While Americans anxiously look at variants that were first identified in the United Kingdom and South Africa in the United States, scientists are finding a number of new variants that have emerged here. What’s more, it seems that many of these variants develop in the same direction and can potentially become contagious threats of their own.
In a study published Sunday, a team of researchers reported seven growing sex lines of the new coronavirus, which was observed in countries across the country. All developed a mutation in the same genetic letter.
“There’s clearly something going on with this mutation,” said Jeremy Kamil, a virologist at the Louisiana State University Health Sciences Center Shreveport. and a co-author of the new study.
It is unclear whether this makes the variants contagious. But because the mutation occurs in a gene that affects how the virus enters human cells, scientists are very suspicious.
“I think there is a clear signature of an evolutionary advantage,” said Dr. Kamil said.
The history of life is full of examples of so-called convergent evolution, in which different generations follow the same path. Birds got wings as they evolved from feathered dinosaurs, for example, just as bats when they evolved from hairy, shaved mammals. In both cases, natural selection gave rise to some flat surfaces that could be slapped to generate lifts, enabling bats and birds to take in the air and fill an ecological niche that other animals could not.
Charles Darwin first recognized convergent evolution by studying living animals. In recent years, virologists have found that viruses can also develop convergently. HIV, for example, originated when various types of viruses spread from monkeys and apes to humans. Many of the generations of HIV got the same mutations that they adapted to our species.
As the coronavirus now branches out into new variants, researchers are taking Darwin’s theory of evolution into action on a daily basis.
Dr. Kamil came across some of the new variants while sequencing samples of coronavirus tests in Louisiana. In late January, he observed an unknown mutation in a number of samples.
The mutation altered the proteins that study the surface of the coronavirus. These are known as vein proteins and are folded chains of more than 1,200 molecular building blocks called amino acids. Dr. Kamil’s viruses all shared a mutation that altered the 677th amino acid.
Dr. Kamil researched these mutant viruses and realized that they all belong to the same sex. The earliest virus in the lineage dates from December 1st. Later it became more common.
On the eve of his discovery, dr. Kamil uploads the genomes of the viruses to an online database used by scientists around the world. The next morning he receives 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 date from October.
The scientists wondered if the lineage they discovered was the only one that had a 677 mutation. Searching the database, dr. Kamil and his colleagues found six other lineages that independently acquired the same mutation on their own.
It is difficult to answer even basic questions about the prevalence of these seven descendants because the United States follows genomes of less than 1 percent of the coronavirus test samples. The researchers found samples of the sex lines that were spread over a large part of the country. But they can not know where the mutations first originated.
“I would currently hesitate to provide a place of origin for any of these generations,” 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 due to the fact that they are more contagious. It may have become more common due to all the travel during the holiday season. Or they may have exploded during superspreader events at pubs or factories.
However, scientists are concerned because the mutation is likely to affect how easily the virus can end up in human cells.
An infection begins when a coronavirus uses the tip of the vein protein to attach to the surface of a human cell. It then releases harpoon-like arms from the base of the pick, pulls itself to the cell and delivers its genes.
Before the virus can carry out this invasion, however, the ear protein must bump into the surface of the cell in a human protein. After contact, the vein can rotate freely and expose its tip of the harpoon.
The 677 mutation changes the vein protein along the place where our proteins call the virus, allowing the acre to be more easily activated.
Jason McLellan, a structural biologist at the University of Texas at Austin who was not involved in the study, calls it an “important advance.” But he warned that the way the coronavirus releases its harpoons is still pretty mysterious.
“It’s hard to know what these substitutes are doing,” he said. “It really needs to be followed up with some extra experimental data.”
Dr. Kamil and his colleagues begin the experiments in the hope of seeing if the mutation does make a difference to infections. If the experiments express their suspicion, the 677 mutation will join a small, dangerous club.
Convergent evolution has also transformed some other spots on the vein protein. The 501st amino acid, for example, has mutated in a number of lineages, including the infectious variants first observed in the United Kingdom and South Africa. Experiments have shown that the 501 mutation changes point by point. That change causes the virus to cling more tightly to cells and infect them more effectively.
Scientists expect coronaviruses to contract into more mutations that give them an advantage – against not only other viruses, but also 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 the mutations do, scientists will have to analyze a much larger sample of coronaviruses collected across the country. But at the moment, they can only look at a relatively meager number of genomes collected by a patchwork of state and university laboratories.
“It is ridiculous that our country does not devise a national strategy to supervise,” said Dr. Cooper said.