June 18, 2024
 
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  • Source: FreePressers
  • 05/30/2024
FPI / May 29, 2024

Researchers in Australia have reported they have found that the dangerous antibodies involved in vaccine-induced blood clots and similar disorders from common cold infections share identical molecular structures.

"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 COVID-19 pandemic in 2021, VITT was recognized as a new condition linked to adenovirus vector-based vaccines, particularly the Oxford-AstraZeneca vaccine," Flinders University noted in a May 26 report.

Flinders University researchers Dr. Jing Jing Wang and Professor Tom Gordon, Head of Immunology at SA Pathology in South Australia, 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.

In the the new Flinders research, the scientists said that VITT was found to be caused by an unusually dangerous blood autoantibody directed against a protein termed platelet factor 4 (or PF4).

Thrombosis is a blood clot within blood vessels that limits the flow of blood.

In separate research in 2023, researchers from Canada, North America, Germany, and Italy described a virtually identical disorder with the same PF4 antibody that was fatal in some cases after a common cold infection.

The Flinders researchers collaborated with the international group 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 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 virus and vaccine structures that initiates the pathological pF4 antibodies,” explains Professor Gordon.

“Indeed, the pathways of lethal antibody production in these disorders must be virtually identical and have similar genetic risk factors. Our findings have the important clinical implication that lessons learned from VITT are applicable to rare cases of blood clotting after adenovirus (a common cold) infections, as well as having implications for vaccine development,” Gordon said.

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