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Surprising Discovery: Researchers have discovered why the blood of many Covid 19 patients accumulates so much. The cause is therefore not the coronavirus itself, but an autoimmune reaction of the body’s own defenses. This leads to a massive release of special antibodies that attack white blood cells and cause blood to pool. This knowledge could open up new therapeutic opportunities for Covid-19.
The corona virus attacks almost the entire body, this now seems clear. One of the components particularly affected are blood vessels and blood. Since the onset of the corona pandemic, doctors have observed that a staggering number of Covid 19 patients suffered from excessive blood clotting. Frequent consequences are thrombosis, pulmonary embolism and even stroke.
“In patients with Covid-19 we see a relentless and self-reinforcing vicious cycle of inflammation and aggregation of blood throughout the body,” explains Yogendra Kanthi of the University of Michigan.
Similarity to an autoimmune disease
But so far it has remained largely unclear what causes this excessive clotting: the virus itself, infection-related inflammation of the vessels, or an immune reaction? “Most patients have normal levels of blood clotting factors, fibrinogen and platelets, which suggests Covid-19 causes a unique prothrombotic condition,” said Kanti, colleague Yu Zuo and her team.
Interestingly, however: in some respects, the excessive thrombotic tendency of patients with Covid-19 is similar to an autoimmune disease, which can also lead to fatal blood clots, the researchers explain. In this so-called antiphospholipid syndrome, the body mistakenly produces antibodies against certain components of the blood, including phospholipids and phospholipid-binding proteins. The accumulation of antibodies on these molecules causes the blood to clump together.
Typical autoantibodies also in patients with Covid-19
Could something similar happen with Covid-19? To find out, scientists analyzed the blood of 172 Covid-19 patients treated in hospital with a serious illness. They specifically looked for eight antibodies typical of antiphospholipid syndrome.
The result: “A good half of the patients with Covid 19 were positive for at least one of these autoantibodies,” reports senior author Jason Knight. A quarter of the patients had two or more of these ApL antibodies. There were clear correlations with the clinical course of Covid 19 disease: the higher the titer of autoantibodies in the patient’s blood, the more severely affected the kidneys, lungs and blood.
Found guilty?
Such a clear connection between the autoantibodies and the severity of the COVID-19 course was unexpected, says Kanthi. “This suggests that these autoantibodies could be the culprits of this vicious circle of blood clots and inflammation that makes many Covid patients sick.” Apparently, SARS-CoV-2 infection directly or indirectly promotes the production of these misdirected antibodies and thus derails blood clotting.
This is supported by the observation that such patients often have white blood cells that are hyperactivated by antibodies, as Kanthi and his colleagues explain. These immune cells then produce extracellular fibers, so-called neutrophil extracellular traps (NETs), which form a kind of network. They usually help fight bacteria, but in this case they do even more blood clotting.
The patients’ antibodies cause the formation of mouse blood clots
To test whether the antibodies from Covid patients are actually the cause of the excessive thrombosis tendency, the scientists conducted an additional experiment with mice. In these cases, they had previously increased the risk of thrombosis due to a slight narrowing of the greater vena cava. Then they isolated ApL antibodies from some Covid-19 patients and injected the animals with the purified, cell-free extract.
It showed: “Antibodies from patients with acute Covid-19 disease produced an astonishing degree of thrombosis in animals – some suffered from the most severe blood clots they have ever seen,” Kanthi says. At the same time, he and his team were able to demonstrate the remarkable hyperactivation of white blood cells and extracellular networks in mice. “We have thus identified a new mechanism that causes blood clots in patients with Covid 19,” the researchers said.
Opportunities for better therapies
The current findings also open up new opportunities for better treatment of this derailed blood clotting. Because in addition to the heparin anticoagulant, which is also administered in many cases of Covid 19, the antiphospholipid syndrome is also treated with the active ingredient dipyridamole. “It’s an old drug that’s safe, cheap, and widely available,” says Kanthi.
Initial tests now suggest that this agent could also help with Covid-19. That is why the research team has already started a clinical trial with dipyridamole. They also recommend testing the effectiveness of a so-called plasmapheresis, the blood wash in which certain components of the blood are filtered in a targeted manner. (Science Translational Medicine, 2020; doi: 10.1126 / science.abd3876)
Those: Michigan Medicine – University of Michigan
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