How the next variant of the coronavirus might appear

With Omicron, those answers still remain a mystery: how did a variant suddenly emerge that looked so different from all of its older cousins? How do you explain your mixture of mutations, many of which are rarely seen in variants of interest?

“When this string of viruses started to come out, it was very difficult for me to understand that it was going to take off,” said Mehul Suthar, a virologist at Emory University.

Viruses change all the time, often in ways that really hurt your chances of survival. But occasionally, these mutations can work in the virus’s favor.

Catch my drift?

The virus you sneeze or cough may be slightly different from the virus you have.

This is because viruses mutate – especially when their genetic code consists of RNA, a close relative of our DNA.

“As the virus reproduces, there are errors in the reproduction of its code,” explained Dr. Mike Ryan, executive director of the WHO’s Health Emergencies Program, in a March briefing. “Most of these errors result in a virus that is either incompetent or simply dies.”

But rarely, these incidents can give the virus an edge. It can become more contagious. Or maybe it’s better at escaping our immunity.

Sarah Kobe, Associate Professor of Ecology and Evolution at the University of Chicago, Explained in an editorial in this week’s New York Times, the transmissibility of the coronavirus will hit a ceiling — eventually. However, it probably won’t stop developing in ways that evade our immune response.

But not all mutations occur in the same way.

“Before implementing Omicron, I think most people in the field would say that we would see an immune leak accumulating these mutations one by one,” Kobe told CNN.

Over time and over hundreds of infections, circulating viruses move further and further away from their ancestors in the evolutionary tree. It is a process known as antigenic drift.

However, while this may explain variants that appear closer together in the evolutionary tree – such as Omicron and its branch BA.2 – it does not explain how Omicron appeared in the first place.

“Omicron surprised everyone,” Kobe said.

Maritje Venter, a professor in the department of medical virology at the University of Pretoria in South Africa, said a “slow change” is unlikely to lead to the use of Omicron.

This means that the virus gradually developed in a population that was not monitored. She said South Africa, where many of the first Omicron specimens were identified, has a good monitoring program.

So it was difficult for a variable like Omicron to slowly infiltrate. Instead, his appearance looked strangely surprising.

“Delta almost disappeared and all of a sudden we saw a completely different Omicron,” said Venter.

gear change

In some cases, viruses do not move away; they saw.

An “antigenic shift” is a more dramatic change that can occur, for example, when viruses in animals reach humans or when two strains infect the same person and exchange genes.

Examples of the latter include rare cases of a hybrid virus containing stretches of delta and omicron genes.

Researchers at Helix, the company that helped Covid-19 testing track a range of variables, identified a cluster of combined Delta-Omicron infections In the United States, there were nearly 30,000 coronavirus samples from late November to mid-February, when both variants circulated.
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Among these samples, the researchers identified 20 cases where people had both variants at the same time. One of these samples showed some evidence that the variants exchanged genes, albeit at low levels. In addition, the researchers found two unrelated cases where the infection originated from hybrid viruses.

“Currently, there is no evidence that the two identified delta-micron recombinant viruses are more transmissible between hosts than the common omicron lineages,” the researchers wrote.

“We don’t call it Deltacron,” Maria Van Kerkhove, WHO’s technical lead on Covid-19, said in a March briefing. “Those are not the terms we use.”

At the time, Van Kerkhove said the combination appeared to be spreading “at very low levels,” but offered the warning that we should test further to get a clearer picture of its prevalence and prevalence — or lack thereof.

However, the ability to switch genes has led to the resurgence of several viruses, most notably the flu.

The genetic material of the flu is made up of several pieces of RNA that can move back and forth when two viruses infect the same cell. This is known as reassembly.

Kobe explained that the coronavirus “can actually do something difficult to understand,” referring to a gene-swapping process called recombination.

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Unlike the flu, the coronavirus has a long strand of RNA as its genetic code. When two strains infect the same cell, its transcription machinery can occasionally jump from one strain to another. This creates random “breakpoints” in the genetic code that are lumped together.

While the flu shuffles entire cards, in a way, each corona has only one card – but it’s a very long card and can be cut and pasted in a variety of ways.

That means the virus has “a lot more evolutionary space that it can be exploited very quickly,” Kobe said.

In her editorial, she and her colleagues describe how we may have only seen the tip of the iceberg when it comes to the number of possible mutations the virus can tolerate and still be able to infect human cells.

While it’s unclear whether recombination is more likely than other pathways to generate the next problematic variant, Kobe said Omicron, in particular, has lit a fire under scientists to understand its origins and the true scope of viable mutations.

“This is the kind of difference that is really difficult to study and predict in the lab,” she said.

Omicron’s secret

There doesn’t seem to be a single interpretation that accurately fits Omicron’s history. But experts revolve around several theories that could explain its sudden appearance last year.

The most common opinion seems to include a prolonged infection in an immunocompromised person.

“They are already developing antibodies, but they are not clearing the virus,” said Venter, who directs the World Health Organization. Scientific advisory group on the origins of new pathogens.
This gives the virus plenty of time to accumulate changes, which could potentially enable it to evade that person’s antibodies and acquire immune resistance.
Another theory, Venter added, is known as reverse zoonosis. This refers to infecting humans with a group of animals, as the virus accumulates new mutations before reverting back to humans. (Actually, this coronavirus has spread widely across the animal kingdom.)

Experts say staying ahead of the virus isn’t just a matter of anticipating your next move. It’s about finding ways to avoid threats and ultimately ensuring the viability of our vaccines.

And it’s not just this virus.

“Most of the pathogens that frequently infect us are able to do so because they evade part of our immunity to earlier infectious strains,” Kobe said.

“Viral evolution is really a real problem in our lives that we may not officially recognize as such.”

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