In most cases, the main symptoms of Covid-19 are fever, cough, shortness of breath. But if the disease is difficult to tolerate, acute renal failure, damage to internal organs and incomprehensible blood clots can be added to them. Doctors suggest that the virus, in fact, can target the vessels, not the lungs.
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Frank Rushicka, an employee of the University Hospital Zurich, began research on unusual symptoms of a respiratory illness in April 2020. During the autopsy of the first coronavirus deceased in the hospital, he discovered that tiny clots and dead cells clogged the capillaries of the lungs, and that inflammation led to the expansion of the blood vessels supplying the organs. He published his observations in a report to the magazine. The Lancet, in which he noted that the virus was aimed at the blood vessels of his patients. “[Covid-19] “This is a vascular problem,” says Rushitska. “The lung is the main battlefield, but it is a blood vessel disease.”
Since the publication of the report, several more studies on this topic have been published. Article published in New England Journal of Medicine, showed that in the lungs of patients who died from Covid-19, there were nine times more blood clots than those who had the H1N1 flu (another respiratory disease), and the number of new blood vessels grew 2.7 times faster.
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A group of scientists from the Leuven Catholic University in Belgium found that endothelial cells (they line the inner surface of blood vessels) play a role in the development of severe Covid-19. Attacking them, the infection causes a change in blood pressure, the formation of blood clots and a violation of blood coagulation. This, in turn, provokes inflammation throughout the body and contributes to the development of acute respiratory distress syndrome (ARDS), which is responsible for most patient deaths.
Belgian studies may help to understand why coronavirus is so dangerous for people with chronic diseases like diabetes, obesity, or cardiovascular disease. In such patients, the state of the blood vessels is already impaired, and SARS-CoV-2 – the pathogen behind Covid-19 – can bring their recovery system out of control. When SARS-CoV-2 enters the lungs, it captures cells that transmit oxygen to the blood, and then invades the endothelial cells. Those, in turn, are destroyed.
The virus prevents the division of human cells, supporting them at a certain point in the cell cycle.
“This is not a silent death when a cell simply dies,” says Neelam Mangalmurti, a resuscitator at a University of Pennsylvania hospital who was not involved in the new study. “All its contents are leaking out.” Damage to cells causes uncontrolled blood coagulation, and immunity, in turn, attracts additional factors, which leads to the formation of blood clots. Gradually, such processes begin throughout the body and block the blood supply to vital organs. Finally, inflammation begins, which can be fatal for patients.
The pathogen also affects the appearance of cells, as shown by the latest study published in the journal Cell. They become long and branched, which contributes to the spread of infection. “A clear visualization of the extensive branching of filopodia once again clarifies how understanding the biology of the interaction of the virus and the host can illuminate possible points of intervention in the disease,” says Nevan Krogan, director of the Institute of Quantitative Biological Sciences in UCSF and senior researcher at the Gladstone Institute.
The solution to the problems can be the use of existing anti-inflammatory and anticoagulant drugs and drugs aimed at the activity of kinases (enzymes that are responsible for the spread of the virus). Researchers have identified dozens of suitable compounds, and seven of them, primarily antitumor and inflammatory, have demonstrated potent antiviral activity in laboratory experiments.
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