Scientists in Houston on Wednesday published an examination of more than 5,000 genetic sequences of coronavirus, showing the continued accumulation of mutations in the virus, one of which could possibly have made it more contagious.
This mutation is related to a higher viral load in patients in the initial diagnosis, the researchers found.
The study, which has not been peer-reviewed, was published Wednesday on the MedRxiv prepress server and appears to be the largest aggregation of genetic virus sequences in the United States. , like the Houston study, concluded that a mutation that alters the design of the “advanced protein” on the surface of the virus may be to blame for the disproportionate spread of this strain.
The new report did not conclude that these mutations have made the virus more lethal. All viruses collect genetic mutations and the maximum are negligible, scientists say. Coronaviruses such as SARS-CoV-2, which causes COVID-19 disease, are solid as viruses go away. because they have a rereading mechanism when replicated.
But mutation is a dice game, and with transmission so widespread in the United States, which continues to see tens of thousands of new infections displayed in both one day and both, the virus has had many opportunities to change, potentially with consequences. embarrassing, according to the study, author James Musser of Houston Methodist Hospital.
“We have given this virus many opportunities,” Musser told The Washington Post. “Right now there’s a mass population. “
Scientists from Weill Cornell Medicine, the University of Chicago, Argonne National Laboratory and the University of Texas at Austin contributed to the study.
David Morens, virologist at the National Institute of Allergy and Infectious Diseases (NIAID), reviewed the new study and said the effects imply the likelihood that the virus, as it moves in the population, has become more communicable and that this “may have implications for our ability. “
Morens noted that this is an exclusive article and that “there is no need to overinterpret what it means. “But the virus, he said, could potentially respond, with random mutations, to interventions such as masking and social est esture, Morens said Wednesday. .
“Wearing masks, washing your hands, all these things are barriers to communicability or contagion, as the virus becomes more contagious, it’s statistically better at bypassing those barriers,” said Morens, senior advisor to Anthony Fauci, director of NIAID.
This has implications for the formulation of the vaccine, he said. As others gain immunity, either through infections or a vaccine, the virus would likely selectively become stressed to escape the human immune response.
“Although we don’t already know, it’s quite imaginable that this coronavirus, when our immunity at the population level becomes high enough, this coronavirus will locate a way to circumvent our immunity,” Morens said. “If that were to happen, we’d be on the same stage as with the flu. We’ll have to hunt down the virus and, as it mutates, we’ll have to play with our vaccine. “
At Houston Methodist, whose primary hospital is a component of Texas Medical Center in downtown Houston and including local hospitals, scientists have been sequencing the genome of 30,000 coronavirus characteristics since early March, when the virus appears to have first reached the metropolitan area of 7. millions of people Paper documents 5,085 sequences.
Research shows that the virus has moved to Houston neighborhoods in two waves, first affected the richest and oldest, and then spread, in the wave of the moment, to other young people and low-income neighborhoods, affecting many Latino residents.
At the same time, while the virus spreads the zip code through the zip code, it collects mutations, many of which affect the complex protein. This arrangement on the surface of the virus, which resembles a tree adorned with rolled ribbons, allows the virus to spread. Enter the cells.
Genetic knowledge shows that the virus arrived in Houston several times, probably first by air. It should be noted that 71% of the viruses that came first were characterized by a now scientifically pointed mutation, which seems to come from China, which increasingly scientific The suspect can give the virus a biological credit in the way it spreads. It is called D614G, in reference to the replacement of an amino acid called aspartic acid (D) with an acid called glycine (G) in a genome region that encodes for the complex protein.
In the wave of the Houston epidemic, the study found that the variant had increased to a prevalence of 99. 9%, completing its dominance over the epidemic. Researchers found that other people affected by the strain had a lot of viruses on top. airways, a chance that the strain will spread more effectively.
Kristian Andersen, an immunologist at the Scripps Research Institute in California, who was not concerned about the new research, downplayed the importance of the new study and said this “only confirms what has already been described: G has a higher frequency over time. “As for the many other mutations discovered through the study, “they simply catalog them, but we don’t know if any of them have functional relevance. “
Musser said the D614G was dominant in Houston and other spaces because it was better suited to human spread. He said the clinical record was not closed on this subject.
“This is not a murder trial, ” said Musser. ” We are no more than a moderate doubt. This is a civil trial and, of course, it is the preponderance of the evidence that I believe compels us all to the same conclusion that there is something biologically different in this strain. Organize this circle of strain relatives. “
Recently, an even broader study of the spread of coronavirus in the UK, in some 25,000 genomes, has also revealed that this variant of the virus outperforms its competition “in a manner consistent with a selective advantage”.
In general, scientists expect the herb variety to announce mutations that help the virus spread better, because it allows it to make more copies of itself, but not necessarily those that make it more virulent. Killing or neutralizing the host wouldn’t help the virus. the virus spreads to more people.
The test revealed 285 different mutation sites that fit a detail of the physical basis of the complex protein, which is the maximum vital component of coronavirus in the sense that it is what allows it to infect and harm humans. had not been observed in the past in other genomes sequenced around the world.
The study describes some of the mutations in the complex protein as “disconcerting”. Although the article does not provide false evidence of an additional evolution of the complex protein, it suggests that these repeated substitutions provide a clue that, when the virus interacts with our framework and immune system, it may be informed of new tricks that respond to your host.
“I think there’s a lot of evidence that’s consistent with the immune variety that works in certain regions of the complex protein,” Musser said.
Actual mutations of the virus occur randomly because it makes mistakes in trying to copy its genome into our cells, but each new case provides more mutations, increasing the chances that one of those mutations will be useful to the virus, just as D614G has already been.
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Just like seasonal flu mutations?
That was my idea when I read this. So do you get the most productive flu vaccine and existing COVID strain every year?