Viral mutations do not slow down. A new subvariant Omicron proves it. 2022-05-01 13:34:29


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During those harrowing days of the pandemic, scientists provided one piece of reassuring news about the new coronavirus: it has slowly mutated. The early booms didn’t seem to have been a consequence. A vaccine, if and when it was invented, may not need regular updating over time.

This proved to be overly optimistic.

The coronavirus, SARS-CoV-2, has billions of opportunities to recreate itself as it spreads across the planet, continues to evolve, creating new variables and subvariables in a clip that kept scientists on guard. Two and a half years after it first spread to humans, the virus has repeatedly changed its structure and chemistry in ways that have baffled efforts to control it completely.

It does not show signs of stability in old age drowsiness. Even with all the changes so far, it still has plenty of evolutionary room to explore, according to virologists who track it closely. What that means in practical terms is that a virus that is already highly contagious can become much more dangerous.

Virologist Robert F. Gary of Tulane University: “It’s possible that this virus has tricks that we haven’t seen yet.” “We know it may not have been quite as contagious as measles yet, but it’s definitely creeping in there.”

The newest member of the rogue gallery of variants and sub variants is BA.2.12.1, part of the omicron gang. Preliminary research indicates that it is 25 percent more transmissible than BA.2 variant This is offline nationally dominantAccording to the Centers for Disease Control and Prevention. The CDC said the drug has spread rapidly in the Northeast in particular, where it accounts for the majority of new infections.

“We have a very highly contagious variant out there. It would be difficult to ensure that no one in America will contract the virus. This is not even a political goal,” President Biden’s new covid-19 coordinator said, Ashish Jhahe said at his inaugural press conference on Tuesday.

He was responding to a question about Vice President Harris, who recently tested positive for the virus and is in isolation. Harris recently got a boost for a second time — her fourth hit from the vaccine.

Her case highlights what has become painfully clear in recent months: No amount of vaccination or booster can create a perfect case. Shield against infection from SARS-CoV-2. However, what vaccines do very well Reduce the risk of serious diseases. This is of great importance in terms of public health, as is the wider use of treatments, such as antiviral drugs. Baxlovid.

All vaccines currently published were based on the genetic sequence of the original strain of the virus that spread in late 2019 in Wuhan, China. They essentially mimic the spike protein of that version of the virus and trigger an immune response that is protective when the real virus appears.

But the variants that have emerged could evade many of the neutralizing antibodies that make up the immune system’s front line of defense.

“It’s developing at a fairly rapid rate,” said Jesse Bloom, a computational biologist at the Fred Hutchinson Cancer Research Center in Seattle. “I think we need to think hard about whether we should update the vaccines, and do that soon.”

BA.2.12.1 takes the novel coronavirus one step further on the infection scale. Its close relative, BA.2, was already more transmissible than the first omicron strain to hit the country in late 2021.

And omicron was more transmissible than delta, delta was more transmissible than alpha, and alpha was more transmissible than earlier variants that did not have the glory of the Greek alphabet name.

Most mutations are not beneficial to the virus. But when mutation offers some advantage, the process of natural selection will favor it.

There are two primary ways a virus can improve its fitness through mutation. The first can be described as mechanical: it can become innately better at infecting a host. It may improve its ability to attach to a future cell. Or perhaps the mutation allows the virus to multiply in greater numbers once the infection has begun—resulting in a person’s viral load and, proportionally, the amount of virus released, potentially infecting other people.

Another strategy involves alternative immunotherapy. The human immune system, when triggered by previous vaccines or infection to be on alert for a particular virus, will release antibodies that recognize and neutralize it. But the mutations make the virus less familiar with the immune system’s forward defense.

Sub-variants continue to emerge: scientists in South Africa have identified BA.4 and BA.5, which have mutations seen in previous variants and can lead to immune evasion.

Osterholm, an infectious disease expert at the University of Minnesota, said: “The evolution is much faster and broader than we initially expected.” “Every day I wake up, I’m afraid there will be a new alternative that we will have to think about. … We are seeing sub-variables from sub-variables.”

