Scientists in Houston on Wednesday published a study of more than 5,000 genetic sequences of the coronavirus, accumulating a constant mutation of the virus, one of which made it more contagious.
Mutations in patients after initial diagnosis are associated with increased viral load, the researchers found.
The study, which has not been peer-reviewed, was posted on the printprint server MedRaxive on Wednesday. It is the largest integration of the genetic sequence of viruses in the United States. A large batch of indexes was published this month by scientists in the United Kingdom, and a study in Houston concluded that a change in the structure of the “spike protein” on the surface of the virus could cause outsiders to spread. That stress.
The new report does not find that the mutation has made the virus worse. All viruses accumulate genetic mutations, and most are insignificant, scientists say. SARS-COVID-2, which causes the disease COVID-19, is relatively stable with the virus, as they have a proofreading mechanism because they mimic.
But every mutation has a role to play, and with such widespread transmission in the United States – which sees thousands of new, confirmed infections every day – the virus has found plenty of opportunities for mutation, with potentially troubling consequences, the study says. James Muzer, author of Houston Methodist Hospital.
“We’ve given the virus many opportunities,” Musser told the Washington Post. “There’s a huge population size right now.”
Scientists from Will 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 findings show that the virus, which has advanced in the population, has become more transmissible and likely. “It could affect our ability to control it.”
Morens notes that this is the same paper, and that “you don’t want to explain further what this means.” But the virus, he said, could potentially respond to interventions – such as wearing masks and social distance – through random change.
“Wearing a mask, washing our hands, are all barriers to transmissibility or infectious infections, but the virus becomes more contagious so it’s better to overcome those barriers,” said Morens, a senior adviser to director Anthony Fauci. NIAID.
This has implications for making the vaccine, he said. As people gain immunity, whether through infection or vaccination, the virus may be under selective pressure to avoid the human immune response.
“Although we do not yet know, it is possible that this coronavirus, when our population-level immunity is high enough, will be able to find a way to get around our immunity.” “If that happened then we would all be in the same situation as the flu. We have to chase the virus, and it turns out, we have to tincture our vaccine. “
At the Houston Methodist, whose main hospital is part of the Texas Medical Center in central Houston and includes hospitals in the area, scientists are searching for a 30,000-character genome of the coronavirus as early as March, when the virus first appeared. Metropolitan area of 7 million people. Paper documents 5,085 sequences.
Research shows that the virus stabilized in two waves from the Houston neighborhood, first attacking wealthy and elderly people, but then in a second wave, spreading to younger people and low-income neighborhoods – affecting many Latinos.
At the same time, as the virus spreads the zip code through the zip code, it coordinates the mutation, affecting many spike proteins. The formation on the surface of the virus, which looks like a tree equipped with curved ribbons, enables the virus to enter the cells.
Genetic data show that the virus arrived in Houston several times, probably by first air travel. Notably, the 1% of viruses that initially arrived were now classified by a scientifically popular mutation that appears to have originated in China, with scientists increasingly skeptical that the virus could have a biological benefit in how it spreads. Called D614G, it refers to a substitute for an amino acid called glycine (G) in the field of the genome that encodes spike proteins.
Through a second wave of outbreaks in Houston, the study found that this variation reached 99.9% broader levels, completing its fury. Researchers have found that people infected with stress have higher levels of the virus in their upper respiratory tract, a potential factor in the spread of stress more effectively.
Christian Anderson, an immunologist at the Scripps Research Institute in California, who was not involved with the new research, denied the importance of the new study. “It just confirms what has already been described – the G frequency increased over time,” he said. As for the numerous changes found by the study, “they just list them, but we don’t know if any of them have any functional relevance.”
Musser said the D614G is increasingly influential in Houston and other areas because it is more suited to spread in humans. He acknowledged that the scientific case was not closed.
“This is not a murder trial,” Musser said. “We are not looking beyond reasonable doubt. This is a civil trial, and clearly, the progress of the evidence that I think pushes us all to a comparison that is biologically something different about that stressful, that stressful family. “
More recently, a large coronavirus study in the United Kingdom based on approximately 25,000 genomes has also found evidence that this type of virus “outperforms its competitors in a way that is consistent with the benefits of choice.”
In general, scientists expect natural selection to favor mutations that help the virus spread more effectively – as it allows more copies to be made on its own – but it doesn’t necessarily make it more viral. Killing or disabling the host will usually not help spread the virus to more people.
The study found 285 different mutation sites that actually alter the physical building blocks of the spike protein, which is the most important part of the coronavirus in the sense that it is the one that infects and harms humans. Forty-nine mutations at these sites have not been found in other sequenced genomes around the world.
This study describes some of the spike’s protein mutations as “disinfecting”. While there is no strong evidence that any additional evolution of the spike protein is taking place in the paper, it suggests that this repeated substitute gives an indication, as the virus interacts with our body and our immune system, that will help learn new tricks that help . He responds to his host.
“I think there is a lot of good evidence that is consistent with immunologic selection acting on specific regions of spike proteins.”
The actual mutation in a virus occurs randomly because it makes the mistake of mimicking its genome within our cells. But each new case offers the chance for more mutations to occur, making it possible that one of these mutations will be useful for the virus, as D614G has clearly already done.
The report is co-authored by Sarah Kaplan and Aaron Stackelberg of the Washington Post.
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