, single-center cohort study that will enroll patients hospitalized for COVID-19 infection and exhibiting a range of disease severity. Blood will be obtained on study days 1, 3±1, 7±1 (and every 7±1 days thereafter up to day 28 while hospitalized), and again at 12 months of follow up. Nasopharyngeal (NP) swabs will be collected on these same study days through day 28, but not at 12 months. These biosamples will be used to study T and B cells, antibody repertoire, and durability of protective immunity, and also to quantify platelet expression of FcγRIIa and circulating EMPs, as described in the protocol.
- Conditions
- Covid19
- Being tested
- Covid-19+ observational
- Medical subject headings
- COVID-19
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Covid-19+ observationalOther
This is observational--there is no intervention
| Study group | Role | What they receive |
|---|---|---|
| Covid-19+ | Hospitalized patients with Covid-19 infection confirmed by PCR test Receives: Other: Covid-19+ observational |
What is being measured
The primary outcome is the main question the study is designed to answer.
To compare the polyfunctionality and frequency of antiviral CD4 and CD8 T cells.
The investigators hypothesize patients with severe disease will have higher frequencies of antiviral T cells that contribute to the cytokine storm observed in the most severe cases of COVID-19.
Measured: Four weeks (while hospitalized)
To compare the polyfunctionality and frequency of antiviral CD4 and CD8 T cells.
The investigators hypothesize patients with severe disease will have higher frequencies of antiviral T cells that contribute to the cytokine storm observed in the most severe cases of COVID-19.
Measured: 12 months after hospital admission
To compare the frequency of plasmablasts (early B cells that produce antiviral antibodies) and plasma antiviral antibody titer during acute infection.
The investigators predict that patients with severe disease will have greater numbers of antiviral plasmablasts and plasma antiviral antibody levels compared to those with mild disease.
Measured: Four weeks (while hospitalized)
To compare the frequency of plasmablasts (early B cells that produce antiviral antibodies) and plasma antiviral antibody titer during acute infection.
The investigators predict that patients with severe disease will have greater numbers of antiviral plasmablasts and plasma antiviral antibody levels compared to those with mild disease.
Measured: 12 months after hospital admission
The number of virus specific CD4 T cells will be measured using flow cytometry.
The investigators hypothesize that severe disease will result in the formation of higher magnitude antiviral B and T cell CHRMS (Medical) #STUDY00001369 Approved: 1/25/2021 4Human subjects protocol form 7/19/19responses during acute disease due to increased viral load and antigen in these patients. The investigators further predict that higher frequency T and B cells during acute disease will correlate with more robust durability of these responses during convalescence.
Measured: Four weeks (while hospitalized)
The number of virus specific CD8 T cells will be measured using flow cytometry.
The investigators hypothesize that severe disease will result in the formation of higher magnitude antiviral B and T cell CHRMS (Medical) #STUDY00001369 Approved: 1/25/2021 4Human subjects protocol form 7/19/19responses during acute disease due to increased viral load and antigen in these patients. The investigators further predict that higher frequency T and B cells during acute disease will correlate with more robust durability of these responses during convalescence.
Measured: Four weeks (while hospitalized)
The number of virus specific CD4 T cells will be measured using flow cytometry.
The investigators hypothesize that severe disease will result in the formation of higher magnitude antiviral B and T cell CHRMS (Medical) #STUDY00001369 Approved: 1/25/2021 4 Human subjects protocol form 7/19/19 responses during acute disease due to increased viral load and antigen in these patients. The investigators further predict that higher frequency T and B cells during acute disease will correlate with more robust durability of these responses during convalescence.
Measured: 12 months after hospital admission
The number of virus specific CD8 T cells will be measured using flow cytometry.
The investigators hypothesize that severe disease will result in the formation of higher magnitude antiviral B and T cell CHRMS (Medical) #STUDY00001369 Approved: 1/25/2021 4Human subjects protocol form 7/19/19responses during acute disease due to increased viral load and antigen in these patients. The investigators further predict that higher frequency T and B cells during acute disease will correlate with more robust durability of these responses during convalescence.
