Great news. Will never know what impact had she not been completely vaccinated
The COVID-19 Science and Medicine Question Thread
- Thread starter Roccus7
- Start date
wader
Well-Known Angler
she's feeling 100% today - returning to work tomorrowsame on this end - my daughter didn't get as ill as it sounds like yours did George - but by yesterday it was down to what felt like an annoying head cold - haven't heard from her today but from the sounds of it yesterday it's pretty well gone - thank God for the vaccines
Evolution is a bi-atch!!! Welcome to "Omidelta", my nomenclature...
pressherald.com/2022/05/26/coronavirus-mutant-now-dominant-in-u-s-contains-ghost-of-pandemic-past/
By LAURA UNGAR May 26, 2022
The coronavirus mutant that is now dominant in the United States is a member of the omicron family but scientists say it spreads faster than its omicron predecessors, is adept at escaping immunity and might possibly cause more serious disease.
Why? Because it combines properties of both omicron and delta, the nation’s dominant variant in the middle of last year.
A genetic trait that harkens back to the pandemic’s past, known as a “delta mutation,” appears to allow the virus “to escape pre-existing immunity from vaccination and prior infection, especially if you were infected in the omicron wave,” said Dr. Wesley Long, a pathologist at Houston Methodist in Texas. That’s because the original omicron strain that swept the world didn’t have the mutation.
The omicron “subvariant” gaining ground in the U.S. — known as BA.2.12.1 and responsible for 58 percent of U.S. COVID-19 cases last week — isn’t the only one affected by the delta mutation. The genetic change is also present in the omicron relatives that together dominate in South Africa, known as BA.4 and BA.5. Those have exactly the same mutation as delta, while BA.2.12.1 has one that’s nearly identical.
This genetic change is bad news for people who caught the original omicron and thought that made them unlikely to get COVID-19 again soon. Although most people don’t know for sure which variant caused their illness, the original omicron caused a giant wave of cases late last year and early this year.
Long said lab data suggests a prior infection with the original omicron is not very protective against reinfection with the new mutants, though the true risk of being reinfected no matter the variant is unique to every person and situation.
In a twist, however, those sickened by delta previously may have some extra armor to ward off the new mutants. A study released before it was reviewed by other scientists, by researchers at Ohio State University, found that COVID patients in intensive care with delta infections induced antibodies that were better at neutralizing the new mutants than patients who caught the original omicron.
“The omicron infection antibody does not appear to protect well against the subvariants compared to delta,” said Dr. Shan-Lu Liu, a study author who co-directs the viruses and emerging pathogens program at Ohio State.
But Liu said the level of protection a delta infection provides depends partly on how long ago someone was ill. That’s because immunity wanes over time.
People who got sick with delta shouldn’t think of themselves as invulnerable to the new subvariants, especially if they’re unvaccinated, Long said. “I wouldn’t say anyone is safe.”
One bright spot? Booster shots can provide strong protection against the new mutants, Liu said. In general, vaccines and prior infection can protect people from the worst outcomes of COVID-19. At this point, scientists say, it’s too early to know if the new mutant gaining ground in the U.S. will cause a significant uptick in new cases, hospitalizations and deaths.
Scientists are still trying to figure out how virulent these new mutants are. Long said he hasn’t seen anything that answers that question for him, but Liu said emerging data points toward more serious illness. Liu said the subvariants have properties suggesting they spread more efficiently cell-to-cell.
The virus “just hides in the cell and spreads through cell-to-cell contact,” Liu said. “That’s more scary because the virus does not come out for the antibody to work.”
Dr. Eric Topol, head of Scripps Research Translational Institute, said the new mutants certainly don’t appear less virulent than previous versions of omicron, and whether they are more virulent or not “will become clear in the months ahead.”
In the meantime, scientists expect the latest powerhouse mutants to spread quickly, since they are more transmissible than their predecessors.
Though home testing makes it tough to track all U.S. COVID cases, data from Johns Hopkins University shows that cases are averaging nearly 107,000 a day, up from about 87,000 two weeks ago. And new hospital admissions of patients with COVID-19 have been trending upwards since around mid-April, according to the Centers for Disease Control and Prevention.
“I’m hopeful that we don’t see a similar increase in hospitalizations that we’ve had in prior waves,” Long said. “But with COVID, any time you have lots of people being infected, it’s just a numbers game. Some of those people are going to be severe. Some of those people are going to need hospitalization. Some of them, unfortunately, are going to pass away.”
