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© Pete Kiehart for The New York Times
Scientists at Duke University sequenced positive coronavirus tests to identify strains circulating in the community on February 3.
As Americans anxiously watch the variants first identified in the UK and South Africa spread to the US, scientists are discovering a number of new variants that originated here. More worryingly, many of these variants appear to be moving in the same direction – potentially becoming contagious threats.
In a study published Sunday, a team of researchers reported seven growing lineages of the novel coronavirus, spotted in states across the country. All of them developed a mutation in the same genetic letter.
“There’s clearly something going on with this mutation,” said Jeremy Kamil, virologist at Louisiana State University Health Sciences Center Shreveport and co-author of the new study.
It is not known if this makes the variants more contagious. But since the mutation appears in a gene that influences how the virus enters human cells, scientists are very wary.
“I think there is a clear signature of an evolutionary advantage,” Dr. Kamil said.
The history of life is full of examples of so-called convergent evolution, in which different lineages follow the same path. Birds have gained wings by evolving from feathered dinosaurs, for example, just as bats have evolved from furry mammals resembling shrews. In either case, natural selection gave birth to a pair of flat surfaces that could be pounded to generate lift – allowing bats and birds to take flight and fill an ecological niche than other animals. could not.
Charles Darwin first recognized convergent evolution by studying living animals. In recent years, virologists have discovered that viruses can also evolve convergently. HIV, for example, arose when several species of the virus passed from monkeys and monkeys to humans. Many of these HIV lines acquired the same mutations when they adapted to our species.
As the coronavirus now splits into new variants, researchers are watching Darwin’s theory of evolution in action, day in and day out.
Dr Kamil came across some of the newer variants while sequencing coronavirus test samples in Louisiana. At the end of January, he observed an unknown mutation in a number of samples.
The mutation altered the proteins that line 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.
While investigating these mutant viruses, Dr. Kamil realized that they all belonged to the same lineage. The first virus in the lineage dates back to December 1. In the following weeks it became more common.
On the evening of his discovery, Dr Kamil uploaded 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 condition, with the same 677 mutation. Their samples dated back to October.
Scientists wondered if the line they had discovered was the only one that had a 677 mutation. Searching the database, Dr. Kamil and his colleagues found six other lines that independently gained the same mutation from them- same.
Even basic questions about the prevalence of these seven lineages are difficult to answer, as the United States is sequencing the genomes of less than 1% of coronavirus test samples. The researchers found bloodline samples scattered across much of the country. But they can’t say where the mutations first appeared.
“I would be very hesitant to give an original location for any of these lines at this time,” 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 in fact the result of their greater contagion. They might have become more common simply because of all the travel during the holiday season. Or they may have exploded during super-spreader events in bars or factories.
Still, scientists are worried that the mutation could presumably 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. It then releases harpoon-shaped arms from the base of the tip, pulling itself towards the cell and delivering its genes.
However, before the virus can make this invasion, the spike protein must strike a human protein on the surface of the cell. After this contact, the point becomes free to twist, exposing its harpoon points.
The 677 mutation changes the spike protein next to where our proteins attack the virus, eventually making 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 “a significant breakthrough.” But he warned that how the coronavirus unleashed his harpoons was still quite a mystery.
“It’s hard to know what these substitutions are doing,” he said. “It really needs to be followed by some more experimental data.”
Dr Kamil and his colleagues begin these experiments, hoping to see if the mutation actually makes a difference in infections. If the experiments confirm their suspicions, the 677 mutation will join a dangerous little club.
The convergent evolution has also transformed a few other points on the spike protein. The 501st amino acid has mutated in a number of lineages, for example, including contagious variants first seen in the UK and South Africa. Experiments have revealed that the 501 mutation alters the very tip of the peak. This change allows the virus to attach more tightly to cells and infect them more efficiently.
Scientists predict that coronaviruses will converge on more mutations that will give them an advantage – not only against other viruses, but also against our own immune system. But Vaughn Cooper, an evolutionary biologist at the University of Pittsburgh and co-author of the new study, said laboratory experiments alone would not be able to reveal the extent of the threat.
To really understand what mutations do, he said, scientists will need to analyze a much larger sample of coronaviruses gathered across the country. But for now, they can only examine a relatively small number of genomes collected by a patchwork of state and university labs.
“It is ludicrous that our country does not come up with a national surveillance strategy,” said Dr Cooper.
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