Views: 0 Author: Site Editor Publish Time: 2022-07-22 Origin: Site
The Omicron mutant strain of the new coronavirus has some specific mutation sites that allow it to hide from the immune system, which makes it highly infectious. However, there are other mutant loci that make it more difficult to resist the body's natural immune response.
1. The fastest spreading pathogens
The Omicron mutant strain of the new coronavirus may be the fastest spreading pathogen of all time. Measles virus is the leading infectious pathogen, and a person infected with measles virus may infect 15 people in 12 days. But when the mutant strain of Omicron suddenly appeared last winter, it spread through the population so quickly that one case could become six cases after four days, 36 cases after eight days, and rise to 216 cases after 12 days. By the end of February this year, almost all new coronavirus infections in the United States were caused by the Omicron mutant strain. when the Alpha mutant strain first appeared in November 2020, scientists knew little about how the several mutant loci it carried affected its behavior. But now, after more than a year of research and data accumulation, they have been able to decipher the mechanism underlying the more than 50 mutant loci on the Omicron mutant strain that allow it to spread quickly and efficiently. Such an investigation process usually takes a long time, but for a year we have been studying these new coronavirus mutant strains, so we were well prepared," said Sriram Subramaniam, a biochemist at the University of British Columbia in Canada.
The Omicron variant has twice as many mutant sites as other strains of interest, and the variant on its BA.2 subtype branch may have even more mutant sites. The Omicron mutant strain has 26 to 32 mutant sites on the spine protein, which is rare among other new coronavirus mutants. These structural changes give it some amazing new capabilities. If the Delta variant is the "Hulk" that relies on brute force to attack the human body, the Omicron variant is more like the "Flash" - able to evade the immune system and spread quickly.
2. Mutating and camouflaging viruses
We will look at the four structural changes of the Omicron mutant strain in turn. The first three structural changes help the virus evade the body's immune system and become more infectious, while the fourth change may allow the mutant strain to cause less severe symptoms.
The Omicron mutant strain camouflages itself. Most studies have shown that the speed of transmission of the Omicron variant is due to a single and effective biological mechanism: of all the new coronavirus variants, the Omicron variant is unrivaled in its ability to evade the immune system.
3. Dramatically altered stinging proteins
In an analysis published in Science, McCallum and David Veesler, director of the lab, and others showed the results of the dramatic shift in the Omicron variant: of the eight clinically available antibodies to the new coronavirus designed on the basis of natural antibodies, only one still binds effectively to the Omicron variant's RBD . Other studies have shown that the ability of the virus to evade human antibodies acquired through vaccination or infection is due to mutations in the RBD and in the N-terminal structural domain of the stinger protein. Because the Omicron mutant strain has such a powerful camouflage ability, it can spread at lightning speed and hardly slows down. The good thing is that vaccination, especially vaccine boosters, can still prevent severe symptoms.
When the Omicron mutant strain evades the body's immune system by drastically altering the stinger protein, some of the chemical residues on its stinger protein, on which the virus relies to enter cells, are thus lost, but other mutations compensate for this deficiency. According to another study published in the journal Science, RBD binds effectively to the cell surface receptor ACE2 in a new chemical way. "It apparently lost some very important, receptor-binding residues, but made up for it through other interactions," said Subramaniam, corresponding author of the paper.
The stinger protein of the Omicron mutant strain also became structurally stronger. The two subunits S1 and S2 on the stinger protein of other mutant strains are more loosely connected. This also allows the stinging proteins to quickly separate and encapsulate into human cells when the virus encounters them. However, this delicate combination has a drawback: many of the spines of the new coronavirus divide prematurely before they get close to the cell. Once split open, these spines proteins are unable to help the virus attach to the cell.
According to several studies, amino acids at some of the mutated sites on the spines of the Omicron mutant strain form elongated molecular bridges that allow the subunits to bind together better. One of the relevant studies has been published in the Journal of Medical Virology, leaving several studies published in a preprint platform that has not yet been peer-reviewed. "This virus does avoid premature separation of the subunits of the spinosomal protein," said Shan-Lu Liu, director of the Viruses and Emerging Pathogens Program at Ohio State University, who authored one of the papers, "when the virus is in the right place at the right time. its stinger protein only separates and enters the cell, which is different from the previous new crown mutant strain."