Coronavirus mutant now dominant in U.S. contains ghost of pandemic past
By LAURA UNGAR May 26, 2022
The coronavirus mutant that is now dominant in the United States is a member of the omicron family but scientists say it spreads faster than its omicron predecessors, is adept at escaping immunity and might possibly cause more serious disease.
Why? Because it combines properties of both omicron and delta, the nation’s dominant variant in the middle of last year.
A genetic trait that harkens back to the pandemic’s past, known as a “delta mutation,” appears to allow the virus “to escape pre-existing immunity from vaccination and prior infection, especially if you were infected in the omicron wave,” said Dr. Wesley Long, a pathologist at Houston Methodist in Texas. That’s because the original omicron strain that swept the world didn’t have the mutation.
The omicron “subvariant” gaining ground in the U.S. — known as BA.2.12.1 and responsible for 58 percent of U.S. COVID-19 cases last week — isn’t the only one affected by the delta mutation. The genetic change is also present in the omicron relatives that together dominate in South Africa, known as BA.4 and BA.5. Those have exactly the same mutation as delta, while BA.2.12.1 has one that’s nearly identical.
This genetic change is bad news for people who caught the original omicron and thought that made them unlikely to get COVID-19 again soon. Although most people don’t know for sure which variant caused their illness, the original omicron caused a giant wave of cases late last year and early this year.
Long said lab data suggests a prior infection with the original omicron is not very protective against reinfection with the new mutants, though the true risk of being reinfected no matter the variant is unique to every person and situation.
In a twist, however, those sickened by delta previously may have some extra armor to ward off the new mutants. A study released before it was reviewed by other scientists, by researchers at Ohio State University, found that COVID patients in intensive care with delta infections induced antibodies that were better at neutralizing the new mutants than patients who caught the original omicron.
“The omicron infection antibody does not appear to protect well against the subvariants compared to delta,” said Dr. Shan-Lu Liu, a study author who co-directs the viruses and emerging pathogens program at Ohio State.
But Liu said the level of protection a delta infection provides depends partly on how long ago someone was ill. That’s because immunity wanes over time.
People who got sick with delta shouldn’t think of themselves as invulnerable to the new subvariants, especially if they’re unvaccinated, Long said. “I wouldn’t say anyone is safe.”
One bright spot? Booster shots can provide strong protection against the new mutants, Liu said. In general, vaccines and prior infection can protect people from the worst outcomes of COVID-19. At this point, scientists say, it’s too early to know if the new mutant gaining ground in the U.S. will cause a significant uptick in new cases, hospitalizations and deaths.
Scientists are still trying to figure out how virulent these new mutants are. Long said he hasn’t seen anything that answers that question for him, but Liu said emerging data points toward more serious illness. Liu said the subvariants have properties suggesting they spread more efficiently cell-to-cell.
The virus “just hides in the cell and spreads through cell-to-cell contact,” Liu said. “That’s more scary because the virus does not come out for the antibody to work.”
Dr. Eric Topol, head of Scripps Research Translational Institute, said the new mutants certainly don’t appear less virulent than previous versions of omicron, and whether they are more virulent or not “will become clear in the months ahead.”
In the meantime, scientists expect the latest powerhouse mutants to spread quickly, since they are more transmissible than their predecessors.
Though home testing makes it tough to track all U.S. COVID cases, data from Johns Hopkins University shows that cases are averaging nearly 107,000 a day, up from about 87,000 two weeks ago. And new hospital admissions of patients with COVID-19 have been trending upwards since around mid-April, according to the Centers for Disease Control and Prevention.
“I’m hopeful that we don’t see a similar increase in hospitalizations that we’ve had in prior waves,” Long said. “But with COVID, any time you have lots of people being infected, it’s just a numbers game. Some of those people are going to be severe. Some of those people are going to need hospitalization. Some of them, unfortunately, are going to pass away.”
Missing some info there Chevy
That's the "good stuff"...
Very interesting stuff, but highlights about the potential dangers of playing with fire. On the other hand, Arson Investigators get much of their knowledge by playing with fire...
In mid-2020, a team of scientists catching bats in Laotian caves discovered coronaviruses that were strikingly similar to the one that had begun wreaking havoc around the world.
In the months since, some of those researchers have been studying one of these mysterious bat viruses in a high-security laboratory in Paris, hoping to discover clues about how its cousin, SARS-CoV-2, went on to become a global threat that has killed an estimated 15 million people.
Their work has been scientifically fruitful. Last year, the scientists discovered that the bat virus was capable of latching on to human cells, at least in Petri dishes. Last month, the team reported more reassuring news: that the virus is not particularly harmful to lab animals. The finding suggests that SARS-CoV-2 evolved its abilities to spread quickly and cause deadly disease only after the two lineages branched apart on the viral evolutionary tree.