Measured: 12 months after hospital admission
To obtain preliminary data on platelet activation in patients hospitalized with COVID-19
To compare platelet activation, measured by platelet surface FcγRIIa while in hospital and 12 months after infection, in patients with severe (i.e., mechanical ventilation in ICU) vs. non-severe (hospitalized, but not in an ICU) COVID-19 disease.
Measured: Four weeks (while hospitalized)
To obtain preliminary data on platelet activation in patients hospitalized with COVID-19
To compare platelet activation, measured by platelet surface FcγRIIa while in hospital and 12 months after infection, in patients with severe (i.e., mechanical ventilation in ICU) vs. non-severe (hospitalized, but not in an ICU) COVID-19 disease.
Measured: 12 months after hospital admission
To obtain preliminary data on endothelial activation in patients hospitalized with COVID-19
To compare endothelial activation, measured by circulating EMPs while in hospital and 12 months after infection, in patients with severe (i.e., mechanical ventilation in ICU) vs. non-severe (hospitalized, but not in an ICU) COVID-19 disease.
Measured: Four weeks (while hospitalized)
To obtain preliminary data on endothelial activation in patients hospitalized with COVID-19
To compare endothelial activation, measured by circulating EMPs while in hospital and 12 months after infection, in patients with severe (i.e., mechanical ventilation in ICU) vs. non-severe (hospitalized, but not in an ICU) COVID-19 disease.
Measured: 12 months after hospital admission
Preliminarily determine if the FcγRIIa and EMPs have utility as biomarkers
To preliminarily determine if the FcγRIIa and EMPs have utility as biomarkers for prediction of thrombotic events and clinical deterioration in hospitalized patients with COVID-19.
Measured: Four weeks (while hospitalized)
Preliminarily determine if the FcγRIIa and EMPs have utility as biomarkers
To preliminarily determine if the FcγRIIa and EMPs have utility as biomarkers for prediction of thrombotic events and clinical deterioration in hospitalized patients with COVID-19.
Measured: 12 months after hospital admission
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted19 May 2021
- Study start3 Feb 2021
- Primary completion30 Jun 2023
- Study completion30 Jun 2023
Why it stopped: Grant application to fund this work was not funded. We won't be posting data for this study.
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Covid19Studies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 16 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Vermont
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Renee Stapleton, University of Vermont
- Investigators
- Renee Stapleton, MD, PhD, Principal investigator, University of Vermont
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04892797
- Sponsor's protocol ID
- 00001369
- Status last verified
- Feb 2025
- First submitted
- 9 Feb 2021
- Last updated
- 14 May 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Study at a glance
From the registry record, last updated by the sponsor on 14 May 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Understanding Immunology and Patient Outcomes of COVID-19: A 1-Year Longitudinal Follow-Up Study of Hospitalized Patients
- ClinicalTrials.gov ID
- NCT04892797
- Acronym / sponsor ID
- 00001369
- Conditions
- Covid19
- Study type
- Observational
- Recruitment status
- TerminatedReason stopped: Grant application to fund this work was not funded. We won't be posting data for this study.
- Enrolment
- 16 participants (actual)
- Lead sponsor
- University of VermontUniversity, hospital or other
- Study start
- 3 Feb 2021 (actual)
- Primary completion
- 30 Jun 2023 (actual)
- Study completion
- 30 Jun 2023 (actual)
- First posted
- 19 May 2021 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The adaptive immune response, consisting of antiviral T and B cells, is critical for providing protection against viruses such as SARS-CoV-2, both during an active infection and later following a subsequent exposure. They can both also potentially contribute to pathogenesis if they are overstimulated. Despite these advances in knowledge, there are still significant gaps in understanding of what constitutes a protective or immunopathologic immune response and its durability.
