A new paper in the New England Journal of Medicine, led by Dr. Wang, decodes deadly blood clots from COVID vaccines, revealing that PF4 antibodies in vaccine-induced thrombosis (VITT) and common cold infections share identical molecular structures.
Research on vaccine-induced immune thrombocytopenia and thrombosis (VITT) is being further explored by researchers from Flinders University and international experts. In 2021, at the height of the COVID-19 pandemic, VITT was identified as a novel illness associated with vaccines based on adenovirus vectors, specifically the Oxford-AstraZeneca vaccine.
It was discovered that an exceptionally hazardous blood autoantibody against the protein known as platelet factor 4 (PF4) was the cause of VITT. Researchers from Canada, North America, Germany, and Italy reported a nearly similar condition in 2023 using the same PF4 antibody. This disorder proved fatal in certain cases following an infection with the common cold virus.
In 2022, a previous study led by Flinders University researchers, Dr. Jing Jing Wang and Flinders Professor Tom Gordon, Head of Immunology at SA Pathology in South Australia, deciphered the PF4 antibody’s molecular code and discovered a genetic risk factor associated with an antibody gene known as IGLV3.21*02.
Collaborative Efforts and Future Implications
The Flinders group and this international team of researchers have now worked together to discover that the molecular fingerprints or signatures shared by the PF4 antibodies in both the traditional adenoviral vectored VITT and the infection-associated VITT caused by adenoviruses are the same.
The first author of the new paper that was published in the esteemed New England Journal of Medicine, Dr. Wang, is a researcher at Flinders University. She claims the findings will also have ramifications for bettering vaccine development.
“These findings, using a completely new approach for targeting blood antibodies developed at Flinders University, indicate a common triggering factor on virus and vaccine structures that initiates the pathological pF4 antibodies,” explains Professor Gordon.
Indeed, these illnesses must share genetic risk factors and have almost identical pathways for the development of deadly antibodies. Our results have significant therapeutic ramifications, including implications for vaccine development and application of VITT lessons to infrequent episodes of blood clotting following adenovirus (common cold) infections, the researcher adds.
Reference: “Antibody Fingerprints Linking Adenoviral Anti-PF4 Disorders” by Jing Jing Wang, Linda Schönborn, Theodore E. Warkentin, Tim Chataway, Leonie Grosse, Paolo Simioni, Stephan Moll, Andreas Greinacher and Tom P. Gordon, 15 May 2024, New England Journal of Medicine.
DOI: 10.1056/NEJMc2402592
The European Medicines Agency service contract and the German Research Foundation (Deutsche Forschungsgemeinschaft) provided funding for the study. The American Society of Hematology’s ASH Global Research Award and the Medical University of Greifswald’s Gerhard Domagk Research Program provided funding for Dr. Schönborn’s research. A Health Seed Grant from the Flinders Foundation funded Dr. Wang.
Recently, GreatGameIndia reported that COVID-19 vaccines led to a rise in a rare autoimmune disease in 2021, as per a new study published in The Lancet’s eBioMedicine.
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