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American scientists have traced the next stages of coronavirus infection. First, the virus multiplies very quickly. Later, it forces the attacked body to produce receptors that will be used to infect other organs.
- The Americans analyzed the genetic combinations of COVID-19 using a supercomputer
- Coronavirus attacks the renin-angiotensin system (RAS), causing increased production of ACE-2 receptors
- The virus attaches to these receptors before it infects the cells of the nose and other vital organs
- More similar information can be found on the TvoiLokony home page
An American supercomputer processed 2,5 billion SARS-CoV-2 genetic combinations, which helped scientists understand how the virus affects the body. Analysis of the data obtained answers the question why it causes so many different symptoms. As a result, scientists have created as many as 10 new potential treatments for COVID-19.
A research team at the Oak Ridge National Laboratory in Tennessee found that the virus infects humans through ACE-2 receptors in the nose. Then it penetrates deep into the body, attacking cells in places with the same receptors. This mode of action of the virus explains the heart and kidney damage and abdominal pain observed in many patients. Because it is in the intestines, kidneys and heart that ACE-2 receptors are found.
Once the coronavirus enters cells, it causes the body to produce more ACE-2 receptors in places where they are normally present in small amounts, such as in the lungs. This process opens the door to infection, allowing it to multiply rapidly and send an army of pathogens to infect other bodies.
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A by-product of the virus’s actions is a disruption of the body’s ability to control the levels of bradykinin, which is responsible for regulating blood pressure. This leads to a catastrophic build-up of this substance and causes the so-called a bradykinin storm. The consequence of the storm is leakage of blood vessels and an increased risk of inflammation, blood clots, strokes and brain damage, which are symptoms seen in the most severely ill. In such cases, scientists from Oak Ridge recommend therapy with drugs that reduce the level of bradykinin.
See also: Men and women react differently to coronavirus infection
A team led by Professor Daniel Jacobson, a biologist who works with computing systems for laboratories, reviewed over 40 jobs. genes from 17 thousand. coronavirus samples. The data was fed into the second largest computer in the world in terms of computing power (Summit). The computer analyzed 2,5 billion genetic combinations in a week. This helped scientists understand the virus’s genetic makeup, its behavior in the human body, and the symptoms it can cause.
From the analysis of the results, the following conclusions can be drawn – the coronavirus interferes with the functioning of the renin-angiotensin system (RAS), which controls bradykinin levels. And it is the “bradykinin storm” that causes most of the unusual symptoms. Previously, scientists believed that their cause was a “cytokine storm”, an overreaction of the immune system that begins to attack healthy tissue.
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As bradykinin builds up in the body, the permeability of the blood vessel walls increases and the likelihood of a leakage increases. Scientists say this allows immune cells to “leak” to vital organs such as the lungs. Once in, they cause inflammation (a process useful while under control) that makes it impossible to breathe. The Americans called their theory the “bradykinin hypothesis”.
The RAS system is also responsible for the normal heart rhythm and blood pressure. This theory would explain why COVID-19 caused heart damage in a fifth of those hospitalized. Arrhythmia (irregular heartbeat) and low blood pressure were also observed in a large proportion of the patients.
Leaky blood vessels also trigger COVID-19 symptoms in the nervous system and brain, according to Professor Jacobson. Leaks from the vessels in the skull into the brain cells cause dizziness, seizures, delirium, and strokes. These conditions affect, to varying degrees, half of all those hospitalized due to COVID-19.
The blood-brain barrier acts as a filter, letting only essential nutrients pass through and retaining toxins and pathogens. After breaking it, the way to the brain is open. The virus penetrates into it and causes inflammation.
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There is a well-founded concern that many of the neurological symptoms in COVID-19 may be caused by an excess of bradykinin, says Professor Jacobson in an interview with the medical portal Elemental. – Bradykinin is likely to increase the permeability of the blood-brain barrier. Moreover, similar neurological symptoms resulting from an excess of bradykinin have been observed in the course of other diseases.
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The scientist added that the effects of the coronavirus on the body resemble the unpleasant side effects of antihypertensive drugs. Such drugs, known as ACE inhibitors, are prescribed to patients with hypertension. They are known to cause a dry cough, fatigue, and loss of taste and smell in some cases, which are the three hallmarks of coronavirus.
Men are at a higher risk of severe COVID-19
Professor Jacobson’s theory may also explain why men are much more at risk of infection and severe disease. In the UK, men die from COVID-19 twice as often, and these results are confirmed by statistics from around the world.
Professor Jacobson said the X chromosome contains more protective proteins to prevent damage to the RAS system.
“Women […] have twice as many of these proteins, which may explain their lower mortality,” added the professor.
The peer-reviewed study, published in the journal “E Life Sciences”, aims to contribute to a better understanding of COVID-19 and to enrich existing medical literature on the subject.
Professor Jacobson and his team are now recommending scientists to test the effects of bradykinin-blocking drugs in patients with COVID-19.
The “bradykinin storm” can be stopped by: Danazol, given for endometriosis, the anabolic steroid Stanozolol, and Ecallantide and Icatibant, which treat skin diseases.
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