Significant knowledge gaps also remain pertaining to the early recognition of COVID patients with increased risk of clinical deterioration who require continued hospitalization and the use of more intensive treatments designed to improve outcomes. Data from non-COVID patients with MI show that platelet surface expression of FcγRIIa, the low-affinity receptor for the Fc fragment of immunoglobulin (Ig) G, identifies patients at high and low risk of subsequent cardiovascular events. Platelet expression of FcγRIIa is increased by interferon γ20 that is significantly elevated in severe COVID-19 infections. The high prevalence of arterial thrombosis among COVID-19 patients and the central role of thrombosis in respiratory failure support the hypothesis that elevated platelet expression of FcγRIIa will identify COVID patients at increased risk of thrombotic complications and clinical deterioration.
In addition to the potential role of platelet activation in thrombosis associated with COIVD-19, the endothelium may also play a significant role. The investigators hypothesize that elevated EMPs in plasma will identify patients at high risk of thrombosis and clinical deterioration.
To begin to address the knowledge gaps above and obtain preliminary data for future large grant submission, the investigators propose a small, prospective, single-center cohort study that will enroll patients hospitalized for COVID-19 infection and exhibiting a range of disease severity. Biosamples will be obtained and used to study T and B cells, antibody repertoire, and durability of protective immunity, and also to quantify platelet expression of FcγRIIa and circulating EMPs, as described in the protocol.
Detailed description
Since December 2019, the novel coronavirus (SARS-CoV-2) and associated COVID-19 illness has spread worldwide. Globally, there are >86 million infections and over 1.8 million confirmed deaths, with the pandemic continuing at record levels throughout the USA. While new data on COVID-19 are emerging daily, several knowledge gaps remain, including understanding of the adaptive immune response to infection, the propensity for infected patients to experience thrombotic events, and identification of biomarkers that might predict clinical deterioration.
The adaptive immune response, consisting of antiviral T and B cells, is critical for providing protection against viruses such as SARS-CoV-2, both during an active infection and later following a subsequent exposure. They can both also potentially contribute to pathogenesis if they are overstimulated. Much has been learned about the T and B cell responses to SARS-CoV-2 since the beginning of the COVID-19 pandemic. The most comprehensive study to date shows that most individuals make a balanced T and B cell response that persists for at least 8 months. Despite these advances in knowledge, there are still significant gaps in understanding of what constitutes a protective or immunopathologic immune response and their durability.
Significant knowledge gaps also remain pertaining to the early recognition of COVID patients with increased risk of clinical deterioration who require continued hospitalization and the use of more intensive treatments designed to improve outcomes. In addition, the identification of low risk patients who can be discharged from the hospital would reduce the use of potentially scarce medical resources, particularly during a surge. Among patients with thrombosis, 49% required critical care and 43% died. Data from non-COVID patients with MI show that platelet surface expression of FcγRIIa, the low-affinity receptor for the Fc fragment of immunoglobulin (Ig) G, identifies patients at high and low risk of subsequent cardiovascular events. Platelet expression of FcγRIIa is increased by interferon γ20 that is significantly elevated in severe COVID-19 infections. Because FcγRIIa amplifies platelet activation, greater expression of FcγRIIa on the surface of the platelet increases platelet reactivity. The high prevalence of arterial thrombosis among COVID-19 patients and the central role of thrombosis in respiratory failure support the hypothesis that elevated platelet expression of FcγRIIa will identify COVID patients at increased risk of thrombotic complications and clinical deterioration.
In addition to the potential role of platelet activation in thrombosis associated with COIVD-19, the endothelium may also play a significant role. The endothelium is a key site of entry for COVID-19 infection and endothelial injury contributes to thrombotic events that increase morbidity and mortality. Endothelial microparticles (EMPs), submicron membranous vesicles indicating endothelial activation and injury, are released by the endothelium into blood and reflect the competency of endothelial function by identifying endothelial activation and injury, which promote thrombosis. Circulating EMPs can be quantified with the use of flow cytometry. The investigators hypothesize that elevated EMPs in plasma will identify patients at high risk of thrombosis and clinical deterioration.
