When she began to develop strange symptoms after having COVID-19, she hoped they weren't related to the virus. She had a mild illness. I have been shot three times. She said she felt protected. She was still sick with a variety of symptoms months later. Hawthorne couldn't get out of bed because of her weakness. She had been looking forward to the diagnosis: long carbon dioxide.
She was desperate and unable to find relief. Hawthorne got in touch with a doctor in Germany who is treating people with blood thinners and a procedure to filter the blood after reading an opinion piece in The Guardian. She hasn't heard back yet, but if she gets the chance to head there for these treatments, she probably will. She doesn't want to wait on her health when she's feeling awful.
Hundreds of studies have tried to unpick its mechanism but have failed. Some scientists, and an increasing number of people with the condition, have been lining up behind the as-yet-unproven hypothesis that tiny, persistent clot might be constricting blood flow to vital organs, resulting in the strange constellation of symptoms that people experience.
The first team to visualize was led by Douglas Kell, a systems Biologist at the University ofLiverpool, UK. The evidence implicating micro-clots is irrefutable, and they want trials of the kind of treatment Hawthorne is considering. Pretorius wrote an article for the Guardian.
There is concern that enthusiasm for the clot hypothesis has outpaced the data. Larger studies and stronger evidence are what they would like to see. They are worried about people seeking out treatments that are not proven to work.
Danny Altmann is an immunologist at Imperial College London. We are all trying to come up with a consensus. We are a long way away from that. It isn't very satisfying.
They met a decade ago. Pretorius neglected to cite some of Kell's research when he studied iron in clotting. They started talking when he reached out. Pretorius says that they decided to work together after having a meeting on the internet. People with a variety of diseases are prone to dense clot that resist breaking down for years. They came up with the idea that some molecule, like iron, could cause these abnormal clots.
fibrinogen is one of the key players in the process of blood clot formation. When an injury occurs, cells release the thrombin, which cuts the fibrinogen into an insolubleProtein A clot can be formed by strands of fibrin loop and criss-cross.
Kell says the web resembles a plate of spaghetti. The clot that the team has identified is different. If you half-boiled the spaghetti and let it all stick together, they would behorrible. The research suggests that the fibrin has misfolded and created a gluey version of itself. Kell says that it doesn't take much to cause a disaster. If the first one changes its structure, all the other ones have to do the same.
Kell and Pretorius have observed the phenomenon in a number of conditions, including diabetes, Alzheimer's disease and Parkinson's disease. The idea didn't gain much traction until now.
Kell and Pretorius were the first to apply their methods to people who had been exposed to the disease. Pretorius says that they looked at clotting in COVID because they do that. A special dye that fluoresces when it binding to amyloid is used in their assays. Under a microscope, researchers can see the glow. 13 healthy volunteers, 15 people with COVID-19, 10 people with Diabetes, and 11 people with long COVID 3 were compared by the team. Pretorius says that the clotting was more than we have previously found in diabetes or any other inflammatory disease. Micro-clots were found in all of the blood samples from 80 people with long COVID.
Pretorius, Kell and their colleagues are the only ones to have published results on micro-clots.
The results of unpublished work have been replicated by a neuroscience professor at a UK university. She and her colleagues used a different method to count the number of blood clot. The team compared people who had never knowingly had COVID-19, people who had had COVID-19 and recovered, and people with long COVID. People with long COVID had a higher number of larger clots than those who had never had it. There was a group that fell in the middle. The team believes that a burst of micro-clots can be created by the SARS-coV-2 infections. Individuals with long COVID seem to keep going.
Some people have fatigue scores that correlate with micro-clot counts. It increases confidence that we are measuring something that is linked to the condition.
Chronic fatigue syndrome, also known as myalgic encephalomyelitis, is a disease that has never been explained. The director of the ME/CFS Collaborative Research Center at Cornell University says that Pretorius and Kell's research has renewed interest. The amount of amyloid in the blood of people with ME/CFS was lower than in people with long COVID 5. Pretorius thinks that clotting is a partial explanation for ME/CFS.
It isn't clear where these micro-clots came from. Pretorius and Kell think that people with long COVID are more likely to be affected by the spikeprotein. The formation of the abnormal clot was caused by the addition of the spikeprotein to the blood from healthy volunteers.
