How COVID-19 can cause dangerous blood clots

New studies suggest that some of the dangerous blood clots in COVID-19 may come from the immune system, which attacks the patient’s body rather than chasing the virus.

It is known Excessive inflammation Excessive immune response can spur thrombus formation in critically ill patients (SN: 6/23/20). Now researchers are making fun of that method. Some of that coagulation may come from autoantibodies that track the molecules that form the cell membrane instead of recognizing foreign invaders. The attack may urge immune cells, called neutrophils, to release a network of genetic material intended to trap viral particles extracellularly.

“Perhaps within the organization, this is a way to control the infection,” says Jason Knight, a rheumatologist at the University of Michigan, Ann Arbor. “But if you do it in the bloodstream, it causes thrombosis, or coagulation very much.”

It may happen at Some COVID-19 patientsYogen Kanthi, a cardiologist at the National Institutes of Health in Bethesda, Maryland, and his colleagues, on November 2, Scientific translation medicine.. In COVID-19, blood clots in the lungs are a major cause of death, Kanti says. Also, when the web traps red blood cells and platelets, blood clots can form, forming sticky clots that can clog blood vessels.

“These are very interesting discoveries,” says Janconers, a clinical hematologist at Harvard Medical School and Brigham and Women’s Hospital in Boston, who was not involved in the study. “There was a lot of speculation about what its existence was. [the auto-antibodies] Means and whether they have a pathogenic role. “

Studies show Autoantibodies can interfere With an immune response to the virus (SN: 9/25/20).Some preliminary studies have also shown that autoantibodies that bind to various targets in the host Common functions In severely ill COVID-19 patients.

Autoantibodies that recognize cell membrane molecules called phospholipids can cause an autoimmune disease called antiphospholipid antibody syndrome (APS). In patients with APS, autoantibodies can activate thrombus-forming cells, and these patients are at increased risk of thrombus formation.

These harmful antibodies can also appear during bacterial or viral infections such as streptococcal pharyngitis and HIV. However, it is difficult to determine if an antibody causes blood clotting during infection, Connors said. In particular, some healthy people can have low levels without forming blood clots.

Severe COVID-19 patients may have high levels of neutrophils, and some have phospholipid-binding antibodies in their blood. So Knight and his colleagues suspected that the antibody might have released traps that cause coagulation in neutrophils.

Of the 172 hospitalized COVID-19 patients included in the study, more than half had autoantibodies that recognized one of three different types of host phospholipids. The presence of these immune proteins was associated with high levels of neutrophils in the blood and proteins that suggested that neutrophils participated in the fight. And when researchers mixed autoantibodies from six COVID-19 patients with laboratory dish-grown neutrophils, the neutrophils threw their nets. In addition, when the team injected the patient’s autoantibodies into the mice, the rodents formed a thrombus. This suggests that people’s coagulation can be caused by immune proteins.

Phospholipid autoantibodies are unlikely to be all, says Thomas Kickler, a hematologist at Johns Hopkins University of Medicine who was not involved in the study. Autoantibodies are probably part of the puzzle, as other inflammatory immune responses also cause blood clots. For example, of the people who participated in this study, 11 patients developed blood clots, and only half of them had autoantibodies.

According to Connors, more work needs to be done to link immune proteins directly to the coagulation of people with COVID-19. However, this study suggests one possible mechanism for how blood clots are formed.

Removing problematic antibodies through a process called plasmaferresis, which filters the liquid portion of the blood, may help severely ill COVID-19 patients who do not respond to other treatments to stop coagulation, Knight said. say. However, the plasma also contains antibodies that recognize and attack the coronavirus. Therefore, if the virus is still replicating in the body, doctors may need to give those patients laboratory-made immune proteins to fight the virus.

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