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Coronavirus is mutating-Washington Post




Medical staff at the University of South Florida Health University conducted a coronavirus test at a community center in Tampa on June 25. (Octavio Jones/Getty Images)

When for the first time Coronavirus cases in Chicago appeared in January, and they have the same genetic characteristics as the bacteria that appeared in China a few weeks ago.

However, after Egon Ozer, an infectious disease specialist at Northwestern University’s Feinberg School of Medicine, examined the genetic structure of virus samples from local patients, he discovered some differences.

The changes of the virus appear again and again. This mutation was related to the outbreaks in Europe and New York, which eventually occupied the city. By May, 95% of all genomes sequenced by Ozer were found.

At first glance, this mutation seems insignificant. About 1300 amino acids can be used as the basis of viral surface proteins. In the mutant virus, the genetic instruction for only one amino acid (number 614) was changed from “D” (short for aspartic acid) to “G” (short for glycine) in the new variant.

But location is important because this transition occurs in the genome that encodes the most important “protrusion protein”. The protruding structure gives the corona virus a coronal outline and allows it to enter human cells in an anti-theft manner. A lock.

And its universality is undeniable. Global researchers have uploaded it to the genomes of about 50,000 new viruses in shared databases, and about 70% carry the mutation, officially named D614G, but scientists more familiarly call it “G”.

In

Dominant coronavirus mutation

Like all coronaviruses, there are a series of characteristic spikes around the core of SARS-CoV-2. These peaks allow the virus to attach to human cells.

The mutation affecting the viral spike protein changes amino acid 614 from “D” (aspartic acid) to “G” (glycine). Studies have shown that this small change (affecting three identical amino acid chains) may make spike protein more effective, thereby enhancing the infectivity of the virus.

Source: GISAID, later report

Aaron Stickberg/Washington Post

In

Dominant coronavirus mutation

Like all coronaviruses, there are a series of characteristic spikes around the core of SARS-CoV-2. These peaks allow the virus to attach to human cells.

The mutation affecting the viral spike protein changes amino acid 614 from “D” (aspartic acid) to “G” (glycine). Studies have shown that this small change (affecting three identical amino acid chains) may make spike protein more effective, thereby enhancing the infectivity of the virus.

Source: GISAID, later report

Aaron Stickberg/Washington Post

In

Dominant coronavirus mutation

Like all coronaviruses, there are a series of characteristic spikes around the core of SARS-CoV-2. These peaks allow the virus to attach to human cells.

The mutation affecting the viral spike protein changes amino acid 614 from “D” (aspartic acid) to “G” (glycine). Studies have shown that this small change (affecting three identical amino acid chains) may make spike protein more effective, thereby enhancing the infectivity of the virus.

Source: GISAID, later report

Aaron Stickberg/Washington Post

In

Dominant coronavirus mutation

Like all coronaviruses, there are a series of characteristic spikes around the core of SARS-CoV-2. These peaks allow the virus to attach to human cells.

The mutation affecting the viral spike protein changes amino acid 614 from “D” (aspartic acid) to “G” (glycine). Studies have shown that this small change (affecting three identical amino acid chains) may make spike protein more effective, thereby enhancing the infectivity of the virus.

Source: GISAID, later report

Aaron Stickberg/Washington Post

In

Dominant coronavirus mutation

Like all coronaviruses, there are a series of characteristic spikes around the core of SARS-CoV-2. These peaks allow the virus to attach to human cells.

The mutation affecting the viral spike protein changes amino acid 614 from “D” (aspartic acid) to “G” (glycine). Studies have shown that this small change affects three identical amino acid chains and may make spike proteins more effective, thereby enhancing the infectivity of the virus.

Source: GISAID, later report

Aaron Stickberg/Washington Post

“G” not only dominated the epidemic in Chicago, but also swept the world. Now, scientists are trying to understand its meaning.

At least four laboratory experiments have shown that this mutation makes the virus more infectious, although none of these works have been peer-reviewed. Another unpublished study led by scientists at Los Alamos National Laboratory asserts that patients with the G variant actually have more viruses in their bodies, which makes them more likely to spread it to others.

This mutation does not seem to make people sick, but more and more scientists worry that this mutation will make the virus more contagious.

“Epidemiological studies and our data together explain why [G variant’s] Hyeryun Choe, a virologist at Scripps Research and the first author of an unpublished unpublished study on the infectivity enhancement of G variants in laboratory cell culture, said the virus is found in Europe The speed of propagation with the United States is indeed very fast. “It’s not just accidental.”

However, there may be other explanations for the predominance of G mutation: prejudice in the location of genetic data collection, and the odds of timing make the mutant virus gain a foothold in susceptible people.

Jeremy Luban, a virologist at the University of Massachusetts Amherst, said: “The most important thing is that we haven’t defined it yet.”

The battle to unravel this mutation mystery exemplifies the scientific challenge during the coronavirus pandemic. Millions of people are infected and thousands of people die every day around the world, so researchers must strike an important balance between getting information quickly and ensuring it is correct.

