7 virus variants found in the U.S. with the same mutation

As Americans anxiously look at the variants first identified in the UK and the spread of South Africa in the United States, scientists are discovering a number of new variants that originated here. Most worryingly, many of these variants appear to be evolving in the same direction – potentially becoming contagious threats of their own.

In a study published on Sunday, a team of researchers reported seven growing strains of the new coronavirus, detected in states across the country. They all developed a mutation in the same genetic letter.

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

It is not clear whether this makes variants more contagious. But because the mutation appears in a gene that influences how the virus enters human cells, scientists are very suspicious.

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

The history of life is full of examples of the so-called convergent evolution, in which different lineages follow the same path. Birds gained wings as they evolved from feathered dinosaurs, for example, just as bats did when they evolved from hairy shrewlike mammals. In both cases, natural selection gave rise to a pair of flat surfaces that could be tapped for support – allowing bats and birds to fly into the sky and fill an ecological niche that other animals could not.

Charles Darwin recognized convergent evolution for the first time when studying living animals. In recent years, virologists have discovered that viruses can also evolve in a convergent way. HIV, for example, came about when several species of viruses went from monkeys and apes to humans. Many of these strains of HIV gained the same mutations as they adapted to our species.

As the coronavirus now branches into new variants, researchers are watching Darwin’s theory of evolution in action, day after day.

Dr. Kamil discovered some of the new variants while he was sequencing samples from coronavirus tests in Louisiana. In late January, he observed an unknown mutation in several samples.

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

Investigating these mutant viruses, Dr. Kamil realized that they all belonged to the same lineage. The oldest virus in the strain dated December 1. In the weeks that followed, it became more common.

On the night of his discovery, Dr. Kamil uploaded the virus genomes 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 state, with the same 677 mutation. Their samples dated back to October.

The scientists wondered if the strain they discovered was the only one to have a 677 mutation. Searching the database, Dr. Kamil and his colleagues found six other strains that independently gained the same mutation on their own.

It is difficult to answer even basic questions about the prevalence of these seven strains because the United States sequences genomes from less than 1% of the coronavirus test samples. The researchers found samples of the strains spread across much of the country. But they can’t say where the mutations first came from.

“I would hesitate to provide a home site for any of these strains at the moment,” said Emma Hodcroft, an epidemiologist at the University of Bern and co-author of the new study.

It is also difficult to say whether the increase in variants is really the result of being more contagious. They may have become more common simply because of all the travel during the holiday season. Or they may have exploded during over-spreading events in bars or factories.

Still, scientists are concerned that the mutation could plausibly affect how easily the virus enters human cells.

An infection begins when a coronavirus uses the tip of the spike protein to attach itself to the surface of a human cell. Then he releases harpoon-like arms from the base of the stake, pulling himself into the cell and handing over his genes.

Before the virus can carry out this invasion, however, the spike protein has to clash with a human protein on the cell’s surface. After this contact, the tip is free to twist, exposing its harpoon tips.

The 677 mutation changes the peak protein close to where our proteins steal the virus, making it easier for the peak to be activated.

Jason McLellan, a structural biologist at the University of Texas at Austin who was not involved in the study, called it “a major breakthrough”. But he warned that the way the coronavirus released its harpoons was still quite mysterious.

“It is difficult to know what these substitutions are doing,” he said. “It really needs to be followed up with some additional experimental data.”

Dr. Kamil and his colleagues are starting these experiments, hoping to see if the mutation really makes a difference in infections. If the experiments confirm his suspicions, mutation 677 will join a small and dangerous club.

Convergent evolution has also turned some other points into the peak protein. The 501st amino acid has mutated in several strains, for example, including the contagious variants seen for the first time in the United Kingdom and South Africa. Experiments revealed that the 501 mutation alters the tip of the ear. This change allows the virus to stick to cells more strongly and infect them more effectively.

Scientists predict that coronaviruses will converge to more mutations that give them an advantage – not just against other viruses, but also against our own immune systems. But Vaughn Cooper, an evolutionary biologist at the University of Pittsburgh and a co-author of the new study, said the laboratory experiments alone would not be able to reveal the extent of the threat.

To really understand what the mutations are doing, he said, scientists will need to look at a much larger sample of coronaviruses collected across the country. But now, they can look only at a relatively small number of genomes collected by a patchwork of state and university labs.

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

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