If the Laotian virus were to ever jump from a bat to a person, the new research suggests, it might cause a mild stomach bug rather than a life-threatening pneumonia. Nevertheless, lab experiments like these rekindle a longstanding debate among scientists about the wisdom of tinkering with viruses that are so closely related to a known pathogen.
Proponents argue that this kind of data is crucial for understanding — and preventing — pandemics. For example, the new studies have tested whether bat viruses could evolve a “furin cleavage site,” a feature of SARS-CoV-2 that allows it to efficiently infect human cells.
“Our motivation was to try to give some insight regarding the origin of Covid,” said Marc Eloit, a virologist at the Pasteur Institute in Paris who is leading the effort.
But critics say that scientists should not run experiments that might make viruses better able to spread among people, given the small but real chance that these altered pathogens might infect lab workers and escape into the outside world.
“For me, the benefits of this work are outweighed by the risks,” said Dr. David Relman, a microbiologist at Stanford University.
The scientists found genetic material from five coronaviruses closely related to SARS-CoV-2. In the feces from a Marshall’s horseshoe bat, they found whole viruses of a strain they named BANAL-236 (a code indicating the virus came from a bat anal swab).
Once back in their lab, the scientists found that BANAL-236 can infect human cells by binding tightly to the same protein that SARS-CoV-2 uses to gain entry. In February, the researchers published these findings in the journal Nature.
Last month, they released a second wave of results, now under review by a scientific journal, in which they investigated the virus’s behavior in laboratory mice and monkeys.
In one experiment, the scientists injected the virus into genetically engineered mice commonly used to study Covid. SARS-CoV-2 replicates quickly in their lungs, just as it does in people, causing them to lose weight and die.
BANAL-236, by contrast, struggled to take hold in the animals’ lungs, producing only about 1 percent of the viruses created in a SARS-CoV-2 infection.
The researchers found that the virus was even milder when they sprayed it into the noses of two monkeys. BANAL-236 replicated mainly in their guts, rather than their lungs.
Dr. Eloit suspects BANAL-236 is milder because it lacks a key feature important to the success of SARS-CoV-2.
After a new SARS-CoV-2 virus is created in a cell, its spike protein changes shape, with an effect like spring-loading a crossbow. When the virus then binds to a new cell, the primed spike protein shoots out molecular bolts that draw it into its new host.
This shape-shifting region of the spike — known as the furin cleavage site — is crucial to the success of SARS-CoV-2. When scientists have engineered viruses lacking this site, the mutants struggle to replicate in the lungs of lab animals or spread to new hosts.
The team based its studies on experiments in which other scientists had injected bird flu viruses into chicken eggs and waited for them to replicate. They then transferred the new viruses into new eggs, and again allowed them to replicate. With every transfer, the virus had a chance to evolve. After 11 transfers, the scientists found that the flu viruses had evolved cleavage sites, making them deadlier to chickens.
In a similar fashion, the Pasteur researchers removed lung tissue from mice infected with BANAL-236 and used the tissue to infect healthy animals. They then repeated the cycle, transferring viruses from mouse to mouse.
In another experiment, they infected a dish of human intestinal cells with BANAL-236, then used the new viruses produced by the cells to infect new dishes.
But for both experiments, Dr. Eloit and his colleagues decided against going as far as 11 transfers, stopping at six.
“From a purely scientific point of view, we wanted to do more than six passages,” Dr. Eloit said. “But we did not want to open the risk to adapting a bat virus to humans.”
BANAL-236 did not gain a furin cleavage site in either experiment. The virus did acquire other mutations, but they did not make it any better at infecting mouse lungs.
Scientists have been running such evolutionary experiments — known as “serial passage” — for more than a century. In fact, vaccines for a number of viruses such as yellow fever were created by growing them in the lab: The viruses evolved in Petri dishes into milder forms that were safe to inject into people.
In 2011, however, a controversy broke out about the safety of serial passage experiments that might produce new human pathogens. At the time, researchers were studying how influenza viruses that cause intestinal infections in birds can evolve into airborne forms that can infect people.
Two teams of researchers sprayed bird flu viruses into the noses of ferrets, waited for the viruses to replicate and then transferred the new viruses to new ferrets. Soon the viruses evolved to become better at replicating in the ferrets.
Some critics said the research was so reckless that it shouldn’t be published, for fear that other researchers would copy the work and accidentally release a new pandemic strain of flu. The United States government halted experiments like these in order to develop a new policy for judging their safety.