There are bits of evidence that show the possible involvement of theProtein. The researchers from Harvard University found a spike in the blood of people with long COVID. A paper from a Swedish group shows that certain peptides in the spike can form amyloid strands on their own. The author of the paper says that it is possible that the misfolded strands give a template.
There are micro-clots in a study participant before and after they were bitten by the CoV-2 bug. The credit goes to E. Pretorius and his team.
A group in California discovered that fibrin can bind to the spike. fibrin forms clot that are harder to degrade when the two proteins bind, according to a report in a preprint 9. How all these puzzle pieces fit together is a mystery.
If the spike is the cause of abnormal clot, it raises the question of whether the instructions contained in the vaccine can induce them. The South African Medical Research Council gave Pretorius and Kell a grant to study the issue. There are rare events associated with the Oxford–AstraZeneca vaccine.
The co-author of the book says that raising safety concerns about the vaccine can be difficult. If this is a medical issue, we have to address that, but we don't want to be too alarmist. Gregory Poland is the director of the vaccine research group at the mayo clinic. He thinks that the virus will have an impressive list of pathophysiologies. I don't know how much of that might be true for the vaccine.
It's plausible that micro-clots could be contributing to long carbon dioxide emissions. The hypothesis seems to fit with some of the data that has come out. People with COVID-19 are more likely to develop blood clot. The virus can cause inflammation and damage to the blood vessels.
The effects of those clot can be seen. Danny Jonigk is a Pathologist at a Medical School in Germany. The capillaries had split and formed new branches to keep the blood flowing. Fresh clot can come from turbulence in the flow that can be caused by the branching.
Some people have a tendency to clot months after the initial infections. About 25% of people who are recovering from COVID-19 have signs of increased clotting that are quite marked and unusual, according to James O'Donnell.
It's not clear if this abnormal clotting response is to blame for any of the symptoms of long COVID or if it's just another unusual phenomenon associated with COVID. O'Donnell said it.
The micro-clot hypothesis is presented by Alex Spyropoulos, a haematologist at the Feinstein Institute for Medical Research. He thinks more work is needed to tie lab markers to symptoms. The authors and other people make huge leaps of faith.
The method Pretorius's team is using to identify micro-clots isn't a standard technique at all according to Jeffrey Weitz. He wants to know if other investigators agree with him. It's hard to detect micro-clots. They can be found in tissue samples, but haematologists prefer to look for markers of abnormal clotting rather than the clot itself.
Large studies of long COVID have not found signs of clotting. A group of people who had been exposed to the disease were examined by an infectious-disease specialist and his colleagues at the National Institutes of Health. They didn't look for micro-c lots. They should have seen some evidence of tissue damage in capillary-rich organs if micro-clots had been the cause. Red blood cells could be damaged by micro-clots. There were no signs of this in any of the tests.
Kell and Pretorius argue that even though no evidence of micro-clots was found, they are still there. Pretorius says that one of the main issues with long COVID is that every single test comes back within the normal range. You don't have a way to diagnose the patients. She wants other researchers to try and duplicate their results. We can have a discussion after that. She says that people with long COVID would be the ultimate proof of causality.
There isn't much evidence of this. Kell, Pretorius and other researchers reported in an early version of a preprint that 24 people with long COVID were treated with a combination of two antiplatelet therapies. The participants reported that they became less tired. They did not have as many micro-c lots. Pretorius and Kell are trying to gather more data before publishing their results. People with long COVID are being treated with these medications. The procedure that filters the fibrinogen and other inflammatory molecule from the blood is being offered by some. Such treatment does not feel right to O'Donnell. He accepts that some people with long COVID are prone to clot, but jumping from a single small study to treating a large group of people is not going to wash in his book. Sneller concurs. Anticoagulating someone is not a good idea. He says that interfering with the blood's ability to clot could be life threatening.
Kell wants to know how to treat long COVID. People are in pain. He says that they are badly unwell. Altmann knows how frustrated that is. He gets a lot of e-mails about the drug trials. It takes so long. Researchers have to follow the process even in the midst of a Pandemic. I don't rubbish anyone's data. He said we are not there yet. Join up the dots and do this correctly.
Nature 608, 662-662.
The article is titled: "D41586 022-0228-7."
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