To begin to address the knowledge gaps above and obtain preliminary data for future large grant submission, the investigators propose a small, prospective, single-center cohort study that will enroll patients hospitalized for COVID-19 infection and exhibiting a range of disease severity. Blood will be obtained on study days 1, 3±1, 7±1 (and every 7±1 days thereafter up to day 28 while hospitalized), and again at 12 months of follow up. Nasopharyngeal (NP) swabs will be collected on these same study days through day 28, but not at 12 months. These biosamples will be used to study T and B cells, antibody repertoire, and durability of protective immunity, and also to quantify platelet expression of FcγRIIa and circulating EMPs, as described in the protocol.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Covid-19+ | – | Other: Covid-19+ observationalHospitalized patients with Covid-19 infection confirmed by PCR test |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- This study will enroll patients hospitalized at the University of Vermont Medical Center who have a positive test result for COVID-19. These patients are expected to have a greater acuity of illness and burden of disease based on the fact that they require inpatient care. Enrolling hospitalized patients ensures a greater opportunity to collect serial biological specimens over the course of the illness due to the proximity of the patient to medical and research staff and UVM laboratories.
Key inclusion criteria (2 listed)
- Adult (≥18 years old) at the time of consent
- Positive COVID-19 PCR test result
Key exclusion criteria (7 listed)
- Expected death or withdrawal of life-sustaining treatments within 3 days
- Hemoglobin ≤7.0 at the time of consent
- Unable to provide consent and no legally authorized representative (LAR) identified or reached by phone
- Pregnant
- Incarcerated
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Covid-19+ observationalThis is observational--there is no intervention | Other | Covid-19+ |
Primary outcome
To compare the polyfunctionality and frequency of antiviral CD4 and CD8 T cells.
Time frame: Four weeks (while hospitalized)
The investigators hypothesize patients with severe disease will have higher frequencies of antiviral T cells that contribute to the cytokine storm observed in the most severe cases of COVID-19.
To compare the polyfunctionality and frequency of antiviral CD4 and CD8 T cells.
Time frame: 12 months after hospital admission
The investigators hypothesize patients with severe disease will have higher frequencies of antiviral T cells that contribute to the cytokine storm observed in the most severe cases of COVID-19.
To compare the frequency of plasmablasts (early B cells that produce antiviral antibodies) and plasma antiviral antibody titer during acute infection.
Time frame: Four weeks (while hospitalized)
The investigators predict that patients with severe disease will have greater numbers of antiviral plasmablasts and plasma antiviral antibody levels compared to those with mild disease.
To compare the frequency of plasmablasts (early B cells that produce antiviral antibodies) and plasma antiviral antibody titer during acute infection.
Time frame: 12 months after hospital admission
The investigators predict that patients with severe disease will have greater numbers of antiviral plasmablasts and plasma antiviral antibody levels compared to those with mild disease.
The number of virus specific CD4 T cells will be measured using flow cytometry.
Time frame: Four weeks (while hospitalized)
The investigators hypothesize that severe disease will result in the formation of higher magnitude antiviral B and T cell CHRMS (Medical) #STUDY00001369 Approved: 1/25/2021 4Human subjects protocol form 7/19/19responses during acute disease due to increased viral load and antigen in these patients. The investigators further predict that higher frequency T and B cells during acute disease will correlate with more robust durability of these responses during convalescence.
The number of virus specific CD8 T cells will be measured using flow cytometry.
Time frame: Four weeks (while hospitalized)
The investigators hypothesize that severe disease will result in the formation of higher magnitude antiviral B and T cell CHRMS (Medical) #STUDY00001369 Approved: 1/25/2021 4Human subjects protocol form 7/19/19responses during acute disease due to increased viral load and antigen in these patients. The investigators further predict that higher frequency T and B cells during acute disease will correlate with more robust durability of these responses during convalescence.
The number of virus specific CD4 T cells will be measured using flow cytometry.
Time frame: 12 months after hospital admission
The investigators hypothesize that severe disease will result in the formation of higher magnitude antiviral B and T cell CHRMS (Medical) #STUDY00001369 Approved: 1/25/2021 4 Human subjects protocol form 7/19/19 responses during acute disease due to increased viral load and antigen in these patients. The investigators further predict that higher frequency T and B cells during acute disease will correlate with more robust durability of these responses during convalescence.
The number of virus specific CD8 T cells will be measured using flow cytometry.
