Immunobiology of vaccine-related clotting after adenovirus vaccines
Official title: The Immunobiology of Vaccine-induced Immune Thrombotic Thrombocytopenia
Funded at Versiti Blood Health, INC. · NIH-11372209 · Data updated 2026-11-12
This research asks how antibodies linked to a rare vaccine-related clotting condition (VITT) interact with specific blood proteins to cause clots after certain COVID-19 vaccines.
Quick facts
| Grant type | P01 program project |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Versiti Blood Health, INC. NIH-funded |
| Lab location | 1 site (Milwaukee, United States) |
| Project start | August 1, 2024 |
| Project end | July 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $498,141 |
| NIH project number | 5P01HL167668-03 |
| Project ID | NIH-11372209 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients who have experienced or are at risk for VITT or related thrombotic disorders may be impacted by advances from this research.
✕Less likely to help
The study is laboratory-focused and may not directly benefit patients who have not encountered VITT or similar conditions.
What this research studies
VITT is a rare problem seen after some adenovirus-based COVID-19 vaccines. The project investigates how antibodies target PF4 and related proteins, and how these interactions might trigger clots in arteries and veins. Using mouse models and laboratory experiments, researchers study where antibodies bind and how the clotting process can be initiated, including how adenoviruses themselves may bind to these proteins. The work aims to map antigen targets and test how different antibody types contribute to VITT pathology.
Why it matters
Potential benefit: A better understanding of VITT could lead to safer vaccines and targeted treatments for people who develop this condition.
How similar studies have gone: Prior work has shown that VITT antibodies interact with PF4 and related proteins, suggesting this line of research could yield actionable insights.
Where this research is happening
-
Versiti Blood Health, INC.
Milwaukee, United States Active
Researchers
- Principal investigator: Poncz, Mortimer — Versiti Blood Health, INC.
- Study coordinator: Poncz, Mortimer
Related research
Other NIH-funded projects on the same topics.
-
New ideas to understand, diagnose, and treat heparin-induced thrombocytopenia
A Mayo Clinic led study will look at the different kinds of HIT antibodies to improve diagnosis and treatment for people with HIT.
-
Second-generation BLVRB inhibitors to help chemotherapy patients with low platelets
A new drug candidate is being developed to raise platelet counts in patients whose cancer treatment lowers them, reducing bleeding risk.
-
Understanding and diagnosing Heparin-Induced Thrombocytopenia (HIT)
A project to understand the immune factors behind HIT and develop faster, more accurate tests to help people who need heparin therapy.
-
Fetal and neonatal platelet allergy: understanding why some babies bleed
A study to understand why maternal antibodies cause serious bleeding in babies with FNAIT, using an animal model and human-relevant clues to improve future care for affected families.
-
Molecular mechanisms behind immune-related low platelets and clots in transfusion medicine
This grant supports a team of researchers to understand how immune factors cause low platelets and abnormal clots, with a focus on transfusion medicine and pediatric to adult patients.
-
Animal model proof-of-concept for TAR syndrome treatment
A researcher is testing new ways to treat TAR syndrome by using a mouse model that mimics the human bone and blood problems.
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.