Some of the studies started up again in recent years. But Dr. Relman of Stanford and others have complained that the current regulations are not transparent enough.
Dr. Eloit said a Pasteur Institute committee that reviews potentially risky biological research authorized his team’s proposal for studying the new bat viruses. The scientists then carried out their experiments at the same level of security as their other work with the coronaviruses, known as Biosafety Level 3, or BSL-3.
Dr. Tom Inglesby, the director of the Johns Hopkins Center for Health Security at the Bloomberg School of Public Health, said it was good that the scientists put thought into these potential risks. But he also said he wanted to see a clear rationale for deciding that six passages were safe.
“It’s not possible to know ahead of time if these experiments would lead to more transmissible or more virulent viruses,” he said. “There’s no hard and fast rule that six is safe and more is not.”
But Thomas Peacock, a virologist at Imperial College London, said he thought that Dr. Eloit and his colleagues had been sufficiently prudent. In earlier studies, he pointed out, the researchers had found that antibodies produced by people during Covid infections were very potent against BANAL-236. That most likely meant that if the virus were to leak out of a lab, it wouldn’t be able to spread very far.
“This virus would probably hit a brick wall in the general population,” Dr. Peacock said. “I don’t really have much issue with the experiments.”
For Dr. Eloit, his team’s inability to produce a furin cleavage site on BANAL-236 in mice or human intestinal cells suggests that the SARS-CoV-2 lineage gained the furin site in bats before spilling over into people. He said it would not have been easy for the virus to gain a furin site after jumping into another species of animal — sometimes called “intermediate hosts” — such as those sold at a market in Wuhan, China. “I do not see any strong arguments in favor of an intermediate host,” Dr. Eloit said.
But scientists who favor the market scenario see the new results in a different light. If the researchers couldn’t spur BANAL-236 to evolve the furin site during serial passage experiments, they reasoned, then it’s unlikely that scientists in a Wuhan lab could have done so with SARS-CoV-2, as some proponents of the “lab leak” theory have suggested.
“This is another nail in the coffin of the lab leak theory that by now should be firmly sealed in the crypt,” said Edward Holmes, a virologist at the University of Sydney.
Dr. Peacock was reluctant to draw strong conclusions from such small-scale experiments. “I think it’s quite a difficult thing to ask to get a furin site after a few passages,” he said.
Dr. Eloit and his colleagues are now exploring the possibility that ancestors of SARS-CoV-2 gained a furin cleavage site while still in wild bats. The virus might have then spread to an intermediate host or directly to people exposed to bats — like those who collect bat guano, hunt bats or eat them.
To test that idea, the scientists are working to obtain more samples from bats in Laos and neighboring countries. Dr. Eloit can’t say whether their hypothesis is more likely than the others, but it is at least one they can investigate.
“Our work as scientists,” he said, “is to explore the working hypotheses that we can explore.”
Bat Virus Studies Raise Questions About Laboratory Tinkering
Working in a laboratory in Paris, scientists gave a close relative of the Covid virus the chance to evolve to be more like its cousin.In mid-2020, a team of scientists catching bats in Laotian caves discovered coronaviruses that were strikingly similar to the one that had begun wreaking havoc around the world.
In the months since, some of those researchers have been studying one of these mysterious bat viruses in a high-security laboratory in Paris, hoping to discover clues about how its cousin, SARS-CoV-2, went on to become a global threat that has killed an estimated 15 million people.
Their work has been scientifically fruitful. Last year, the scientists discovered that the bat virus was capable of latching on to human cells, at least in Petri dishes. Last month, the team reported more reassuring news: that the virus is not particularly harmful to lab animals. The finding suggests that SARS-CoV-2 evolved its abilities to spread quickly and cause deadly disease only after the two lineages branched apart on the viral evolutionary tree.
If the Laotian virus were to ever jump from a bat to a person, the new research suggests, it might cause a mild stomach bug rather than a life-threatening pneumonia. Nevertheless, lab experiments like these rekindle a longstanding debate among scientists about the wisdom of tinkering with viruses that are so closely related to a known pathogen.
Proponents argue that this kind of data is crucial for understanding — and preventing — pandemics. For example, the new studies have tested whether bat viruses could evolve a “furin cleavage site,” a feature of SARS-CoV-2 that allows it to efficiently infect human cells.
“Our motivation was to try to give some insight regarding the origin of Covid,” said Marc Eloit, a virologist at the Pasteur Institute in Paris who is leading the effort.
But critics say that scientists should not run experiments that might make viruses better able to spread among people, given the small but real chance that these altered pathogens might infect lab workers and escape into the outside world.