Time frame: 12 months after hospital admission
The investigators hypothesize that severe disease will result in the formation of higher magnitude antiviral B and T cell CHRMS (Medical) #STUDY00001369 Approved: 1/25/2021 4Human subjects protocol form 7/19/19responses during acute disease due to increased viral load and antigen in these patients. The investigators further predict that higher frequency T and B cells during acute disease will correlate with more robust durability of these responses during convalescence.
To obtain preliminary data on platelet activation in patients hospitalized with COVID-19
Time frame: Four weeks (while hospitalized)
To compare platelet activation, measured by platelet surface FcγRIIa while in hospital and 12 months after infection, in patients with severe (i.e., mechanical ventilation in ICU) vs. non-severe (hospitalized, but not in an ICU) COVID-19 disease.
To obtain preliminary data on platelet activation in patients hospitalized with COVID-19
Time frame: 12 months after hospital admission
To compare platelet activation, measured by platelet surface FcγRIIa while in hospital and 12 months after infection, in patients with severe (i.e., mechanical ventilation in ICU) vs. non-severe (hospitalized, but not in an ICU) COVID-19 disease.
To obtain preliminary data on endothelial activation in patients hospitalized with COVID-19
Time frame: Four weeks (while hospitalized)
To compare endothelial activation, measured by circulating EMPs while in hospital and 12 months after infection, in patients with severe (i.e., mechanical ventilation in ICU) vs. non-severe (hospitalized, but not in an ICU) COVID-19 disease.
To obtain preliminary data on endothelial activation in patients hospitalized with COVID-19
Time frame: 12 months after hospital admission
To compare endothelial activation, measured by circulating EMPs while in hospital and 12 months after infection, in patients with severe (i.e., mechanical ventilation in ICU) vs. non-severe (hospitalized, but not in an ICU) COVID-19 disease.
Preliminarily determine if the FcγRIIa and EMPs have utility as biomarkers
Time frame: Four weeks (while hospitalized)
To preliminarily determine if the FcγRIIa and EMPs have utility as biomarkers for prediction of thrombotic events and clinical deterioration in hospitalized patients with COVID-19.
Preliminarily determine if the FcγRIIa and EMPs have utility as biomarkers
Time frame: 12 months after hospital admission
To preliminarily determine if the FcγRIIa and EMPs have utility as biomarkers for prediction of thrombotic events and clinical deterioration in hospitalized patients with COVID-19.
Results and safety
The study was stopped early (reason given: Grant application to fund this work was not funded. We won't be posting data for this study.). Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 14 May 2025.
- Individual participant dataSharing planned: Undecided
Related trials for Covid19
Not yet recruitingPhase 1
Phase I Open-Label Safety Trial of Pembrolizumab for Neurological Post- Acute Sequelae of SARS-CoV-2 (PD1-PASC I)
Post-Acute COVID-19 Syndrome
Active, not recruitingPhase 1
A Safety and Immunogenicity Trial of OCU500, ChAd36 Vector Encoding SARS-CoV-2 Spike Vaccine Via Intranasal and Inhalational Routes in Previously Vaccinated Adults
COVID-19
Active, not recruiting
Intervention to Address Disparate Mental Health Consequences of COVID-19 Pandemic on Latinx and African Newcomers
Mental Health Issue, Mental Health Disorder
Recruiting
Home-Based Exercise Tele-Rehabilitation After COVID-19
Post SARS-CoV2 (COVID-19)
Not yet recruitingPhase 1
A Safety, Reactogenicity and Immunogenicity Trial of RVX-sCPD9 Booster Intranasal COVID-19 Vaccine
COVID -19
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Renee Stapleton, MD, PhD principal investigator
University of Vermont
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Covid19, run by University of Vermont at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 7 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: stopped early, as of the sponsor's last update on 14 May 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study was stopped early (reason given: Grant application to fund this work was not funded. We won't be posting data for this study.). Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
To compare the polyfunctionality and frequency of antiviral CD4 and CD8 T cells. (time frame: Four weeks (while hospitalized)). The study lists 14 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 14 May 2025.