Spike protein mutation

The mutation in the spike protein of the SARS-CoV-2 virus changed only one amino acid in about 1,300 chains, but it may change the way the virus attacks human cells. The mutation (called D614G) first appeared in January and was found in the main variant of coronavirus.

New samples every week

In Nextrain’s global subsample

Proportion of samples with D614G mutation

No sample ratio

D614G mutation

The data includes 3,006 samples collected on June 24.

Source: Nextstrain, GISAID

Joe Fox/Washington Post

Spike protein mutation

The mutation in the spike protein of the SARS-CoV-2 virus changed only one amino acid in about 1,300 chains, but it may change the way the virus attacks human cells. The mutation (called D614G) first appeared in January and was found in the main variant of coronavirus.

New weekly sample in Nextrain’s global subsample

Proportion of samples with D614G mutation

No sample ratio

D614G mutation

The data includes 3,006 samples collected on June 24.

Source: Nextstrain, GISAID

Joe Fox/Washington Post

Spike protein mutation

The mutation in the spike protein of the SARS-CoV-2 virus changed only one amino acid in about 1,300 chains, but it may change the way the virus attacks human cells. The mutation (called D614G) first appeared in January and was found in the main variant of coronavirus.

New weekly sample in Nextrain’s global subsample

Proportion of samples with D614G mutation

Proportion of samples without D614G mutation

The data includes 3,006 samples collected on June 24.

Source: Nextstrain, GISAID

Joe Fox/Washington Post

Spike protein mutation

The mutation in the spike protein of the SARS-CoV-2 virus changed only one amino acid in about 1,300 chains, but it may change the way the virus attacks human cells. The mutation (called D614G) first appeared in January and was found in the main variant of coronavirus.

New weekly sample in Nextrain’s global subsample

Proportion of samples with D614G mutation

Proportion of samples without D614G mutation

The data includes 3,006 samples collected on June 24.

Joe Fox/Washington Post

Source: Nextstrain, GISAID

Better locking options

SARS-CoV-2 is a new coronavirus that causes the coronavirus covid-19, and can be considered a very destructive anti-theft. It cannot survive or reproduce on its own, it will split into human cells and choose its biological mechanism to make thousands of copies of itself. This leaves traces of damaged tissue and triggers an immune system response, which can be catastrophic for some people.

This replication process is confusing. Although coronavirus has a “proofreading” mechanism to replicate its genome, it often makes mistakes or mutations. Most mutations have no effect on the behavior of the virus.

But since the viral genome was first sequenced in January, scientists have been looking for meaningful changes. And few gene mutations are more important than those that affect spike protein. The spike protein is the most powerful tool of the virus.

The protein attaches to the respiratory cell ACE2, and the receptor opens the cell and slides the virus inside. The more effective the spike protein, the easier it is for the virus to invade its host. Even if the original variant of the virus appeared in Wuhan, China, it is clear that the spike protein on SARS-CoV-2 is already very effective.

SARS-CoV-2 uses its spikes to bind to the ACE2 receptor and enter the cell.

The viral RNA is released into the cell. Cells read and read RNA and produce proteins.

These proteins are assembled into new copies of the virus, and then continue to infect more cells.

Aaron Stickberg/Washington Post

SARS-CoV-2 uses its spikes to bind to the ACE2 receptor and enter the cell.

The viral RNA is released into the cell. Cells read and read RNA and produce proteins.

These proteins are assembled into new copies of the virus, and then continue to infect more cells.

Aaron Stickberg/Washington Post

The viral RNA is released into the cell. Cells read and read RNA and produce proteins.

These proteins are assembled into new copies of the virus, and then continue to infect more cells.

SARS-CoV-2 uses its spikes to bind to the ACE2 receptor and enter the cell.

Aaron Stickberg/Washington Post

SARS-CoV-2 uses its spikes to bind to the ACE2 receptor and enter the cell.

The viral RNA is released into the cell. Cells read and read RNA and produce proteins.

These proteins are assembled into new copies of the virus, and then continue to infect more cells.

Aaron Stickberg/Washington Post

Choe said, but the situation may be better. Since the outbreak of Severe Acute Respiratory Syndrome in 2003, he has studied spike protein and its binding to ACE2 receptor.

The spike protein of SARS-CoV-2 has two parts, which sometimes do not bind well. Qiao said that in this virus that appears in China, the outer part of the virus often falls off. Equipped with this wrong pickaxe, the virus can hardly invade the host cell.

Choe said: “I think this mutation can just make up.”

Choe and her colleagues used proxy viruses in human Petri dishes to study two versions of the gene, and found that the virus with the G variant had more spike proteins, and these proteins were more likely to circulate outside. small. In laboratory experiments, this increased the virus’s infectivity by about 10 times.

This mutation does not seem to cause the patient’s prognosis to deteriorate. Choe said that it also did not change the virus’s response to antibodies to patients with the D variant, suggesting that the vaccine developed based on the original virus version will be effective against the new strain.

