As Americans anxiously watch changes first marked in the United Kingdom and South Africa spread in the United States, scientists are discovering several new changes that have come here. More worryingly, many of these variables appear to be evolving in the same direction – becoming the infectious risks themselves. In a study posted Sunday, a team of researchers described seven growing strains of the novel coronavirus, which has been seen in states across the country. All of them have developed mutations in the same genetic letter.
“There’s clearly something going on with this trend,” said Jeremy Kamil, a pathologist at Louisiana Shreveport State University’s Center for Health Sciences and co-author of the new study. It is unclear whether it makes the changes more contagious. But because there is a mutation in a gene that affects how the virus enters human cells, the scientists are very skeptical. “I think there is a clear name for the benefit of evolution,” Kamil said.
A biography is full of examples of so-called homogenous evolution, in which different lines follow the same path. Birds got wings as they grew from feathered dinosaurs, for example, just like bats did when they came out of hairy mammals, like a screw. In each case, natural selection caused a pair of flat surfaces that could be shaken to generate a lift – allowing bats and birds alike to move into the sky and fill an ecological space that is not. other animals could.
Charles Darwin identified homogenous evolution by studying living animals. In the last few years, virologists have discovered that viruses can also emerge. HIV, for example, arose when several species of viruses passed from monkeys and apes to humans. Many of these strains of HIV received the same mutations as they did for our sex.
As the coronavirus now enters new variants, researchers are monitoring Darwin’s theory of evolution in action, both inward and outward.
Kamil skipped over some of the new variants while following samples from coronavirus tests in Louisiana. At the end of January, he saw an unusual change in several samples.
The mutation altered the proteins that clog the surface of the coronavirus. Called spike proteins, they are complex chains of more than 1,200 molecular building blocks called amino acids. Kamil’s viruses all shared a mutation that altered the 677th amino acid.
Examining these mutant viruses, Kamil realized that they all belonged to the same line. The earliest virus in the line was dated to December 1st. In recent weeks, it has become more common.
On the afternoon of his discovery, 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 discovered the same variant in their state, with the same 677 mutation. Their samples went to October.
The scientists were wondering if the line they found was the only one that had a 677 mutation. Examining the database, Kamil and his colleagues found six other lines that had the same mutation on their own.
It is difficult to answer even fundamental questions about the frequency of these seven sequences because the United States follows genomes from less than 1% of coronavirus test samples. The researchers found samples from the lines scattered across much of the country. But they can’t tell where the changes first happened.
“I would be very reluctant to give a place of origin for any of these lines right now,” 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 variables is due to being more contagious. They may have become more common just because of how much they travel over the holiday season. Or they may have exploded at superspreader events at bars or factories.
However, scientists are concerned because the simulation could affect the easy entry of the virus into human cells.
Infection begins when a coronavirus uses the crop of the spike protein to penetrate the surface of a human cell. He then extends harp-like arms from the base of the spike, pulling himself to the cell and delivering his genes.
Before the virus can carry out this attack, however, the spike protein must invade human proteins on the surface of the cell. After that communication, the free spike twists, revealing its harp suggestions.
Mutation 677 changes the spike protein next to where our proteins are spying on the virus, 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, said it was “an important step forward. But he warned that the way the coronavirus spread his harp was still a mystery.
“It’s difficult to find out what these agents are doing,” he said. “Some more experimental data needs to be followed up. ”
Kamil and his colleagues are embarking on these experiments, hoping to see if the mutation is actually making a difference to diseases. If the tests hold out their suspicions, a 677 mutation will turn into a dangerous little club.
Congenital evolution has altered a few other spots on the spike protein as well. The 501st amino acid has been circulated in several series, for example, incorporating the infectious variables first observed in the United Kingdom and South Africa. Tests have shown that the 501 mutation changes the very top of the spike. That change allows the virus to enter more dense cells and capture them more efficiently.
Scientists expect coronaviruses to come together in more mutations that will benefit them – 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 tests alone would not be able to reveal the magnitude of the risk.
To better understand what mutations are, he said, scientists need to study a much larger sampling of coronaviruses collected from across the country. But for now, they can only look at a very small number of genomes collected by a trout operation of a state and university laboratory.
“It’s strange that our country is not coming up with a national strategy for monitoring,” Cooper said.
Carl Zimmer. c.2021 New York Times Company