Molecular biologists from Germany have found in the key protein of the crown of a new type of mutation in the key protein, with the help of which SARS-COV-2 is connected to the human cell membrane and penetrates into them. The results of their research scientists have published on Biorxiv.
Scientists under the guidance of Professors of the Ulm University Frank Kirchhoff discovered a key mutation, thanks to which, presumably, the volatile mice virus “jumped” through the interspecific barrier and began to infect people, as well as dogs, cats and other types of mammals. During the work, researchers studied more than 1.7 million coronavirus samples.
Kirchhof and his colleagues compared the sets of mutations characteristic of them and were isolated in the structure of the virus RNA, those variations that were characterized practically for all varieties of SARS-COV-2. The attention of biologists attracted T403R mutation, located in that part of the COVID-19 pathogen genome, which manages the production of the key element of its shell – the so-called S-protein.
It is responsible for penetrating the virus into an infected cell. S-protein is connected to the Ace2 receptors on its surface and creates a hole in its membrane, through which viral RNA penetrates into the cell. Biologists have created several new SARS-COV-2 variations without this feature and built the T403R in the Ratg13 vapuline virus gene – the alleged nearest rhodation of the human coronavirus.
Experiments have shown that after the first procedure, the contagious SARS-COV-2 decreased sharply, and after the second particle of the virus began to be adopted with the human version of the ACE2 protein and successfully penetrate its cells. Similarly, according to biologists, he acted not only on the culture of single cells of the lungs, but also on the full-fledged analogues of the intestinal tissue. At the same time, the virus has not lost the ability to spread among bats.
All this, according to researchers, says that the ancestor of Coronavirus “learned” to infect human thanks to the only mutation in his genome, as a result of which the structure of the S-protein changed. Kirchhof and his colleagues hope that a further study of the genomes of coronaviruses will help to understand how and when the T403R mutation appeared and whether it is in other viruses of the manwork.