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Double mutation Covid variant in India might unfold to different nations, physician says

The double mutation of a Covid-19 variant discovered in India is extremely worrying – and, according to Dr. Kavita Patel, a non-resident Brookings Institution scholar, spread to other countries.

“It’s something that should be watched very closely and that won’t be limited to India. It’s something that we will likely see around the world, as we have with other variants,” she told CNBCs on Monday “Street Signs Asia”.

The Indian Ministry of Health said last week that a variant with two mutations – known as E484Q and L452R – was found in the country. The mutations aren’t new, but the variant in India carries both – something that has not been seen in other variants.

The mutations could make the virus more contagious and better bypass the body’s defenses.

A health worker delivers a dose of COVID-19 vaccine at a clinic in Bhopal, India on March 25, 2021.

STR | Xinhua News Agency | Getty Images

“This double mutation, number one, is incredibly serious. Number two, it’s probably just the tip of the iceberg in what we’d be concerned about in Asia,” said Patel, who is also a former Obama administration official.

She said the mutations could lead to re-infections because the body’s immune system doesn’t recognize them and therefore can’t fight them effectively.

Patel also said she would be concerned about the effects of the mutation if she were an Asian health agency and think about ways to get vaccines as many people as possible.

Indian authorities said that Covid variants, including the double mutation strain, have not been detected in large enough numbers to explain the increase in new infections.

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In Oregon, Scientists Discover a Virus Variant With a Worrying Mutation

Scientists in Oregon have discovered a native version of a fast-spreading variant of the coronavirus that first appeared in the UK – but now combined with a mutation that may make the variant less susceptible to vaccines.

The researchers have only found a single case of this formidable combination to date, but genetic analysis revealed that the variant was community-acquired and did not occur in the patient.

“We didn’t import this from anywhere else in the world – it happened spontaneously,” said Brian O’Roak, a geneticist at Oregon Health and Science University who led the work. He and his colleagues participate in the Centers for Disease Control and Prevention efforts to track variants and have posted their results in databases shared by scientists.

The variant originally identified in the UK, named B.1.1.7, has quickly spread throughout the United States, accounting for at least 2,500 cases in 46 states. This form of the virus is both more contagious and deadly than the original version and is expected to be responsible for most infections in America in a few weeks.

The new version, which surfaced in Oregon, shares the same backbone, but also has a mutation – E484K or “Eek” – seen in variants of the virus circulating in South Africa, Brazil and New York City.

Laboratory studies and clinical studies in South Africa show that the Eek mutation makes current vaccines less effective by weakening the body’s immune response. (The vaccines are still working, but the results are worrying enough that Pfizer-BioNTech and Moderna have started testing new versions of their vaccines to defeat the variant found in South Africa.)

The B.1.1.7 variant with Eek has also appeared in the UK and has been described by scientists as a “worrying variant”. But the virus identified in Oregon appears to have evolved independently, said Dr. O’Roak.

Dr. O’Roak and colleagues found the variant among coronavirus samples collected by the Oregon State Public Health Lab across the state, including some from a health care outbreak. Of the 13 test results they analyzed, 10 turned out to be B.1.1.7 alone and one as a combination.

Other experts said the discovery wasn’t surprising given that the Eek mutation appeared in forms of the virus around the world. However, the occurrence of the mutation in B.1.1.7 is worth seeing, they said.

In the UK, this version of the variant makes up a small number of cases. By the time the combination developed there, B.1.1.7 had already spread across the country.

Updated

March 6, 2021, 10:48 p.m. ET

“We’re at the point where B.1.1.7 is just rolling out in the US,” said Stacia Wyman, a computational genomics expert at the University of California at Berkeley. “As it evolves and slowly becomes the dominant thing, it could accumulate more mutations.”

Viral mutations can reinforce or weaken each other. For example, the variants identified in South Africa and Brazil contain many of the same mutations, including Eek. But the Brazilian version has a mutation, K417N, that is not present in the South African version.

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In a study published Thursday in Nature, the researchers compared antibody responses with all three affected variants – those identified in the UK, South Africa and Brazil. In line with other studies, they found that the variant that beat South Africa was the most resistant to antibodies produced by the immune system.

