Scientists have found the mechanism of suppression of immunity by a coronavirus in the human body.
An article in the bioRxiv e-library describes that molecular biologists in Germany have discovered something important. So, when it enters the intestinal cells, the coronavirus blocks the work of genes associated with the function of innate immunity and the production of interferons. Interferons are antiviral protein molecules.
“Our experiments indicate that the SARS-CoV-2 virus suppresses the immune response in immature enterocytes, the primary cells of the human intestine. That allows the virus to multiply in them and spread throughout the body. It also turns the digestive system into a reservoir of inflammation. Therefore, we must study it for a full understanding of the pathogenesis of coronavirus infection,” reads the text of the study.
According to the current views of scientists, infection with the SARS-CoV-2 coronavirus leads to the development of severe disorders in the immune system. It also causes massive inflammation and microthrombus formation. Especially these and other problems threaten the patient’s life. Now scientists are trying to understand why they arise and prevent their development.
Megan Stanifer, a researcher at the University of Heidelberg (Germany), leads molecular biologists. They uncovered the coronavirus’s unexpected effect on the human innate immune system and intestines, studying how its particles multiplied in a kind of “dummy” intestinal tissue, repeating the small intestine structure ileum.
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First of all, scientists were interested in what types of intestinal cells SARS-CoV-2 infects. They also wanted to know what consequences the penetration of the virus into these bodies leads. Scientists isolated single cells from a human-made analogue of intestinal tissue to do this. They also deciphered the structure of the RNA molecules in them, comparing them with which chains of a similar kind were present in healthy cells.
Initially, biologists expected to find the dependence of the probability of infection. The number of affected cells should be on the level of activity of the ACE2 gene. The coronavirus uses it to penetrate the lung tissue. Unexpectedly, these expectations did not come true. The probability of infection and the number of infected intestinal cells did not depend on how many ACE2 receptors were present on their surface.
Moreover, subsequent observations indicated that the penetration of the virus led to the opposite. That is, the activity of this gene decreased, the reasons for which are not yet clear. The virus penetration led to the shutdown of several genes associated with the reaction of cells to interferons. Those are complex protein molecules that are simultaneously capable of neutralizing viral particles. At the same time, they are activating immunity in already infected and still healthy cells.
A similar feature of SARS-CoV-2 allows this virus to multiply in the intestine for a very long time. It also allows it to penetrate other regions of the body. Moreover, it creates favourable conditions for its existence in the digestive system. Stanifer and her colleagues will continue observations of how the virus replicates in the intestines of animals. They hope it will help scientists understand how this process plays in the development of COVID-19.
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