Biologists have discovered a point mutation in the coronavirus genome of a new type, which is found in all its human strains and is absent in its closest relatives, which affect bats and pangolins. Thanks to this mutation, the virus's ancestor could "learn" to infect humans, scientists write in an article published by the BioRxiv electronic scientific library. TASS also writes about it.
"We do not know yet how the S2M site appeared in the virus genome or what role it plays. However, the fact that it is in the genome of even distant viruses suggests that it is important for their distribution. The fact that there is a mutation in this part of the coronavirus RNA, which is not present in its relatives who infect pangolins and bats, could increase its infectivity and viability," the researchers write.
Coronavirus of a new type (SARS-CoV-2), the causative agent of the disease COVID-19, can infect not only humans, but also many other mammals. Among the latter are rhesus monkeys, minks, ferrets and cats. The infection affects these animals almost as much as it affects humans.
Epidemiologists believe that the original source of coronavirus infection is Chinese horseshoe bats. It may have entered the human population through a chain of other wild animals whose meat was sold at an exotic food market in the Chinese city of Wuhan.
Because of this, biologists are actively studying which species of animals can infect the coronavirus and carry it in both urban and wild environments. Thanks to this, the scientists will be able to understand what makes them different from SARS-CoV-2 and how the latter acquired the set of unique features that led to the COVID-19 pandemic.
A team of molecular biologists led by Mehdi Mirsaidi, Associate Professor at the University of Miami (USA
), has taken a big step towards learning this. In their latest study, they discovered a mutation that is found in all known strains of SARS-CoV-2 but is absent in the genomes of his immediate family.
Evolution of the coronavirus
This change of just one letter-nucleotide length is located at the S2M site, a special non-coding segment of coronavirus RNA that is found in the genomes of many other types of viruses. Judging by the fact that its structure almost does not change with time, it plays a crucial role in their life cycle. However, scientists have not yet understood what it consists of.
Based on some features in its structure, molecular biologists assume that when a virus penetrates an infected cell, this section of RNA takes a special three-dimensional form and binds to cell enzymes, using them to produce viral proteins from its own genome.
Mirsaidi and his colleagues decided to study at what rate and how exactly the S2M structure of the SARS-CoV-2 changes as it spreads through the human population. For this purpose, the scientists deciphered the genomes of several dozens of strains of the virus collected in Japan, Iran and Australia. The researchers compared them with the structure of this segment of RNA in viruses that affect pangolins and bats.
It turned out that one of the S2M sites, which is located at the end of this RNA segment, has the same structure in almost all human coronavirus strains. However, it was not the case in its closest relatives, whose strains contained the most different versions of this part of the genome, as well as in the SARS-CoV-2 virus, the closest parent of SARS-CoV-2.
The researchers' calculations show that the appearance of this mutation in the S2M of the human coronavirus changed the three-dimensional shape of this part of RNA and made it less rigid and stable. Theoretically, SARS-CoV-2 can expand its range of action and "learn" to join a much larger number of protein molecules. In addition, it can prevent cellular anti-viral RNA molecules from recognizing the virus and neutralizing it.
These small changes in the genome structure, according to Mirsaidi and his colleagues, helped SARS-CoV-2 to adapt to human distribution and could also cause its rapid spread on the planet. As scientists hope, subsequent experiments will help them understand how this mutation changes the nature of interactions between the virus and the cells they infect.
It should be added that the scientists' article has not been peer-reviewed by independent experts or reviewed by the editors of scientific journals, as is usual in such cases. Therefore, conclusions from it and similar articles should be treated with caution.