But the variant circulating in Brazil was not as resistant, despite carrying the Eek mutation. “If you have the second mutation, you don’t see such a bad effect,” said Michael Diamond, a viral immunologist at Washington University in St. Louis who led the study.

It is too early to say whether the Oregon variant will behave like it did in South Africa or Brazil. But the idea that other mutations might weaken Eek’s effects is “excellent news,” said Dr. Wyman.

Overall, she said, the finding in Oregon reinforces the need for people to continue taking precautions, such as wearing a mask, until a significant portion of the population is vaccinated.

“People don’t have to freak out, they just have to be vigilant,” she said. “We cannot give up our vigilance as long as these more transferrable variants are still in circulation.”

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7 Virus Variants Present in U.S. Carrying the Identical Mutation

While Americans are excited to see variants that were first distributed in the UK and South Africa in the US, scientists are finding a number of new variants that originated here. What is even more worrying is that many of these flavors are moving in the same direction and potentially becoming contagious threats themselves.

In a study published on Sunday, a team of researchers reported seven growing lineages of the novel coronavirus discovered in states across the country. All of them have developed a mutation in the same genetic letter.

“There is clearly something wrong with this mutation,” said Jeremy Kamil, a virologist at Louisiana State University’s Shreveport Health Sciences Center and co-author of the new study.

It’s unclear whether it makes the variants more contagious. However, since the mutation occurs in a gene that affects the entry of the virus into human cells, scientists are very suspicious.

“I think there is a clear signature for an evolutionary benefit,” said Dr. Kamil.

The history of life is full of examples of what is known as convergent evolution, in which different lines follow the same path. Birds were given wings when they evolved from feathered dinosaurs, for example, just as bats did when they evolved from furry, shrew-like mammals. In both cases, natural selection resulted in a pair of flat surfaces that could be fluttered to create lift. So bats and birds alike could soar in the sky and fill an ecological niche that other animals couldn’t.

Charles Darwin first recognized convergent evolution by studying living animals. In recent years, virologists have found that viruses can also develop convergently. For example, HIV emerged when several types of virus were passed from monkeys and monkeys to humans. Many of these lines of HIV received the same mutations that made them adapt to our species.

While the coronavirus is now branching into new variants, researchers observe Darwin’s theory of evolution in action every day.

Dr. Kamil stumbled upon some of the new variants while sequencing samples from coronavirus tests in Louisiana. At the end of January he observed an unfamiliar mutation in a series of samples.

The mutation changed the proteins that examine the surface of the coronavirus. Known as spike proteins, they are folded chains of more than 1,200 molecular building blocks called amino acids. Dr. Kamil’s viruses all shared a mutation that changed the 677th amino acid.

When Dr. Kamil examined these mutant viruses, he found that they all belonged to the same lineage. The earliest virus in the line dates back to December 1st. It became more common in later weeks.

On the evening of his discovery, Dr. Kamil uploaded the genomes of the viruses to an online database used by scientists around the world. The next morning he received an email from Daryl Domman of the University of New Mexico. He and his colleagues had just found the same variant in their condition with the same 677 mutation. Your samples are from October.

The scientists wondered if the line they discovered was the only one that had a 677 mutation. Dr. Kamil and colleagues examined the database and found six other lineages that independently received the same mutation.

It is difficult to answer even basic questions about the prevalence of these seven lineages because the United States sequences genomes from less than 1 percent of coronavirus test samples. The researchers found samples from the lineages that were scattered across much of the country. But they cannot tell where the mutations first originated.

Updated

Apr. 14, 2021, 3:56 p.m. ET

“At the moment I would be quite reluctant to give a place of origin for one of these lines,” said Emma Hodcroft, epidemiologist at the University of Bern and co-author of the new study.

It’s also hard to tell if the increase in variants is actually due to their being more contagious. They might have become more frequent simply because of all the travel during the holiday season. Or they exploded during superspreader events in bars or factories.

Still, scientists are concerned because the mutation could plausibly affect how easily the virus gets into human cells.

