Main paper: pubmed.ncbi.nlm.nih.gov/41671482/

What this gives us is a clear explanation for why this clotting happened in some people and not most others. It also gives vaccine researchers a clearer target to avoid when designing future adenovirus-based vaccines.

The researchers tested this directly. When they reversed that key K31E change in the lab, the clot-causing effect disappeared. That gave strong evidence that this was a real mechanism, not just an association.

That one change, called K31E, shifted the antibody so it bound more strongly to PF4 instead of pVII. PF4 is a normal blood protein released by platelets. Once antibodies started binding PF4, they could activate platelets and drive clotting.

Then one extra change happened inside some antibody-making cells. This is called a somatic hypermutation. In plain language, it is a small DNA change that can happen naturally while the immune system is refining an antibody.

The antibodies first recognised a part of adenovirus called pVII. An antibody is a protein made by the immune system to stick to a target. pVII is one of the virus proteins inside the adenovirus used in these vaccines.

But that gene version on its own was not enough. The study says there also had to be repeat exposure to adenovirus, meaning the immune system had likely seen adenovirus before and then saw it again through the vaccine.

The new study found that most patients carried a certain inherited antibody gene version called IGLV3-2102 or IGLV3-2103. In simple terms, they were born with a version of an immune gene that made this reaction more possible.

This was mainly seen after AstraZeneca and Johnson & Johnson COVID vaccines. These used an adenovirus delivery system. It was not the same issue seen with the mRNA vaccines from Pfizer or Moderna.

The paper is about VITT. That stands for vaccine-induced immune thrombocytopenia and thrombosis. In simple terms, this means dangerous blood clots together with low platelets. Platelets are blood cells that help clots form.

Researchers have identified the cause of clotting seen after some COVID vaccines. In certain people, a common inherited gene version plus prior adenovirus exposure led to an immune mistake that triggered clotting.

www.bbc.com/news/live/cg... (edited) GOV.UKUK Covid-19 Inquiry: Vaccines and therapeutics (Module 4) ReportThe UK Covid-19 Inquiry’s fourth report considers the development and rollout of vaccines across the UK and treatment of Covid-19 using existing and new medications.

Likewise, funding for those affected post-COVID also needs to exist. Right now, they are also a forgotten population, living with serious long term illness without enough research, treatment options, or clinical support.

These patients should not be forgotten. Funding needs to be allocated now for biological research, better case definition, and clinical trials, so people have a real chance of answers and treatment.

This should not be treated as a closed issue just because the rollout worked at population level. A public health success overall can still leave a smaller group with major unmet medical needs.

If the government accepts that some people have been seriously harmed, then support should go beyond payouts. It should include research funding, dedicated clinical pathways, and treatment development.

The report seems much more focused on future planning, future trust, future safety systems, and future pandemic readiness. Those issues matter. But they do not replace action for the people already living with severe illness now.

Without that work, patients may stay stuck in the same position: too ill to return to normal life, but without clear answers, proven treatments, or specialist services built around their condition.

Research into pathology means research into the actual disease process in the body. In simple terms, it means finding out what has changed, which systems may be affected, and why symptoms continue in some people.

What is missing is a serious plan for the people who are ill right now. Where is the funding for research into what is biologically going wrong in these patients? Where is the plan for treatment studies and proper clinical support?

But money alone does not solve the main problem. Most affected patients may never receive a payout. And even for those who do, a payment does not remove a life changing illness or restore their health.

The report does mention people who were harmed. It says the Vaccine Damage Payment Scheme should be reformed, and that the maximum payout should rise from £120,000 to at least £200,000.

The UK Covid Inquiry says the vaccine rollout was a major success overall. But for people living with serious long term illness after vaccination, the report still does not seem to offer a real plan for research, treatment, or clinical care.

Due to MCAS my diet consists of ONLY sweet potatoes & beef mince. 800g of sweet potatoes and 300g of mince for breakfast, lunch, dinner, every day for 3 years.

And I’ve recently realised I probably eat more sweet potatoes per year than anyone in the western world. Great record.

Main paper: doi.org/10.64898/202...

Important caveats: this was a small preprint study, it was cross-sectional, and the groups were not age-matched. So it cannot prove cause, and it needs replication in larger studies. But it does add another signal pointing toward ongoing blood and immune abnormalities in Long COVID.

They also connect this to broader Long COVID blood findings reported in other studies, including endothelial dysfunction, platelet changes, and fibrin-rich microclots. The idea is that these processes may be linked parts of the same wider problem.

The authors interpret this as possible evidence of ongoing thromboinflammation. That means inflammation linked to abnormal clotting activity. They suggest these platelet-monocyte clumps may reflect continued platelet activation and immune system activation in Long COVID.

The images supported the numbers. Both the imaging flow method and confocal microscopy showed platelet attachment to monocytes, and Long COVID samples more often showed more complex attachment patterns with several platelets on one monocyte.

In healthy controls, these clumps increased somewhat with age. But in Long COVID, the levels were already high and did not show a clear age link. The authors argue this suggests the increase may relate to disease status, not simply age.