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American scientists have published a study of more than 5,000 genetic sequences of the coronavirus, which reveals the continued accumulation of mutations of the virus, one of which may have made it more contagious.
That mutation is associated with a higher viral load among patients at the time of initial diagnosis, the researchers in Houston found.
The study, which has not been peer-reviewed, was published on Thursday (NZT) on the MedRxiv prepress server. It appears to be the largest single aggregation of virus genetic sequences in the United States.
Scientists in the UK published a larger batch of sequences this month and, like the Houston study, concluded that a mutation that changes the structure of the “spike protein” on the surface of the virus may be driving the massive spread of that virus. Pressure.
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The new report did not find that these mutations made the virus more lethal. All viruses accumulate genetic mutations and most are negligible, scientists say. Coronaviruses like SARS-CoV-2, which causes Covid-19 disease, are relatively stable as viruses progress, because they have a proofreading mechanism as they replicate.
But each 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 confirmed infections daily, the virus has had abundant opportunities to change, potentially with problematic consequences, the study said. author James Musser of Houston Methodist Hospital.
“We have given this virus a lot of opportunities,” Musser said. The Washington Post. “There is a huge population right now.”
Scientists from Weill Cornell Medicine, the University of Chicago, 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 findings point to the likelihood that the virus, as it has moved through the population, has become more transmittable, and that this “may have implications for our ability to control it.”
Morens noted that this is a unique article and that “it is not advisable to over-interpret what this means.” But the virus, he said, could potentially be responding, through random mutations, to interventions like wearing masks and social distancing, Morens said.
“Wearing masks, washing our hands, all of those things are barriers to transmissibility or contagion, but as the virus becomes more contagious, it is statistically better to get around those barriers,” said Morens, senior advisor to Anthony Fauci, director of the NIAID.
This has implications for vaccine formulation, he said. As people acquire immunity, either through infections or a vaccine, the virus could be under selective pressure to evade the human immune response.
“Although we don’t know yet, it is quite 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 the flu. We will have to chase the virus and as it mutates, we will have to play with our vaccine.”
At Houston Methodist, whose main hospital is part of the Texas Medical Center in downtown Houston and which includes hospitals in the area, scientists have been sequencing the 30,000-character genome of the coronavirus since early March, when the virus appears to have arrived by first time. the metropolitan area of 7 million inhabitants. The document documents 5,085 sequences.
Research shows that the virus moved into Houston neighborhoods in two waves, first affecting wealthier and older people, but then spreading, in the second wave, to younger people and low-income neighborhoods, affecting many Latino residents.
At the same time, as the virus spread zip code to zip code, it collected mutations, many of which affected the spike protein. That structure on the surface of the virus, which resembles a tree adorned with curly ribbons, allows the virus to enter cells.
Genetic data shows that the virus reached Houston many times, presumably initially by air. Notably, 71 percent of the viruses that initially arrived were characterized by a now scientifically famous mutation, which appears to have originated in China, which scientists increasingly suspect may give the virus a biological advantage in the way it is spread. spread.
It’s called D614G, referring to the replacement of an amino acid called aspartic acid (D) with one called glycine (G) in a region of the genome that encodes the spike protein.
For the second wave of the outbreak in Houston, the study found that this variant had risen to 99.9 percent prevalence, completing its dominance of the outbreak. The researchers found that people infected with the strain had higher virus loads in their upper respiratory tracts, a potential factor in causing the strain to spread more effectively.
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 increased in frequency over time.” As for the numerous other mutations the study finds, “they just catalog them, but we don’t know if any of them have any functional relevance.”
Musser said that D614G has been increasingly dominant in Houston and other areas because it is better adapted to spread between humans. He acknowledged that the scientific case is not closed on this matter.
“This is not a murder trial,” Musser said. “We are not looking beyond a reasonable doubt. This is a civil judgment, and clearly, it is the preponderance of the evidence that I think forces us all to the same conclusion, which is that there is something biologically different about that strain, what a family of strains “.
Recently, the even larger study of the spread of the coronavirus in the UK, based on some 25,000 genomes, also found evidence that this variant of the virus outperforms its competitors “in a consistent way with a selective advantage”.
In general, scientists would expect natural selection to favor mutations that help the virus spread more effectively, as that allows it to make more copies of itself, but not necessarily the ones that make it more virulent. Killing or incapacitating the host would generally not help the virus spread to more people.
The study found 285 separate mutation sites that actually change a physical building block of the spike protein, which is the most important part of the coronavirus in the sense that it is what allows it to infect and harm humans. Forty-nine of the changes at these sites had not been seen before in other sequenced genomes around the world.
The study characterizes some of the spike protein mutations as “puzzling.” While the article does not present strong evidence that further evolution of the spike protein is occurring, it does suggest that these repeated substitutions hint that as the virus interacts with our bodies and immune systems, it may be learning new tricks that help your host respond.
“I think there is pretty good evidence that it is consistent with immunological selection acting on certain regions of the spike protein,” Musser said.
Actual mutations in the virus happen randomly, as it makes mistakes when trying to copy its genome inside our cells. But each new case gives the possibility of more mutations occurring, increasing the possibility that one of these mutations is useful for the virus, as D614G apparently already has been.
