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Scientists Decode Deadly Blood Clot Disorder Triggered by COVID Vaccines

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Researchers from Flinders University, along with international experts, have discovered that the PF4 antibodies causing VITT after adenovirus vector-based COVID-19 vaccination share identical molecular signatures with those found in similar cases following natural adenovirus infection. This finding, using a new approach developed at Flinders, has significant implications for understanding the genetic risk factors and improving future vaccine development.

New research has shown that the dangerous PF4 antibodies involved in vaccine-induced thrombosis (VITT) and similar disorders from common cold infections share identical molecular structures, highlighting implications for future vaccine development and disease management.

New research conducted by Flinders University and global specialists is deepening our knowledge of vaccine-induced immune thrombocytopenia and thrombosis (VITT). During the peak of the led a previous study in 2022 that cracked the molecular code of the PF4 antibody and identified a genetic risk factor related to an antibody gene termed IGLV3.21*02.

Jing Jing Wang and Tom Gordon

Flinders University immunology researchers Dr. Jing Jing Wang and Professor Tom Gordon. Credit: Flinders Foundation

Collaborative Efforts and Future Implications

Now, the Flinders group has collaborated with this international group of researchers to find that the PF4 antibodies in both adenoviruses infection-associated VITT and classic adenoviral vectored VITT share identical molecular fingerprints or signatures.

The research will also have implications for improving vaccine development, says Flinders University researcher Dr. Wang, the first author on the new article that was published in the eminent New England Journal of Medicine.

“These findings, using a completely new approach for targeting blood antibodies developed at Flinders University, indicate a common triggering factor on DOI: 10.1056/NEJMc2402592

The research was supported by the German Research Foundation (Deutsche Forschungsgemeinschaft) and a European Medicines Agency service contract. Dr. Schönborn was supported by the ASH Global Research Award from the American Society of Hematology and by the Gerhard Domagk Research Program through the Medical University of Greifswald. Dr. Wang was supported by a Flinders Foundation Health Seed Grant.



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