Massive genetic study shows coronavirus mutates and potentially evolves amid rapid spread in United States


Scientists in Houston on Wednesday published a study of more than 5,000 genetic sequences of the coronavirus, which reveals the continued build-up of mutations in the virus, one of which may have made it more contagious.

This mutation is associated with a higher viral load in patients upon initial diagnosis, the researchers found.

The study, which has not been peer reviewed, was published Wednesday on the MedRxiv preprint server. It appears to be the largest single aggregation of genetic sequences for the virus in the United States. A larger batch of footage was released this month by scientists in the UK and, like the Houston study, concluded that a mutation that alters the structure of the ‘spike protein’ on the surface of the body. virus can be at the origin of the disproportionate spread of this tension.

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The new report did not find that these mutations made the virus any more deadly. All viruses accumulate genetic mutations, and most are insignificant, scientists say. Coronaviruses such as SARS-CoV-2, which causes covid-19 disease, are relatively stable as viruses disappear because they have a replay mechanism when they replicate.

But every mutation is a roll of the dice, and with transmission so widespread in the United States – which continues to see tens of thousands of new infections confirmed every day – the virus has had many opportunities to change, potentially with uncomfortable consequences. , said study author James Musser of the Methodist Hospital in Houston.

“We gave this virus a lot of chances,” Musser told the Washington Post. “There is a huge population there right now. “

Scientists from Weill Cornell Medicine, the University of Chicago, the Argonne National Laboratory and the University of Texas at Austin also contributed to the study.

David Morens, a virologist at the National Institute of Allergy and Infectious Diseases (NIAID), reviewed the new study and said the results indicate the likelihood that the virus, as it spreads in the population , has become more transmissible, and that this “may have implications for our ability to control it.” “

Morens noted that this is a single document and that “you don’t want to overinterpret what that means”. But the virus, he said, could potentially respond – through random mutations – to interventions such as mask wearing and social distancing, Morens said Wednesday.

“Wearing masks, washing your hands, all of these things are barriers to transmissibility or contagion, but as the virus becomes more contagious it is statistically better to bypass these barriers,” said Morens, senior adviser Anthony Fauci, Director of NIAID.

This has implications for vaccine formulation, he said. As people gain immunity, whether through infections or a vaccine, the virus could be put under selective pressure to evade the human immune response.

“While we don’t know it yet, it’s entirely possible that this coronavirus, when our population-level immunity is high enough, this coronavirus will find a way around our immunity,” Morens said. “If that happened, we would be in the same situation as with the flu. We will have to chase the virus away, and as it mutates, we will have to tinker with our vaccine. “

At Houston Methodist, whose main hospital is part of the Texas Medical Center in central Houston and which includes area hospitals, scientists have been sequencing the genome of 30,000 characters of the coronavirus since early March, when the virus appeared to be arrived for the first time in the metropolitan area of ​​7 million inhabitants. The article documents 5,085 sequences.

Research shows that the virus moved through Houston neighborhoods in two waves, hitting the wealthiest and oldest people first, but then spreading, in wave two, to younger and older people. to low-income neighborhoods – affecting many Latino residents.

At the same time, as the virus spread zip code by zip code, it was compiling mutations, many of which affected the spike protein. This structure on the surface of the virus, which resembles a tree adorned with coiled ribbons, allows the virus to enter cells.

Genetic data shows that the virus has arrived in Houston on several occasions, probably first by air. Notably, 71% of the viruses that initially arrived were characterized by a now-famous mutation, which appears to originate from China, which scientists increasingly suspect gives the virus a biological advantage in the way it spreads. It’s called D614G, in reference to the substitution of an amino acid called aspartic acid (D) for another called glycine (G) in a region of the genome that codes for the spike protein.

During the second wave of the epidemic in Houston, the study found that this variant jumped to 99.9% prevalence – completing its dominance of the epidemic. The researchers found that people infected with the strain had higher viral loads in their upper respiratory tract, a potential factor in making the strain more efficient.

Kristian Andersen, an immunologist at the Scripps Research Institute in California, who was not involved in the new research, downplayed the importance of the new study. He said it “just confirms what has already been described – G has increased in frequency over time.” As for the many other mutations discovered by the study, “they just catalog them, but we don’t know if any of them have functional relevance.”

Musser said D614G is increasingly dominant in Houston and other areas because it is better suited for spread among humans. He acknowledged that the scientific file is not closed on this issue.

“This is not a murder trial,” Musser said. “We are not looking beyond a reasonable doubt. This is a civil lawsuit and obviously it’s the preponderance of evidence that I think forces us all to the same conclusion that there is something biologically different about this strain, this family of strains.

Recently, the even larger study into the spread of the coronavirus in the UK, based on around 25,000 genomes, also found evidence that this variant of the virus distances its competition “in a manner consistent with selective advantage”.

In general, scientists would expect natural selection to favor mutations that help the virus spread more efficiently – as this allows it to make more copies of itself – but not necessarily those that make it. more virulent. Killing or neutralizing the host would generally not help the virus spread to more people.

The study found 285 distinct mutation sites that actually alter a physical building block of the spike protein, which is the most important part of the coronavirus in that it is what allows it to infect and harm humans. Forty-nine of the changes at these sites had not previously been observed in other genomes sequenced around the world.

The study calls some of the spike protein mutations “puzzling.” While the article does not present strong evidence that further evolution of the spike protein occurs, it suggests that these repeated substitutions give a clue that when the virus interacts with our body and immune system, it may learn. new tricks that help he responds to his host.

“I think there is very good evidence that is consistent with immunological selection acting on certain regions of the spike protein,” Musser said.

The virus’s real mutations happen randomly because it makes mistakes while trying to copy its genome into our cells. But each new case gives a chance for more mutations to occur, which increases the chances that one of those mutations will be useful to the virus, just as D614G apparently already has.

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Sarah Kaplan and Aaron Steckelberg of the Washington Post contributed to this report.


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