Gary, Tulane’s scientist, points out that mutations in the virus do not change its appearance significantly. In fact, he said, even the highly mutated variants don’t look much different from the original Wuhan strain, or different from other coronaviruses that cause the common cold. These are minor changes.

Garry has software that allows him to create a graphic image of the virus, and even rotate it, to monitor the sites of mutations and draw conclusions about why they are important. On Friday, when asked about BA.2.12.1, and why it is spreading, he indicated that it contains a mutation, called S704L, that likely destabilizes part of the spike protein on the virus’s surface. Essentially, this softens part of the height in a way that facilitates infection.

The S704L mutation distinguishes this variant from BA.2.

The number “704” refers to position 704 of an amino acid on a chain of about 1,100 amino acids that make up a protein. S is one of the types of amino acids (“serine”) that appears in the original strain of the virus, and L (“lysine”) is what is found after the mutation. (The mutation is caused by a change in one nucleotide, or “letter,” in the genetic code of the virus; three nucleotides code for an amino acid.)

Today the virus is circulating in the United States on an immune landscape much different from the one it first encountered in early 2020. Between vaccinations and infections, not many people are completely gullible to the virus. The CDC’s latest data She reports that the virus has successfully infected nearly 200 million people in the country of about 330 million. Among children and teens, about three in four have been infected, the CDC estimates.

For the new CDC study, researchers looked at blood samples from thousands of people and looked for an antibody that was found after a natural infection, but not found after vaccination. The CDC concluded that the omicron variant managed to traverse the US population during the winter almost as if it were an entirely new virus. By that time, the country had been largely vaccinated. However, approximately 80 million people were infected for the first time in that omicron wave.

In the family tree of this coronavirus, the omicron is a distant cousin of delta, alpha and other variants that circulated earlier – it came out of the viral left field. No one is sure of the omicron’s origin, but many disease experts assume it came from an immunocompromised patient with a long-term illness, and the virus continued to use mutations to evade the immune system’s efforts to get rid of it.

Omicron was less likely to kill a person than previous variants. But infectious disease experts are clear on this point: Future variants could be more pathogenic.

As if mutation weren’t a problem enough, the virus has another trick up its sleeve: recombination. It occurs when two different strains simultaneously infect one host and intertwine their genes. The process of recombination is the origin of what is known as omicron XE. This recombinant likely appeared from a person co-infected with the original omicron variant and the BA.2 subvariate.

This has always been possible in theory, but identifying the actual combinations provides “proof of concept,” said Jeremy Le Pen, a virologist at the University of Massachusetts Medical School.

The worst-case scenario would be the emergence of a variant or recombinant that renders current vaccines largely ineffective in preventing severe disease. But this has not happened yet. No ‘recombinants’ such as omicron or other recent variants and subvariants have been deployed.

This is the first catastrophic pandemic to occur in the era of modern genetic sequencing. A century ago, no one knew what a coronavirus was, and even “virus” was a relatively new concept. But today, with millions of virus samples analyzed at the genetic level, scientists can track mutations almost in real time and watch the virus evolve. Scientists all over the planet have uploaded millions of sequences to the database known as GISAID.

Genomic sequencing has significant limitations with it, although scientists can track changes in the genome, they do not automatically know what each of these changes does to the virus. What mutations are most important is a question that can be discerned through laboratory experiments, modeling, or epidemiological surveillance, but it is not always simple or straightforward.

Erica Savier, head of the La Jolla Institute of Immunology, speculates that the omicron has mutations that alter the virus in ways not yet understood but make it more resistant to neutralization by antibodies.

“You may have picked up some new tricks that we haven’t uncovered yet,” Safire said. “It’s hard to neutralize what I expected, based on the number of mutations alone.”

The reality check comes from Jeremy Kamel, assistant professor of microbiology and immunology at Louisiana State University Health Shreveport: “These are all SARS-CoV-2.”

What he means is that these are all variants of the same virus, despite what appears to be an enormous amount of mutation. In contrast, a person who develops one of these new variants will have the same disease as people who have been infected previously.

“They contracted the virus,” he said.