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Wednesday, November 30, 2022

Virus mutation is not slowing down. The new Omicron subvariant proves it.

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During those dreadful early days of the pandemic, scientists offered a piece of reassuring news about the novel coronavirus: It slowly mutated. The initial mutations did not appear to be consequential. A vaccine, if and when it was invented, may not need to be updated regularly over time.

This proved to be overly optimistic.

The coronavirus, SARS-CoV-2, has had billions of chances to reconfigure itself as it has spread across the planet, and it continues to evolve, generating new variants and subvariants at a clip that has given scientists the opportunity to reconfigure themselves. Kept on toes. Two and a half years after it first spread to humans, the virus has repeatedly changed its structure and chemistry in ways that have confused efforts to bring it under complete control.

And it’s not showing signs of settling into a sleepy old age. Even with all the changes so far, according to virologists who are tracking it closely, it still has abundant evolutionary space to explore. What this practically means is that a virus that is already highly contagious can become even more prevalent.

“There are probably tricks in this virus that we haven’t seen yet,” said virologist Robert F. Gary of Tulane University. “We know it’s probably not quite as contagious as measles yet, but it’s creeping in there, for sure.”

The latest member of the gangsters gallery is variants and subvariants named BA.2.12.1, part of the Omicron gang. According to the Centers for Disease Control and Prevention, preliminary research suggests it is about 25 percent more transmissible than the BA.2 subvariant, which is currently dominant nationally. The CDC said the subvariant has spread particularly rapidly in the Northeast, where it accounts for the majority of new infections.

“We have a very contagious form. It will be difficult to make sure there is no covid in the US. It is not even a policy goal,” Ashish Jha, President Biden’s new Covid-19 coordinator, told his inaugural news on Tuesday. Said in the briefing.

He was responding to a question about Vice President Harris, who recently tested positive for the virus and went into isolation. Harris was recently promoted for the second time – his fourth shot of the vaccine.

His case highlights what has become painfully clear in recent months: No amount of vaccination or boosting can create an ideal shield against infection with SARS-CoV-2. However, vaccines work very well, significantly reducing the risk of serious disease. This is of huge consequence in terms of public health, as is the widespread use of therapeutics such as the antiviral PaxLovid.

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

But the variants that have emerged may evade many of the neutralizing antibodies that are the immune system’s front line of defense.

“It’s evolving quite rapidly,” said Jesse Bloom, a computational biologist at the Fred Hutchinson Cancer Research Center in Seattle. “I think we need to consider aggressively whether we should be updating vaccines, and do it sooner.”

BA.2.12.1 brings the new coronavirus one more step up the infectivity scale. Its close relative, BA.2, was already more permeable than the first Omicron strain that arrived in the country in late 2021.

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And Omicron was more permeable than Delta, and Delta was more permeable than Alpha, and Alpha was more permeable than earlier variants, which did not glorify the name of the Greek alphabet.

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

There are two fundamental ways in which a virus can improve its fitness through mutation. The first can be described as mechanical: it may be instinctively better at infecting a host. Perhaps this receptor improves its ability to bind to the cell. Or perhaps the mutation allows the virus to replicate in greater numbers once the infection has begun – increasing the viral load in the individual and, correspondingly, the amount of virus that can infect other people.

The second strategy involves resolving immunity. The human immune system, when prompted by a vaccine or previous infection to become aware of a specific virus, will deploy antibodies that recognize and neutralize it. But the mutations make the virus less familiar with the immune system’s front-line defense.

Subvariants keep coming: Scientists in South Africa have identified BA.4 and BA.5, which have mutations that were seen in earlier variants and can lead to decreased immunity.

“The development is much faster and more extensive than we initially expected,” said Michael T. Osterholm, an infectious disease specialist at the University of Minnesota. “Every day I wake up, I’m afraid there will be a new subvariant we have to consider. … We’re seeing subvariants of subvariants.”

Tulane scientist Gary explains that the mutation in the virus does not dramatically change its appearance. In fact, he said, even the heavily mutated variants don’t appear to be much different from the original Wuhan strain, or different from other coronaviruses that cause the common cold. These are subtle changes.

Gary has a software program that allows him to create a graphic image of the virus, and even rotate it, to observe the locations of mutations and get an idea of ​​why they matter. to put. On Friday, when asked about BA.2.12.1, and why it is spreading, he noted that it has a mutation, named S704L, that possibly destabilizes a part of the spike protein on the surface of the virus. gives. This essentially loosens part of the spike in a way that facilitates infection.

This S704L mutation separates this subvariant from BA.2.

The “704” refers to the 704th position for an amino acid on the chain of approximately 1,100 amino acids that make up a protein. S is a type of amino acid (“serine”) seen in the original strain of the virus, and L (“leucine”) is followed by mutation. (The mutation is caused by a change in one nucleotide, or “letter” in the virus’s genetic code; three nucleotides encode for one amino acid.)

The virus is spreading in the United States today on an immunological landscape that first emerged in early 2020. Between vaccination and infection, there are no people completely naive to the virus. The latest figures from the CDC show that the virus has managed to infect about 200 million people in the country, which has a population of about 330 million. The CDC estimates that among children and adolescents, about three out of four have been infected.

For the new CDC study, researchers looked at blood samples from thousands of people and looked for antibodies that are found after a natural infection but not after vaccination. The CDC concluded that the Omicron variant managed to plow through the population of the United States during the winter, as if it were an entirely new virus. By that time, mass vaccination had taken place in the country. And yet, about 80 million people were infected for the first time in that omicron wave.

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On the lineage tree of this coronavirus, Omicron is a distant cousin of delta, alpha and other variants that spread earlier – it originated from the virological left field. No one is sure of the origin of the omicron, but many pathologists believe that it came from an immunocompromised patient with a very long illness, and the virus mutated to evade the immune system’s efforts to clear it. continued to use.

Omicron had less mercy for killing someone than in previous variants. But infectious disease experts are clear on this point: Future forms may be more pathogenic.

As if mutation weren’t enough of a problem, the virus has another trick up its sleeve: recombination. This occurs when two different strains infect the same host simultaneously and their genes become entangled. The recombination process is the origin of what is known as Omicron XE. That recombinant probably emerged from an individual co-infected with the original Omicron variant and the BA.2 subvariant.

In theory this was always possible, but identification of the actual recombinant provides “proof of concept,” says Jeremy Luban, a virologist at the University of Massachusetts Medical School.

The worst-case scenario would be the emergence of a variant or recombinant that makes current vaccines largely ineffective at preventing serious disease. But so far it hasn’t happened. And no “recombinant” spread like Omicron or other more recent variants and subvariants.

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

This has a major limitation of genomic sequencing, as although scientists can track changes in the genome, they do not automatically know what each of those changes is doing to the virus. Which mutation matters most is a question that can be identified through laboratory experiments, modeling or epidemiological surveillance, but is not always simple or clear.

Erica Sapphire, president of the La Jolla Institute for Immunology, speculates that there are mutations in the omicron that mutate the virus in ways not yet understood, but which make it more resistant to antibody-mediated neutralization.

“It may have acquired some new tricks that we haven’t uncovered yet,” Safire said. “Based on the number of mutations alone, it’s harder to neutralize than I expected.”

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

What he means is that they are all variations of the same virus, despite what seems like a lot of mutation. Similarly, someone who becomes infected with one of these new forms gets the same disease as people who have been infected before.

“He got Covid,” he said.

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