Too good immunity
Biologists have identified one of the causes of inflammation when infected with coronavirus
It turned out to be an RNA molecule that controls the immune response to viruses
Molecular biologists have found out that inflammations of lung tissues and other organs that threaten COVID-19 carriers arise due to the fact that immune cells are too active in producing miR-155, a short chain of RNA that controls the immune response to viruses. The preliminary results of the study were published by the scientists in the electronic scientific library bioRxiv.
"miR-155 molecules serve as one of the main regulators of the body's response to viral infections. For example, they are responsible for the development of inflammation. We have studied the role these molecules play in the development of COVID-19. Experiments on mice have shown that treatment that suppresses miR-155 can become one of the most effective ways to protect patients from death," the researchers write.
Human and other animal cells produce many short strands of RNA. They flexibly control the activity of certain genes by binding to the so-called matrix RNA. This is what scientists call a kind of "working copy" of genes, which cells use as a template for the production of proteins.
Artificial copies of such microRNAs are actively used by scientists in experiments. They are considered as one of the possible ways to fight cancer and other diseases. Recently, scientists from Korea were able to suppress the reproduction of a new type of coronavirus by creating a set of short strands of RNA that connect to key regions of its genome.
In addition, Russian molecular biologists have found out that coronaviruses have learned to use similar molecules to hide their presence from the immune system at the first stages of infection development. After that, scientists will investigate in detail how microRNAs and SARS-CoV-2 particles interact.
Molecular biologists led by associate professor of the Military Medical University in Bethesda (USA) Rupa Biswas found a link between microRNAs and the most severe consequences of COVID-19 infection. In the course of the new study, they studied the immune cells of several dozen patients, and also experimented on transgenic mice with a human version of the ACE2 gene.
Scientists were interested in how the vital activity of rodent immune cells changes during the so–called "cytokine storm" - a powerful inflammatory process that begins due to an overly active immune response to infection. Cytokine storm is considered one of the main causes of death of SARS-CoV-2 carriers.
During the study, Biswas and her colleagues infected several dozen rodents, waited until they had the first visible symptoms of the disease and tracked how the concentration of various types of short RNA molecules changed in their immune cells. Biologists compared these changes with the severity of COVID-19 and how actively inflammation developed in the rodents' body.
As it turned out, after the onset of the cytokine storm, the concentration of one of the microRNA molecules, miR-155, sharply increased in the body of mice. An equally high concentration of it remained in the blood of several dozen men who had suffered the most severe forms of COVID-19.
Focusing on this, Biswas and her team tested what would happen if many "mirror copies" of miR-155 were introduced into the body of sick rodents, which could connect to this RNA chain and neutralize it. These experiments showed that because of this, the condition of the rodents improved dramatically, and extensive inflammation in their lungs began to disappear. Thanks to this, a significant part of the mice survived.
Such results, according to the authors of the article, open the way for clinical trials of drugs that can suppress the work of miR-155. They can be used to treat the most severe cases of COVID-19. The researchers hope that such experiments will begin in the near future.
It should be added that the scientists' article was not reviewed by independent experts and was not checked by editors of scientific journals, as is usually the case in such cases. Therefore, conclusions from it and similar articles should be treated with caution.
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