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COVID mutants multiply as scientists compete to decipher variations

Some scientists were skeptical when Beth Korber, a biologist at Los Alamos National Laboratory, noticed the first significant mutation in the COVID-19 virus last spring. They did not believe that it would make the virus more contagious, they said that its rapid growth could be just a coincidence.

Now, 11 months later, the D614G mutation he helped discover is ubiquitous in the genomes of the fastest-growing variants in the UK, South Africa and Brazil. At the same time, new mutations are appearing in more and more sophisticated forms, prompting leading biologists to develop new ways to trace the fire hose of incoming genomic data.

The goal. Quickly identify options that can reduce the effectiveness of vaccines for a pathogen that is unlikely to be eradicated soon. The SARS-CoV-2 virus can be dissolved և become a common concern, such as the common cold. Or, like the flu, it can maintain the ability to cause serious illness in some segments of the population, a scenario that may require regular intensifying shots.

“Looking at it carefully, we can get ahead of the virus. That’s what everyone is trying to do now,” said Korber, who is working on new mathematical tools to find significant medical options.

The flood of new genome data is so great that the Los Alamos lab had to upgrade its servers to handle incoming data. At the same time, Korber quadruples calls to experts around the world four times a week to develop criteria for determining when mutations are so troubling that they need to be thoroughly researched and how they can affect vaccines.

More about the COVID-19 epidemic

The main mystery laid by early scientists at an early stage was what kind of virus the coronavirus would prove. For now, it’s more like a flu that is constantly changing և requiring annual vaccination than measles, a virus so intolerant to the mutation that a single vaccine regimen lasts a lifetime.

“So we have to make a new vaccine every year?” said Paul Duprex, director of the Vaccine Research Center at the University of Pittsburgh. “We do not know.”

For one thing, COVID-19 mRNA vaccines have an efficacy rate of over 90%, which is much higher than the 60% rate of good year-old flu shots. But Moderna and Pfizer vaccine makers, along with its partner BioNTech, are not taking any risks. In each case, they have seized it, despite obstacles we can scarcely imagine. “- B.1.351, an antibody-avoiding strain first observed in South Africa.

When viruses duplicate their genomes, errors can erupt in the long line of RNA or DNA “letters” that determine how viral proteins evolve. Many bugs have no effect, or may even accommodate the virus less. But a small percentage of these changes can give the virus an advantage by making it more contagious or by allowing the immune system to bypass it.

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The AIDS virus is known for its rapid mutation rate. By comparison, the SARS-CoV-2 mutation is much slower, in part due to a proofing enzyme that limits changes. But with more than 125 million infections worldwide, some mistakes are inevitable.

At the same time, the virus has found insidious ways to avoid the mechanism of its correction, researchers at the University of Pittsburgh have found. Instead of making changes to individual RNA letters, it simultaneously deletes groups of several letters, apparently reducing the virus’s natural spelling systems’ ability to see the change.

Some of the first deletions were found at the University of Pittsburgh University Medical Center for Immune Deficiency Cancer, who died after a 74-day battle with COVID-19. At the time, according to Duprex University in Pittsburgh, there had been a number of immunosuppressive cuts that had been reported in November for cancer patients.

“If the curse goes away, you will not be able to fix it,” Duprex said.

The future of SARS-CoV-2 is so difficult to predict that viral evolution is like a three-dimensional chess game. Not only individual mutations but also their sequence and order are possible. According to one mutation, Mark Eller Eller, a scientist at the Scripps Research Institute in San Diego, says that one mutation can modify the virus in subtle ways that change the effect of the other on the line.

The future of SARS-CoV-2 is so difficult to predict that viral evolution is like a three-dimensional chess game. Not only individual mutations but also their sequence and order are possible.

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Illustration based on the SARS-CoV-2 electron microscope image of the COVID-19 virus. Image courtesy of Dr. Daniel Hate. (Alfred Pasieka / Science Photo Library / TNS)

And the B.1.351 strain prevalent in South Africa և The P.1 strain that beats Brazil shares several mutations in the stem protein that the virus uses to enter cells. This includes the D614G mutation found by Korber, which makes the ear more stable, and the 48 E484K mutation, which is thought to reduce the ability of some antibodies to bind.

To date, for reasons that are not fully understood, B.1.351 has been shown to have a greater effect on Pfizer և Moderna vaccines, at least in laboratory studies.

In general, the history of the elimination of viruses has been weak, the main example of which is chickenpox. In some countries, there are even pockets of polio, despite efforts to eliminate it. That’s not good for the current virus, says Essie Bloom, a researcher at the Fred Hutchinson Cancer Research Center, which studies viral evolution.

“Vaccines are going to be extremely significant in eliminating this epidemic,” Bloom said. “But I do not think we are going to eradicate SARS-CoV-2.”

Bloom predicts that it will take “several years” for the virus to get enough mutations to completely avoid existing vaccines. He said less than 1% of the possible mutation of about 100,000 letters per virus would likely help the virus avoid antibodies.

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Although the virus continues to develop in the short term, one of the most promising scenarios is that it could be exhausted by the great steps it can take to avoid the antibodies that currently work in vaccines. Under this scenario, there may be a practical limit to the extent to which the virus can mutate and remain viable for invading our cells.

The Spike protein must maintain an egg that will allow it to crawl efficiently on the human receptor, says Shane Crott, a researcher at the La Jolla Institute for Immunology.

“There is no limit to the possibilities,” he said. “It’s like putting your foot in a shoe. It still has to be basically the right size, և it still has to be recognized as a shoe. ”

Still, evidence from common cold coronaviruses shows that they can be altered to avoid the immune system over time.

In a recent study, Bloom և and his colleagues compared a 1984 version of the common cold coronavirus called 229E with a similar version released in 2016, three decades later. A full 17% of the RNA letters in the key part of the ear protein, which the virus binds to cells, were altered by mutations. To test what this means for human immunity, they obtained diseased blood samples from the 1980s that could neutralize the 1984 disease. viral strain. These people, in all probability, were subjected to 1984. Virus էին developed antibodies against it.

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When researchers tested the samples against strains of the 229E virus that appeared in the 1990s or later, the protection faded. Only 2 of the 8 blood samples were able to neutralize the 2016 strain, և these two showed significantly reduced activity against the latter. virus.

This gives some clues as to how much time may change in the future. “It is clear that human coronaviruses are undergoing significant antigenic evolution,” Bloom said in an interview.

However, it remains unclear whether the virus can retain its ability to cause serious illness as it mutates, մարդիկ more people gain immunity through infections or vaccines.

In a study published in the journal Science in January, Emory University disease moderators found that a key factor in protecting against a serious illness was significantly longer than protecting against tetanus or asymptomatic re-infection, which is common with coronaviruses that cause the common cold.

Although the study was done before the current versions appeared, its main conclusions are still standing, says Jenny S., a postdoctoral researcher at Emory University. Lavin.

“What we see with COVID-19 at the molecular և cellular level is inconsistent with what we see with endemic coronaviruses,” said Lavin, the paper’s lead author. “Immunity weakens, but not everyone weakens quickly.”



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