Scientists from Cardiff University and the Arizona State University believe they have found the likely cause of blood clotting in some recipients of the Oxford-AstraZeneca COVID-19 vaccine.
AstraZeneca Vaccine/Courtesy of Rafapress
Scientists believe they have found the likely cause of blood clotting in some recipients of the Oxford-AstraZeneca COVID-19 vaccine.
Researchers from Cardiff University and Arizona State University investigated why some people who were given the vaccine developed thrombosis with thrombocytopenia syndrome (TTS), a clotting disease that can lead to death. The incidences of TTS were rare during clinical trials and the vaccine rollout, but given the potential danger, some countries decided early this year to suspend use of the product, including the European Union and the United States.
This prompted the scientists, alongside AstraZeneca, to conduct further research into the causative factors. One of the vaccine’s components is an adenovirus vector that works to deliver immunity instructions into human cells. This vector sometimes binds to the platelet factor 4 (PF4) in the blood, triggering the clotting, mainly in people with COVID-19 infections — hence the name vaccine-induced immune thrombotic thrombocytopenia (VITT).
VITT figures are not low enough to be dismissed, with 73 deaths recorded in the U.K. out of the 150 million doses rolled out. On the other hand, the UK Health Security Agency has also said that the same vaccine helped prevent the deaths of over 80,000 patients. While some industry observers believe that the benefits outweigh the risks, knowing why TTS is happening is crucial to prevent it from occurring.
So, the researchers used state-of-the-art computational simulations to observe the electrostatic interaction mechanism between three types of adenovirus with PF4 and then later confirmed findings using surface plasmon resonance. After evaluating the three — chimpanzee adenovirus Y25 (ChAdOx1), human adenovirus type 5 (HAd-V-C5) and human adenovirus type 26 (HAdV-D26) — the scientists found that ChAdOx1 had a strong negative charge, which meant that it attracted PF4, which has a positive charge. This led them to suggest that if ChAdOx1 were modified, the threat of TTS could be significantly reduced.
“Our team continues to investigate the mechanisms which underpin TTS and how this interaction with PF4 may lead to this rare side effect,” Dr. Alexander Baker, an honorary research fellow at Cardiff and the study’s lead author, told Biospace.
Further study is required to confirm these observations, but the discovery could be significant to creating and developing future vaccine products containing ChAdOx1. For now, as researchers have seen what could trigger the clotting, the next steps would be to find ways to prevent it. AstraZeneca has also expressed its willingness to move forward with the research so it could eventually remove the problem from its doses.
Details of the study are published in the journal Science Advances.
