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Beyond Omicron: what's next for COVID's viral evolution - Nature.com

Beyond Omicron: what's next for COVID's viral evolution - Nature.com

Beyond Omicron: what's next for COVID's viral evolution - Nature.com
Dec 07, 2021 6 mins, 1 sec

As the world sped towards a pandemic in early 2020, evolutionary biologist Jesse Bloom gazed into the future of SARS-CoV-2.

Like many virus specialists at the time, he predicted that the new pathogen would not be eradicated.

But it’s not clear whether these reinfections are the result of fading immune responses in their human hosts or whether changes in the virus help it to dodge immunity.

To find out, Bloom got hold of decades-old blood samples from people probably exposed to 229E, and tested them for antibodies against different versions of the virus going back to the 1980s.

The same held true for blood samples from the 1990s: people had immunity to viruses from the recent past, but not to those from the future, suggesting that the virus was evolving to evade immunity.

“Now that we’ve had almost two years to see how SARS-CoV-2 evolves, I think there are clear parallels with 229E,” says Bloom.

Variants such as Omicron and Delta carry mutations that blunt the potency of antibodies raised against past versions of SARS-CoV-2.

How SARS-CoV-2 evolves over the next several months and years will determine what the end of this global crisis looks like — whether the virus morphs into another common cold or into something more threatening such as influenza or worse.

They expect SARS-CoV-2 eventually to evolve more predictably and become like other respiratory viruses — but when this shift will occur, and which infection it might resemble is not clear.

Researchers are learning as they go, says Andrew Rambaut, an evolutionary biologist at the University of Edinburgh, UK.

When a virus first starts spreading in a new host, the lack of pre-existing immunity means that there is little advantage to be gained by evading immunity.

But this gain was nothing like the leaps in transmissibility that researchers would later observe with the variants Delta and Alpha, says Sarah Otto, an evolutionary biologist at the University of British Columbia in Vancouver, Canada.

They also carried mutations similar or identical to those spotted in SARS-CoV-2 in people with compromised immune systems whose infections lasted for months.

Many researchers expected that a descendant of Alpha — which seemed to be the most infectious of the bunch — would pick up additional mutations, such as those that evade immune responses, to make it even more successful.

Compared with other variants, including Alpha, Delta multiplies faster and to higher levels in the airways of infected individuals, potentially outpacing initial immune responses against the virus.

“At some point, I would expect that increased transmissibility will stop happening,” says Bloom.

Other established human viruses do not make the leaps in infectivity that SARS-CoV-2 has in the past two years, and Bloom and other scientists expect the virus to eventually behave in the same way.

One way for the virus to thread this needle would be to evolve to grow to lower levels in people’s airways, but maintain infections for a longer period of time, increasing the number of new hosts exposed to the virus, says Rambaut.

“Ultimately there’s going to be trade-off between how much virus you can produce and how quickly you elicit the immune system.” By lying low, SARS-CoV-2 could ensure its continued spread.

The assertion that viruses evolve to become milder “is a bit of a myth”, says Rambaut.

“A lot of us were expecting the next weird variant to be a child of Delta, and this is a bit of a wild card,” says Aris Katzourakis, a specialist in viral evolution at the University of Oxford, UK.

The swift rise in cases of Omicron in South Africa suggests that the new variant has a fitness advantage over Delta, says Tom Wenseleers, an evolutionary biologist and biostatistician at the Catholic University of Leuven in Belgium.

Instead, he and other researchers suspect that Omicron’s rise may be largely due to its ability to infect people who are immune to Delta through vaccination or previous infection.

But if the variant is spreading, in part, because of its ability to evade immunity, it fits in with theoretical predictions about how SARS-CoV-2 is likely to evolve, says Sarah Cobey, an evolutionary biologist at the University of Chicago in Illinois.

As gains in SARS-CoV-2’s infectivity start to slow, the virus will have to maintain its fitness through overcoming immune responses, says Cobey.

That evolutionary path, towards immune evasion and away from gains in infectivity, is common among established respiratory viruses such as influenza says Adam Kucharski, a mathematical epidemiologist at the London School of Hygiene and Tropical Medicine.

“The easiest way for the virus to cause new epidemics is to evade immunity over time.

Evolving to evade immune responses such as antibodies could also carry some evolutionary costs.

It’s also possible that repeated exposure to different versions of spike — through infection with different virus strains, vaccine updates or both — could eventually build up a wall of immunity that SARS-CoV-2 will have difficulty overcoming.

Mutations that overcome some people’s antibody responses are unlikely to foil responses across an entire population, and T-cell-mediated immunity, another arm of the immune response, seems to be more resilient to changes in the viral genome.

Such constraints might slow SARS-CoV-2’s evasion of immunity, but they are unlikely to stop it, says Bloom.

How SARS-CoV-2 evolves in response to immunity has implications for its transition to an endemic virus.

To predict what these outbreaks will look like, scientists are investigating how quickly a population becomes newly susceptible to infection, says Kucharski, and whether that happens mostly though viral evolution, waning immune responses, or the birth of new children without immunity to the virus.

“My feeling is that small changes that open up a certain fraction of the previously exposed population to reinfection may be the most likely evolutionary trajectory,” says Rambaut.

“Even a virus like measles, which has essentially no ability to evolve to evade immunity, is still around,” says Bloom.

If SARS-CoV-2 follows this path — aided by vaccines that provide strong protection against severe disease — “it becomes essentially a virus of kids,” says Rambaut.

The influenza A virus, which drives global seasonal influenza epidemics each year, is characterized by the rapid evolution and spread of new variants able to escape the immunity elicited by past strains.

But if SARS-CoV-2 evolves to evade immunity more sluggishly, it might come to resemble influenza B.

How quickly SARS-CoV-2 evolves in response to immunity will also determine whether — and how often — vaccines need to be updated.

Although other respiratory viruses, including seasonal coronaviruses such as 229E, offer several potential futures for SARS-CoV-2, the virus may go in a different direction entirely, say Rambaut and others.

The sky-high circulation of the Delta variant and the rise of Omicron — aided by inequitable vaccine roll-outs to lower-income countries and minimal control measures in some wealthy countries such as the United States and the United Kingdom — offer fertile ground for SARS-CoV-2 to take additional surprising evolutionary leaps.

For instance, a document prepared by a UK government science advisory group in July raised the possibility that SARS-CoV-2 could become more severe or evade current vaccines by recombining with other coronaviruses.

“There may be multiple directions that the virus can go in,” Rambaut says, “and the virus hasn’t committed.”.

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