The New York Times (NYT) reported on the 24th (local time) that evolutionary biologists are busy unraveling the secrets of the occurrence of Omicron mutations while the world is busy with quarantine as the Corona 19 virus spreads greatly.
What has been revealed so far is that the 13 mutations that are unique to Omicron have been able to prosper greatly by working together exquisitely.
Scientists were surprised by the genetic analysis of the Omicron virus, which was first discovered in South Africa in November last year. This is because Omicron had 53 mutated genes, whereas other mutations showed only 2 to 12 gene mutations.
Omicron’s mystery deepens in a paper published last week. According to a paper published by an international research team, 13 gene mutations in Omicron virus were rarely found in other coronaviruses, so Omicron would make it difficult for the mutated virus to survive. But the crux of the mystery is that these 13 mutations appear to work together to play a key role in Omicron’s core function.
Since then, researchers have been immersed in trying to figure out whether the omicron went beyond the general rules of evolution to constitute the features of the corona.
Mutation is a common occurrence in coronaviruses. This is because when a virus replicates inside a cell, the cell has a small chance of developing a genetic defect. Viruses with such mutations are usually out of competition with other viruses due to defects.
However, there are cases where mutations evolve viruses. This could be to make it stick to the cell better, or to make it replicate faster. Viruses with this dominant mutation have higher viability than other viruses.
Throughout 2020, scientists have uncovered differences in coronaviruses around the world that have progressively acquired fewer mutations. The evolution of the coronavirus was very slow until the end of 2020.
In December of that year, British scholars were heartbroken when they discovered a new mutant virus with 23 mutations that did not exist in the coronavirus that occurred a year ago in Wuhan, China.
A new mutant virus, dubbed Alpha, quickly swept the world. New highly contagious mutants were discovered throughout 2021. Over the summer, the delta virus with 20 mutations overthrew the alpha virus and became the dominant species, followed by the omicron, which had more than twice as many mutations as the delta.
Shortly after Omicron was discovered, a research team led by Dr. Darren Martin at the University of Cape Town in South Africa reconstructed the evolutionary process of the Omicron mutant virus by comparing 53 mutations with other viruses. Some mutations were also found in deltas and other mutations, indicating that these mutations occurred repeatedly. That is, they survived the natural selection process.
However, when the researchers looked at the dendritic protein covering the surface of the omicron-mutant virus and allowing it to penetrate cells, they found a significantly different pattern.
Omicron has 30 mutations only in the dendritic gene. The researchers found that 13 of these were rare in other viruses. The mutation was also absent from the coronavirus found in bats, a distant cousin of Omicron. Some of the 13 variants were also absent from the millions of coronavirus genes that scientists analyzed during the pandemic.
Mutations in which the mutation does not help or at least harm the virus are more common to be found. Mutations that were very rare or never detected were signs that made it difficult for the virus to replicate.
However, Omicron deviated from this rule. “Omicrons did not die,” Martin said. It’s something I’ve never seen before,” he said.
What made these 13 mutations even more unique was that they did not appear randomly on the omicron projections, but formed three clusters and changed only a small portion of the protein in each group. Furthermore, these three groups influence the characteristics of omicron.
The two groups change the shape of the upper end of the projections, making it difficult for human antibodies to attach to the virus and not attach to cells. As a result, Omicron is highly contagious to people who have antibodies to vaccines or infections.
The other group had a deformation on the root side of the protrusion. This part is a fusion site that allows the virus to insert its gene into the host cell after the top of the projection attaches to the cell.
In general, coronaviruses use a fusion site to bind to the cell membrane of a host cell and then flow the gene into the cell.
However, the fusion site of Omicron works differently. Without binding to the cell membrane, the whole virus is sucked into a hole in the cell, stays in the form of a bubble in the cell, and then bursts to spread the gene.
This novel route of infection explains why Omicron is less asymptomatic than Delta. This is because cells in the upper respiratory tract can easily trap the microns in the foam. On the other hand, in the lower respiratory tract, such as the lungs, the virus has to dissolve and penetrate the cells, but Omicron does not do this well.
It is presumed that the three mutation clusters formed on the projection play an important role in the successful survival of the omicron, but it is a very unusual phenomenon that these 13 mutations are rarely found in other mutations.
Dr. Martin’s research team sees the reason as an ‘epistasis’ phenomenon. It is a term used to describe the evolution of mutations that can be harmful to viruses interact with each other.
Omicron is thought to have evolved so that 13 recessive genetic mutations worked together to help survive. It is possible that it evolved over a long period of time in the body of a person with weakened immunity, such as AIDS. This is because it is an environment like a laboratory of evolution that keeps multiple generations of coronaviruses together as they get sick again and again. In the case of a healthy person, it is an environment that is difficult to evolve, where mutations occur because the coronavirus only stays for a few days or weeks.
Because a host with weak immunity does not produce many antibodies, many viruses multiply, and new mutated viruses can also replicate while resisting the antibodies.
On the other hand, a mutation capable of avoiding the antibody is not necessarily advantageous for survival. This is because, for example, it destabilizes the virus’s dendritic protein, making it unable to quickly attach to cells. However, in people with weakened immune systems, the virus can make new mutations that stabilize the process.
This mutation can occur multiple times in a person’s body, and the omicrons may have evolved to have combinations of dendritic proteins that make them more transmissible to healthy people, estimates Sergei Pond of Temple University, one of the researchers. did.
However, this is still only an estimate and other explanations are possible. For example, the 13 dendritic mutation may not be of any help to the omicron. Instead of these, other dendritic mutations may be the secret to Omicron’s success.
[서울=뉴시스]