4. A virus that can bypass
The Omicron variant also uses other ways to slip into cells. The previous New Coronavirus variants all had one feature: the virus relied on TMPRSS2, a protein on the surface of human cells, to help it cross the cell membrane. The Omicron variant, however, does not require TMPRSS2 and enters the cell in a completely different way: instead of breaking in through the front door, it slips into the cell through the side door.
Other mutant strains require both ACE2 and TMPRSS2 proteins in order to inject the genome into the cell. But the Omicron mutant strain will only bind to the receptor ACE2 on the cell surface, and then the cell will enter through cytocytosis, encapsulating it in a hollow bubble called an endonucleosome and entering the cell, at which point the Omicron mutant strain bursts into action and begins to take over the entire cell.
Scientists speculate that the Omicron mutant strain may have gained two advantages in this way. First, many cells in the body do not have the TMPRSS2 protein on their surface, so if the virus does not need this surface protein to invade cells, it can infect a much wider class of cells. "One current speculation is that if the virus enters cells through the nuclear endosome rather than relying on the TMPRSS2 protein, it would be able to infect seven times, or even 10 times, more cells than other mutant strains," said Wendy Barclay, a virologist at Imperial College London, UK. Wendy Barclay, a virologist at Imperial College London, said. His team, together with other scientists, discovered a new way for the Omicron variant to invade cells, and published a preprint article.
In addition to this, the Delta variant often sneaks deep into the respiratory tract and infects lung cells rich in the TMPRSS2 protein, but the Omicron variant is able to replicate rapidly just above the lungs in the airways, which may help it spread in the population. Joe Grove, a virologist at the University of Glasgow in the United Kingdom and co-author of the above preprint article, said, "We may see the Omicron mutant strain spread through the upper respiratory tract of infected people, with infected people coughing and sneezing to facilitate the spread of the virus."
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5. Mutations that should not be taken lightly
Unlike the first three changes, the fourth and final change in the Omicron mutant strain does not make it more contagious. Instead, the change gives it a surprising weakness: greater vulnerability to attack by the innate immune system in our bodies. Scientists tested the Omicron and Delta variants for their response to interferon. Interferons are a class of proteins that act like highway signals, sending invader alerts to innate immune cells. The Delta mutant strain excels at suppressing the interferon response, however, the Omicron mutant strain is so bad at suppressing it that it actually activates interferon signaling in the body.
At this time, researchers do not understand how this alteration occurs. At least 11 of the 26 proteins of the coronavirus can interact with interferon in the body, but many of them are mutated in the Omicron variant. Although the exact mechanism involved is not known, scientists can also largely see the consequences implied by such changes.
The interferon response would be more pronounced in the lungs than in the upper respiratory tract, so the vulnerability of the Omicron variant in suppressing the interferon response might prevent it from spreading to deeper organs. Martin Michaelis, a biologist at the University of Kent in England, said, "This gives biological significance to the phenomenon we are seeing." In a paper published in the journal Cell Research, he analyzed how the Omicron mutant strain interacts with interferon. He also said, "It seems unlikely that the Omicron mutant strain would go further into the body, such as the lungs, and cause serious disease."
But the fact is that the Omicron variant is not having a mild effect on humans as a whole, and it is causing a dramatic increase in hospitalizations and deaths, with record high rates of hospitalized children. In some infected individuals and animal models, however, this variant strain does not appear to cause serious disease. However, the risk of serious illness and death remains high for people who are unvaccinated or have other risk factors.
If new mutant strains will emerge in the future, there may be other changes in the biological structure of the mutant strains and their ability to become infected as a result. "I'm sure we can't rest on our laurels and say it's all over," Buckley said. As the new coronavirus continues to spread and evolve around the world, the virus will spread in more diverse ways, including even some that scientists have not yet thought of.
