Can you explain this latest development and how it can deepen our understanding of these side effects?
Everyone wants to understand what causes the very rare blood clotting problems seen with the so-called adenoviral vector vaccines developed by Astra-Oxford and J&J. What’s unusual about these problems is that they are blood clots that form in odd-numbered parts of the body, such as the sinus vein of the brain, along with a reduction in platelets. which normally results in bleeding. If we know why they are happening, maybe we can find a way to prevent them. To this end, it is already known that some Astra and J&J vaccinees develop an antibody against what is called platelet factor 4, which then leads to a reduction in the number of platelets. But what about blood clots? This is what this study attempts to answer. And I’m afraid some people have taken the results of these experiments as suggesting a solution. But this is not the case. These are very interesting experiences, but that is what they are. Their lab analysis seems to suggest that Astra and J&J’s vaccines – which target the “spike protein,” or rod-shaped structures stuck on the outside of the virus – could produce soluble chunks of this protein. They then hypothesize that these soluble spike proteins could bind to so-called ACE2 receptors inside human blood vessels and trigger an inflammatory cascade that leads to blood clotting.
How credible is this report? Does this seem like a plausible explanation for the blood clots we see if confirmed by further research?
From an experimental point of view, it looks good. The problem is, the authors, in my opinion, have gone a little too far, even in naming their finding as “vaccine-induced COVID-19 mimicry” syndrome. They don’t show any real evidence to back up their hypothesis. Some key steps are needed to prove that this is, in fact, how vaccines cause blood clots, called thromboses.
What would the process of confirming this, and if valid, vaccine remediation look like? Is there a regulatory or scientific precedent?
Several things can be done. The first is to prove that people vaccinated with adenoviral vaccines do have a soluble spike protein in their bloodstream and that it is higher than those who have been inoculated with messenger RNA injections (Pfizer Inc. -BioNTech SE and Moderna Inc.). Next, they must show that there is indeed inflammation at the site of blood clots involving immune complexes with soluble spike protein and anti-spike antibodies. In addition, if there is indeed a soluble spike protein produced in sufficient quantities for matter, we need data on the course over time and its relationship to the evolution of neutralizing antibodies. The authors hypothesize that the reason why the coagulation problem is rare is that neutralizing antibodies generally tend to form in time to bind to the soluble spike protein and prevent it from sticking to ACE2 receptors in the body. inside the blood vessels, and “neutralize” them. All this remains to be proven.
But if after taking these steps the assumption turns out to be correct, that would be relatively good news, wouldn’t it? Rather than a fundamental problem with this whole class of vaccines, maybe the solution is simply to modify the spike protein?
Wouldn’t that be great? Companies could go back and change their vaccines. But then they would have to prove that the modified vaccines are just as effective and, more importantly, that they don’t cause side effects. It would involve vaccinating hundreds of thousands of people to test this. I don’t know how feasible this is.
Does the fact that J & J’s vaccine apparently has a lower rate of these events than Astra’s give the theory extra credence?
The key word here is “apparently”. We have to wait for a lot more data. I will not be convinced that the J&J vaccine has a lower rate of such events until I see data on the same number of vaccinations as the Astra vaccine. It is possible that this is the case, however, given that the two use different adenoviruses, spike sequences, and manufacturing processes. The authors try to use this as potential evidence to support their hypothesis, but given the immaturity of the data, I don’t think it’s a given.
What happens with existing vaccines and existing production if the hypothesis turns out to be true?
Countries are still using vaccines, so this study alone is unlikely to change anything. Like I said, we need a lot more clinical data before anyone actually accepts this as a cause and effect situation. But if the hypothesis were to hold true, then indeed these existing vaccines would have to be replaced with new ones that have the modification. It would all take time. This does not mean that it would not be desirable to find a solution. These shots are seen as essential in the race to vaccinate the world and tame the virus, so if we could remove the threat of these rare but potentially deadly side effects from the equation, that would be a big step forward. But we are not there yet.