“For me, the benefits of this work are outweighed by the risks,” said Dr. David Relman, a microbiologist at Stanford University.
The furin site
The bat virus at the center of Dr. Eloit’s experiments came to light on an expedition to limestone caves in northern Laos in the summer of 2020. A team of Laotian and French researchers caught bats flying out of the caves and took samples of their saliva, blood, urine and feces.The scientists found genetic material from five coronaviruses closely related to SARS-CoV-2. In the feces from a Marshall’s horseshoe bat, they found whole viruses of a strain they named BANAL-236 (a code indicating the virus came from a bat anal swab).
Once back in their lab, the scientists found that BANAL-236 can infect human cells by binding tightly to the same protein that SARS-CoV-2 uses to gain entry. In February, the researchers published these findings in the journal Nature.
Last month, they released a second wave of results, now under review by a scientific journal, in which they investigated the virus’s behavior in laboratory mice and monkeys.
In one experiment, the scientists injected the virus into genetically engineered mice commonly used to study Covid. SARS-CoV-2 replicates quickly in their lungs, just as it does in people, causing them to lose weight and die.
BANAL-236, by contrast, struggled to take hold in the animals’ lungs, producing only about 1 percent of the viruses created in a SARS-CoV-2 infection.
The researchers found that the virus was even milder when they sprayed it into the noses of two monkeys. BANAL-236 replicated mainly in their guts, rather than their lungs.
Dr. Eloit suspects BANAL-236 is milder because it lacks a key feature important to the success of SARS-CoV-2.
After a new SARS-CoV-2 virus is created in a cell, its spike protein changes shape, with an effect like spring-loading a crossbow. When the virus then binds to a new cell, the primed spike protein shoots out molecular bolts that draw it into its new host.
This shape-shifting region of the spike — known as the furin cleavage site — is crucial to the success of SARS-CoV-2. When scientists have engineered viruses lacking this site, the mutants struggle to replicate in the lungs of lab animals or spread to new hosts.
Serial passage
Gaining a furin cleavage site may have been a crucial step in the evolution of SARS-CoV-2. To explore that possibility, Dr. Eloit and his colleagues ran lab experiments to give BANAL-236 a chance to evolve new traits, such as a furin cleavage site.The team based its studies on experiments in which other scientists had injected bird flu viruses into chicken eggs and waited for them to replicate. They then transferred the new viruses into new eggs, and again allowed them to replicate. With every transfer, the virus had a chance to evolve. After 11 transfers, the scientists found that the flu viruses had evolved cleavage sites, making them deadlier to chickens.
In a similar fashion, the Pasteur researchers removed lung tissue from mice infected with BANAL-236 and used the tissue to infect healthy animals. They then repeated the cycle, transferring viruses from mouse to mouse.
In another experiment, they infected a dish of human intestinal cells with BANAL-236, then used the new viruses produced by the cells to infect new dishes.
But for both experiments, Dr. Eloit and his colleagues decided against going as far as 11 transfers, stopping at six.
“From a purely scientific point of view, we wanted to do more than six passages,” Dr. Eloit said. “But we did not want to open the risk to adapting a bat virus to humans.”
BANAL-236 did not gain a furin cleavage site in either experiment. The virus did acquire other mutations, but they did not make it any better at infecting mouse lungs.
Scientists have been running such evolutionary experiments — known as “serial passage” — for more than a century. In fact, vaccines for a number of viruses such as yellow fever were created by growing them in the lab: The viruses evolved in Petri dishes into milder forms that were safe to inject into people.
In 2011, however, a controversy broke out about the safety of serial passage experiments that might produce new human pathogens. At the time, researchers were studying how influenza viruses that cause intestinal infections in birds can evolve into airborne forms that can infect people.
Two teams of researchers sprayed bird flu viruses into the noses of ferrets, waited for the viruses to replicate and then transferred the new viruses to new ferrets. Soon the viruses evolved to become better at replicating in the ferrets.
Some critics said the research was so reckless that it shouldn’t be published, for fear that other researchers would copy the work and accidentally release a new pandemic strain of flu. The United States government halted experiments like these in order to develop a new policy for judging their safety.
Some of the studies started up again in recent years. But Dr. Relman of Stanford and others have complained that the current regulations are not transparent enough.
Dr. Eloit said a Pasteur Institute committee that reviews potentially risky biological research authorized his team’s proposal for studying the new bat viruses. The scientists then carried out their experiments at the same level of security as their other work with the coronaviruses, known as Biosafety Level 3, or BSL-3.