Infection begins when a coronavirus uses the tip of the spike protein to attach itself to the surface of a human cell. It then releases harpoon-like arms from the base of the spike, pulls toward the cell, and supplies its genes.

Before the virus can make this invasion, however, the spike protein must encounter a human protein on the surface of the cell. After this contact, the spike is free to rotate, exposing its harpoon tips.

The 677 mutation changes the spike protein next to where our proteins cut into the virus, which may make it easier to activate the spike.

Jason McLellan, a structural biologist at the University of Texas at Austin who was not involved in the study, called it “an important advance.” But he warned that the way the coronavirus unleashed its harpoons was still pretty mysterious.

“It’s hard to know what these substitutions do,” he said. “There really needs to be some additional experimental data added.”

Dr. Kamil and his colleagues begin these experiments in the hope that the mutation actually makes a difference to infections. If the experiments confirm their suspicions, the 677 mutation will join a small, dangerous club.

Convergent evolution has transformed several other locations on the spike protein as well. For example, the 501st amino acid is mutated in a number of lineages, including the contagious variants first seen in the UK and South Africa. Experiments have shown that the 501 mutation changes the tip of the tip. This change allows the virus to attach itself more tightly to cells and infect them more effectively.

Scientists believe that coronaviruses will converge on more mutations that will give them an advantage – not just against other viruses, but also against our own immune system. However, Vaughn Cooper, an evolutionary biologist at the University of Pittsburgh and co-author of the new study, said laboratory experiments alone could not reveal the extent of the threat.

To really understand what the mutations are doing, scientists need to analyze a much larger sample of coronaviruses from across the country. Currently, however, they can only look at a relatively small number of genomes collected from a patchwork of government and university laboratories.

“It is ridiculous that our country is not developing a national strategy for surveillance,” said Dr. Cooper.

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Pfizer Says Its Vaccine Works In opposition to Key Mutation in Contagious Variants

Pfizer and BioNTech announced on Friday that their Covid vaccine is effective against one of the mutations in the new contagious variants in the UK and South Africa.

Independent experts said the results were good news, but warned that each of these coronavirus variants have several different potentially dangerous mutations that have not yet been studied. So it’s possible that one of these mutations could affect the effectiveness of the vaccine.

“It’s the first step in the right direction,” said Dr. John Brooks, the chief medical officer of the Covid-19 emergency department at the Centers for Disease Control. “I hope the additional work that comes out in the future matches this insight.”

The new variant, known as B.1.1.7, first gave cause for concern in December when British researchers found it was rapidly becoming more common in people with Covid-19. Since then, it has appeared in 45 countries.

Subsequent research has confirmed that it has the ability to spread more easily from person to person. On Friday, Public Health England published a new study on B.1.1.7 in which researchers estimated that the variant is 30 to 50 percent more transmissible than other forms of the virus.

The viral line that leads to B.1.1.7 has accumulated 23 mutations. Of particular concern to scientists are eight mutations that affect the gene for a protein called spike on the surface of coronaviruses. That’s because the viruses use the spike protein to capture human cells. It is possible that one or more of them will help B.1.1.7 enter cells more successfully.

One of these mutations, known as N501Y, is of particular concern. Experiments have shown that it allows the virus to bind more tightly to cells. And it has appeared in other lines of the coronavirus as well, including a variant identified in South Africa in December. This variant, named B.1.351, quickly spread across the country and has so far expanded to a dozen other countries.

In the new study, which went online Thursday and has not yet undergone a formal scientific review, researchers from the University of Texas Medical Department conducted an experiment to see if the Pfizer BioNTech vaccine was against viruses with the N501Y mutation works. They found that in cells in the laboratory, the mutated virus could not infect human cells mixed with antibodies from vaccinated people. The antibodies clung to the coronaviruses, preventing them from entering cells. Despite the N501Y mutation, the experiment showed that the antibodies produced by the vaccine were still able to bind to the viruses.

“This indicates that the key N501Y mutation found in the emerging variants in the UK and South Africa does not create resistance to the immune responses induced by the Pfizer BioNTech vaccine,” the companies said in a press release .