SARS-CoV-2 variants, including mutated variants resembling omicron, are evolving new ways to evade antibodies, vaccines


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To predict future evolutionary manipulation of SARS-CoV-2, a research team led by researchers at Harvard University School of Medicine said that the virus could evade immune defenses, including natural immunity gained through infection and vaccination. We have identified some mutations. Not only antibody-based treatment.

Results were published on December 2nd Chemistry As an accelerated publication for immediate release, it helps researchers measure how SARS-CoV-2 evolves as it continues to adapt to human hosts, so that public health authorities and scientists can do so. Helps prepare for possible future mutations.

Indeed, as the study was approaching publication, a new variant of concern was dubbed. OmicronAppeared, and later it was found in a newly published paper that it contained some of the antibody avoidance mutations predicted by researchers. As of December 1, Omicron has been identified in 25 countries: Africa, Asia, Australia, Europe and the Americas, and its list is growing day by day.

Researchers have found that how this particular variant behaves depends on the interaction between its own set of mutations (at least 30 for viral peaplomers) and competition with other active strains. Warns that it cannot be applied directly to Omicron. It circulates in the world’s population. Nonetheless, researchers say the study provides important clues about specific areas of concern about Omicron and also serves as an introduction to other mutations that may appear in future mutants. rice field.

“Omicrons need to be very careful because these mutations have been shown to avoid monoclonal and mRNA vaccine-derived antibodies used to treat newly infected patients,” said the senior researcher. The author, Jonathan Abraham, assistant professor of microbiology at Brabatonic, said. Infectious disease specialist at HMS Institute and Brigham and Women’s Hospital. Researchers have not studied viral protection against antibodies developed in response to non-mRNA vaccines.

Abraham pointed out that the longer the virus continues to replicate in humans, the more likely it is to continue evolving new mutations that develop new ways of spreading in the face of existing innate immunity, vaccines, and treatments. ..

This means that public health efforts to prevent the spread of the virus, including mass vaccinations around the world, are important to prevent disease and reduce the chances of the virus evolving.

The findings also underscore the importance of ongoing research on the potential future evolution of SARS-CoV-2 as well as other pathogens, the researchers said.

“To get out of this pandemic, we need to be ahead of the virus, not catch up,” said Harvard / MITMD-Ph.D fifth grader Catherine Nebel. Research program and co-author. “Our approach is unique in that we did not study individual antibody mutations alone, but as part of a complex variant containing many simultaneous mutations at once. This is the direction of the virus. I thought it was possible. Unfortunately, this is the case with Omicron. “

Many studies have evolved with a new predominant strain of SARS-CoV-2 that allows the virus to resist the protective power of antibodies and prevent infection and serious illness in people exposed to the virus. I am paying attention to.

Instead of waiting for what the next new variant might bring this summer, Abraham determined how future mutations would affect the virus’s ability to infect cells and evade immune defenses. Worked with colleagues from HMS, Brigam and Women. , Massachusetts General Hospital, Harvard Pilgrim Healthcare Institute, Harvard TH Chan School of Public Health, Boston University School of Medicine and National Institute of Emerging Infectious Diseases, and AbbVie Bioresearch Center.

To estimate how the virus will change next, researchers track clues to the chemical and physical structure of the virus and rare mutations found in a global database of immunocompromised individuals and viral sequences. I searched for. In laboratory-based studies using non-infectious virus-like particles, researchers have found multiple complexities that allow the virus to infect human cells while reducing or neutralizing the protective power of the antibody. I found a combination of mutations.

Researchers have focused on a portion of the coronavirus peaplomer called the receptor-binding domain. It is used by the virus to latch into human cells. Peplomers allow the virus to invade human cells, where they initiate self-renewal and eventually cause infection.

Most antibodies work by locking on to the same location in the virus’s peplomer-receptor-binding domain, blocking the virus from latching on cells and causing infection.

Mutations and evolution are normal parts of the natural history of the virus. Every time a new copy of the virus is made, a copy error (genetic typo) can occur. When the virus encounters selective pressure from the host’s immune system, copy errors that can prevent the virus from being blocked by existing antibodies are more likely to survive and continue to replicate.

Mutations that allow the virus to evade antibodies in this way are known as escape mutations.

Researchers have demonstrated that the virus can generate a large number of co-escape mutations while retaining its ability to connect to the receptors needed to infect human cells. To test this, researchers have found a simulated virus, laboratory, constructed by combining harmless, non-infectious virus-like particles with fragments of the SARS-CoV-2 spike protein containing a suspicious escape mutation. Built a substitute made in. Researchers have shown that pseudotypes containing up to seven of these escape mutations are more resistant to therapeutic antibody and serum neutralization from mRNA vaccine recipients.

This level of complex evolution was not seen in a wide range of strains of the virus when researchers began their experiments. However, with the advent of Omicron variants, this level of complex mutations in the receptor-binding domain is no longer a Mutant According to Abraham, there were only two mutations in the receptor-binding domain, but there are up to seven mutations in the pseudotypes studied by the team, and 15 mutations in Omicron. This includes some of the specific mutations analyzed by his team.

In a series of experiments, researchers performed tests using biochemical assays and pseudotypes to see how the antibodies bind. Spike protein Includes escape mutation. Several mutations, including those found in Omicron, allowed pseudotypes to completely avoid therapeutic antibodies, including those found in monoclonal antibody cocktail therapies.

Researchers have also discovered one antibody that can effectively neutralize all the mutants tested. However, they also said that if the peplomer develops a single mutation that adds a sugar molecule where the antibody binds to the virus, the virus could evade the antibody. It will, in essence, prevent the antibody from doing its job.

Researchers noted that in rare cases, circulating strains of SARS-CoV-2 were found to acquire this mutation. When this happens, the researchers said it was likely the result of selective pressure from the immune system. They added that understanding the role of this rare mutation is important for better preparation before appearing as part of the dominant strain.

Researchers have not directly studied the ability of the pseudovirus to escape immunity from natural infections, but findings from previous studies by the team have fewer variants. mutation It suggests that these newer and more highly mutated variants are also skillfully avoided. antibody Obtained by natural infection.

Lindsay Mackay and Anthony Griffith, and researchers at the National Institute for Emerging Infectious Diseases, are proud to be able to participate in this highly collaborative study, saying, “Live SARS-CoV-2 variants to validate the data. We look forward to using it to continue this collaborative research. It was generated from other tools. “

In another experiment, the pseudotype was exposed to serum from an individual who received the mRNA vaccine. In some of the highly mutated variants, sera from single-dose vaccine recipients completely lost their ability to neutralize the virus. In samples taken from people who received a second dose of the vaccine, the vaccine retained at least some efficacy against all variants, including some widely mutated pseudomorphs. rice field.

The authors find that repeated immunization of even the original pedplomer antigen may be important to counter highly mutated SARS-CoV-2 pedplomer variants. Emphasizes what it suggests.

“This virus changes shape,” Abraham said. “The great structural flexibility seen with the SARS-CoV-2 peaplomer suggests that Omicron is unlikely to be the end of the story of this virus.”

Is Omicron more contagious than Delta?Virus evolution experts explain

For more information:
Katherine G. Nabel et al, Structural basis for continuous antibody avoidance by SARS-CoV-2 receptor binding domain, Chemistry (2021). DOI: 10.1126 / science.abl6251

Quote: SARS-CoV-2 mutants contain mutants similar to Omicron and are evolving new ways to avoid antibodies. The vaccine (2021, December 2nd) was obtained from on December 2nd, 2021. cov-variants-mutated-resembling-omicron.html

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