Dr. Tom Inglesby, the director of the Johns Hopkins Center for Health Security at the Bloomberg School of Public Health, said it was good that the scientists put thought into these potential risks. But he also said he wanted to see a clear rationale for deciding that six passages were safe.
“It’s not possible to know ahead of time if these experiments would lead to more transmissible or more virulent viruses,” he said. “There’s no hard and fast rule that six is safe and more is not.”
But Thomas Peacock, a virologist at Imperial College London, said he thought that Dr. Eloit and his colleagues had been sufficiently prudent. In earlier studies, he pointed out, the researchers had found that antibodies produced by people during Covid infections were very potent against BANAL-236. That most likely meant that if the virus were to leak out of a lab, it wouldn’t be able to spread very far.
“This virus would probably hit a brick wall in the general population,” Dr. Peacock said. “I don’t really have much issue with the experiments.”
Origins of Covid
Other researchers agreed with Dr. Eloit that the research could shed light on how and when SARS-CoV-2 spilled over into people.For Dr. Eloit, his team’s inability to produce a furin cleavage site on BANAL-236 in mice or human intestinal cells suggests that the SARS-CoV-2 lineage gained the furin site in bats before spilling over into people. He said it would not have been easy for the virus to gain a furin site after jumping into another species of animal — sometimes called “intermediate hosts” — such as those sold at a market in Wuhan, China. “I do not see any strong arguments in favor of an intermediate host,” Dr. Eloit said.
But scientists who favor the market scenario see the new results in a different light. If the researchers couldn’t spur BANAL-236 to evolve the furin site during serial passage experiments, they reasoned, then it’s unlikely that scientists in a Wuhan lab could have done so with SARS-CoV-2, as some proponents of the “lab leak” theory have suggested.
“This is another nail in the coffin of the lab leak theory that by now should be firmly sealed in the crypt,” said Edward Holmes, a virologist at the University of Sydney.
Dr. Peacock was reluctant to draw strong conclusions from such small-scale experiments. “I think it’s quite a difficult thing to ask to get a furin site after a few passages,” he said.
Dr. Eloit and his colleagues are now exploring the possibility that ancestors of SARS-CoV-2 gained a furin cleavage site while still in wild bats. The virus might have then spread to an intermediate host or directly to people exposed to bats — like those who collect bat guano, hunt bats or eat them.
To test that idea, the scientists are working to obtain more samples from bats in Laos and neighboring countries. Dr. Eloit can’t say whether their hypothesis is more likely than the others, but it is at least one they can investigate.
“Our work as scientists,” he said, “is to explore the working hypotheses that we can explore.”
If you care to read a well-written piece about the new Omicron Variants, read away...
By Jeremy Kamil
Dr. Kamil is a virologist and associate professor of microbiology and immunology at Louisiana State University Health Shreveport.
The blitz of Omicron variants has felt like one long wave. And many questions have arisen amid the tumult. Are we seeing the emergence of entirely new coronavirus variants that are impervious to immunity from vaccines and previous infections? If we keep getting reinfected, is it inevitable that most of us will end up developing long Covid?
In short, the answer is no.
As a virologist, it’s important to me that people understand Covid-19 remains a great concern. But this does not excuse or license a misdiagnosis of the current situation.
Let’s start with what is true. BA.5, one of the most recent Omicron variants to emerge, is everywhere. It unquestionably has an advantage in terms of transmissibility over previous Omicron lineages, most likely because it’s better at evading our existing repertoire of antibodies.
BA.5 and its close cousin BA.4 have a key mutation that enables them to sneak past an important class of so-called broadly neutralizing antibodies. These particular antibodies did a great job of preventing infections from a wide swath of earlier variants.
That’s changed in some ways.
In recent weeks I’ve watched many vaccinated friends and family members get infected with the coronavirus for the first time. The most concerning of these are cases like a colleague of mine who was infected in May and again in June, both times becoming ill.
Thankfully, reinfection a few weeks after recovery is not the norm. Scientists have shown that people who previously contracted Covid-19 are less likely to get infected with the variant du jour than people who had never seen the virus, and this trend holds true for Omicron. Early research from Qatar that has not yet been peer-reviewed showed that people who had a BA.1 infection in, say, January were significantly less likely to experience a BA.4 or BA.5 breakthrough infection months later. While more research on this is welcome, these findings are consistent with how immunity, played out at the population level, helps explain the rise, fall and magnitude of epidemic waves.
Antibodies remain a powerful defense against this coronavirus. They do many things to protect us, while also flagging the virus for destruction by other elements of the immune system. Even though some studies have found that Omicron variants may induce weaker antibody responses than earlier variants, this is most likely because Omicron causes less severe disease, thanks to immunity from vaccines and prior infections.