Choe has uploaded the manuscript describing the study to the BioRxiv website, where scientists can publish “preprinted” research that has not been peer-reviewed. She has also submitted the paper to an unpublished academic journal.

Strain G is uniquely infectious, so that scientists are attracted to it even without looking for mutations.

Neville Sanjana, a geneticist at the New York Genome Center and New York University, tried to find out which genes could allow SARS-CoV-2 to penetrate human cells. However, in an experiment based on the gene sequence of early virus cases in Wuhan, he tried to infect the cells with this virus form. Then, the research team switched to a model virus based on the G variant.

“We were shocked,” Sanjana said. “Voilà! It’s just a huge increase in viral transduction.” They repeated the experiment in many types of cells, and the infectivity of each variant increased many times.

Their findings were published as a preprint of BioRxiv, and generally coincided with what Choe and other laboratory scientists have seen.

But the New York team provided different explanations for why this variant is so contagious. Choe’s research suggests that the mutation makes the spike protein more stable, and Sanjana said that experiments over the past two weeks (not yet publicly available) indicate that the improvement is actually in the infection process. He hypothesized that the G variant was more efficient in starting to invade human cells and take over its reproductive mechanisms.

Luban has also been trying the D614G mutation, and he was led to a third possibility: his experiments showed that this mutation caused the spike protein to change shape when it binds to the ACE2 receptor, thereby improving its ability to fuse with host cells. .

Ruban said that different methods of making model viruses may explain these differences. “But obviously, things are happening.”

Unanswered question

Kristian Andersen, a Scripps virologist who did not participate in any research, said that although the experiments were compelling, they were not decisive. Scientists need to figure out why they have found different mechanisms for the same effect. All research must still pass peer review and must be copied using the real version of the virus.

Andersen said that even then, it is too early to say that the speed of the G variant spreads from person to person.

Anderson Brito, a computational biologist at Yale University, pointed out that previous cell culture experiments were wrong. Early experiments with the malaria drug hydroxychloroquine showed that it can effectively fight the coronavirus in the Petri dish. The drug was touted by President Trump and approved by the US Food and Drug Administration (FDA) for emergency use in hospitalized covid-19 patients. However, after there was evidence that the drug was “unlikely effective” to resist the virus and pose a potential security risk, the authorization was withdrawn this month.

To date, the largest research on transmission comes from Bette Korber, a computational biologist at Los Alamos National Laboratory, who has established one of the world’s largest viral genome databases to track HIV. In late April, she and colleagues at Duke University and the University of Sheffield in the United Kingdom released their working draft, believing that the mutation promoted the spread of the virus.

By analyzing sequences from more than twenty regions around the world, they found that most of the places where the original virus dominated before March were eventually replaced by mutant versions. This conversion is particularly evident in the United States: 96% of the early sequences here belong to the D variant, but by the end of March, almost 70% of the sequences contained G amino acids.

British researchers have also found that people with the G variant have more virus particles in their bodies. Scientists write that although this higher viral load does not seem to make people sick, it may explain the rapid spread of the G variant. People with more virus shedding ability are more likely to infect others.

The Los Alamos draft was rigorously reviewed when it was released in the spring, and many researchers doubt it.

Anderson said: “There are too many deviations in the data set here, you can’t control it, and you may not know it exists.” In the United States, 90% of infections have not been found and countries with limited public health infrastructure are still trying to keep up with the increasing number of countries. At the time of the case, insufficient data meant “we can’t answer all the questions we want to answer.”

Pardis Sabeti, a computational biologist at Harvard University and the Broad Institute, pointed out that the vast majority of the genomes sequenced came from Europe and the United States where the G variant first appeared. These infections are believed to have been introduced by European travelers before the country closed. Undetected within a few weeks. This can at least partially explain why it is so dominant.

She said that the success of the mutation may also be the “founder effect.” Arriving in places like northern Italy (the vast majority of sequencing infections are caused by G mutations), it is easy to buy among older people who are basically unprepared, and then spread it unconsciously everywhere.

Scientists may be able to exclude these alternative explanations by conducting more rigorous statistical analysis or controlled experiments on animal populations. With the continuous accumulation of research on the D614G mutation, researchers began to believe its importance.

Northwestern University virologist Judd Hultquist said: “I think we are slowly reaching consensus.”

Anderson said that solving the mystery of the D614G mutation will not change much in the short term. He said: “We can’t deal with D.” “If G transmits better, we won’t be able to cope.”

Scientists say, but it is still important to understand how the genome affects viral behavior. Identifying emerging mutations allows researchers to track their spread. Knowing which genes affect how the virus spreads, public health officials can make efforts to control the virus. Once therapeutic agents and vaccines are distributed on a large scale, a basic understanding of the genome will help to identify when drug resistance begins to develop.

Sabeti said: “Understanding the means of communication is not a panacea, but it will help us respond better.” “This is a race against time.”


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