Our immune system works much like a wise yet frugal investor, calibrating responses according to the magnitude and extent of the various danger signals sensed during infection. Generally speaking, the greater the symptoms and disease from infections like Covid or the flu, the stronger the antibody response. When existing antibodies are good enough to keep disease to a minimum (because fewer virus particles succeed in replicating in the body), we tend to see much lower amounts of antibodies than when someone ends up hospitalized from the coronavirus. Vaccines are a great way around that problem: They stimulate our immune systems to make antibodies, and other tailored defenses, even when there is no disease.
Right now the immunological makeup of the population is a mix. People who were infected with prior variants may now be catching Omicron infections, even if they’re also vaccinated. People who have never had Covid may be getting it now. It’s true that some people who got infected from an earlier Omicron variant in December, January or even more recently are catching BA.5 now, and becoming sick from it.
Alas, this current situation, where some are newly susceptible to infection while others remain protected, is no friend to nuance. It’s difficult to generalize broadly and make bold predictions concerning how well an individual or a population will hold up against infection now or later. But despite Omicron’s knack for circumventing antibodies, it’s clear that prior immunity, be it from vaccines or previous infections, protects from severe outcomes such as death and hospitalization. There has yet to be a variant that negates the benefits of vaccines.
Recently, an early study, which was not peer-reviewed, argued that reinfections are just as dangerous as primary infections, but there is by no means a consensus on this among scientists and medical experts. (The study only really showed that getting reinfected is worse than not being reinfected.) Other scientists are concerned about the long-term risks of multiple reinfections. However, there is no debate that prior immunity, in most cases, reduces the severity of subsequent infections. Catching the coronavirus more than once or after vaccination does not necessarily put someone at risk for the most serious and chronically debilitating forms of long Covid, though more research is needed to understand what might predispose someone to that.
The Food and Drug Administration should move swiftly to authorize new booster shots that target Omicron variants. The existing data suggest that updated shots, even based on earlier Omicron lineages, would be more effective at preventing infections than continuing to use the current vaccine boosters, which are based on the original 2019 coronavirus spike.
In the meantime, if you are eligible, it’s wise to get boosted with the currently available shots, which are still outstanding at preventing hospitalization and death. (This is especially critical for older people .) Wearing a mask when mixing indoors and avoiding indoor dining when case numbers are high remains advisable for those who’d prefer not to kick the tires on their existing immunity. Fortunately, monoclonal antibody cocktails are available that remain effective against BA.5. One such product, Evusheld, is given prophylactically to protect patients, while others are used to treat severe infections. Paxlovid, which can be taken at home, may also be a good option for people who test positive and are eligible for it.
Most immunologists I know are cautiously optimistic about our long-term prospects. We don’t know exactly what this virus will do next, and we should never be dismissive of those who have a high risk profile or are dealing with long Covid. Nonetheless, most of us can have faith in our immune systems, especially when we make use of vaccines and boosters. Recorded history may hold little precedent for the ongoing Covid-19 pandemic. But this is not our immune systems’ first rodeo.
Setting the Record Straight on Variants and Reinfections
By Jeremy Kamil
Dr. Kamil is a virologist and associate professor of microbiology and immunology at Louisiana State University Health Shreveport.
The blitz of Omicron variants has felt like one long wave. And many questions have arisen amid the tumult. Are we seeing the emergence of entirely new coronavirus variants that are impervious to immunity from vaccines and previous infections? If we keep getting reinfected, is it inevitable that most of us will end up developing long Covid?
In short, the answer is no.
As a virologist, it’s important to me that people understand Covid-19 remains a great concern. But this does not excuse or license a misdiagnosis of the current situation.
Let’s start with what is true. BA.5, one of the most recent Omicron variants to emerge, is everywhere. It unquestionably has an advantage in terms of transmissibility over previous Omicron lineages, most likely because it’s better at evading our existing repertoire of antibodies.
BA.5 and its close cousin BA.4 have a key mutation that enables them to sneak past an important class of so-called broadly neutralizing antibodies. These particular antibodies did a great job of preventing infections from a wide swath of earlier variants.
That’s changed in some ways.
In recent weeks I’ve watched many vaccinated friends and family members get infected with the coronavirus for the first time. The most concerning of these are cases like a colleague of mine who was infected in May and again in June, both times becoming ill.
Thankfully, reinfection a few weeks after recovery is not the norm. Scientists have shown that people who previously contracted Covid-19 are less likely to get infected with the variant du jour than people who had never seen the virus, and this trend holds true for Omicron. Early research from Qatar that has not yet been peer-reviewed showed that people who had a BA.1 infection in, say, January were significantly less likely to experience a BA.4 or BA.5 breakthrough infection months later. While more research on this is welcome, these findings are consistent with how immunity, played out at the population level, helps explain the rise, fall and magnitude of epidemic waves.
Antibodies remain a powerful defense against this coronavirus. They do many things to protect us, while also flagging the virus for destruction by other elements of the immune system. Even though some studies have found that Omicron variants may induce weaker antibody responses than earlier variants, this is most likely because Omicron causes less severe disease, thanks to immunity from vaccines and prior infections.
Our immune system works much like a wise yet frugal investor, calibrating responses according to the magnitude and extent of the various danger signals sensed during infection. Generally speaking, the greater the symptoms and disease from infections like Covid or the flu, the stronger the antibody response. When existing antibodies are good enough to keep disease to a minimum (because fewer virus particles succeed in replicating in the body), we tend to see much lower amounts of antibodies than when someone ends up hospitalized from the coronavirus. Vaccines are a great way around that problem: They stimulate our immune systems to make antibodies, and other tailored defenses, even when there is no disease.
Right now the immunological makeup of the population is a mix. People who were infected with prior variants may now be catching Omicron infections, even if they’re also vaccinated. People who have never had Covid may be getting it now. It’s true that some people who got infected from an earlier Omicron variant in December, January or even more recently are catching BA.5 now, and becoming sick from it.
Alas, this current situation, where some are newly susceptible to infection while others remain protected, is no friend to nuance. It’s difficult to generalize broadly and make bold predictions concerning how well an individual or a population will hold up against infection now or later. But despite Omicron’s knack for circumventing antibodies, it’s clear that prior immunity, be it from vaccines or previous infections, protects from severe outcomes such as death and hospitalization. There has yet to be a variant that negates the benefits of vaccines.
Recently, an early study, which was not peer-reviewed, argued that reinfections are just as dangerous as primary infections, but there is by no means a consensus on this among scientists and medical experts. (The study only really showed that getting reinfected is worse than not being reinfected.) Other scientists are concerned about the long-term risks of multiple reinfections. However, there is no debate that prior immunity, in most cases, reduces the severity of subsequent infections. Catching the coronavirus more than once or after vaccination does not necessarily put someone at risk for the most serious and chronically debilitating forms of long Covid, though more research is needed to understand what might predispose someone to that.
The Food and Drug Administration should move swiftly to authorize new booster shots that target Omicron variants. The existing data suggest that updated shots, even based on earlier Omicron lineages, would be more effective at preventing infections than continuing to use the current vaccine boosters, which are based on the original 2019 coronavirus spike.
In the meantime, if you are eligible, it’s wise to get boosted with the currently available shots, which are still outstanding at preventing hospitalization and death. (This is especially critical for older people .) Wearing a mask when mixing indoors and avoiding indoor dining when case numbers are high remains advisable for those who’d prefer not to kick the tires on their existing immunity. Fortunately, monoclonal antibody cocktails are available that remain effective against BA.5. One such product, Evusheld, is given prophylactically to protect patients, while others are used to treat severe infections. Paxlovid, which can be taken at home, may also be a good option for people who test positive and are eligible for it.
Most immunologists I know are cautiously optimistic about our long-term prospects. We don’t know exactly what this virus will do next, and we should never be dismissive of those who have a high risk profile or are dealing with long Covid. Nonetheless, most of us can have faith in our immune systems, especially when we make use of vaccines and boosters. Recorded history may hold little precedent for the ongoing Covid-19 pandemic. But this is not our immune systems’ first rodeo.
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New COVID boosters could mark turning point in pandemic
The Food and Drug Administration is expected to authorize new Pfizer and Moderna booster shots to fight the Omicron subvariants that have been triggering the vast majority of new U.S. COVID-19 cases for months. A combined 175 million doses should be available shortly after Labor Day.
What to Know About the New Booster Shots
New shots targeting the latest version of the Omicron variant will be available soon. When should you get yours? Here’s what experts recommend.With fall and winter looming, along with an anticipated seasonal surge in Covid cases, the Centers for Disease Control and Prevention greenlit a new tool for battling the pandemic: updated booster shots. The Food and Drug Administration authorized the shots earlier this week.
The new shots target the Omicron subvariant BA.5, the dominant version of the virus. Here’s what you need to know.
When will new boosters be available?
The updated boosters could roll out within days.It typically takes around one to two weeks after you get the shot for your antibodies to “kick in,” Aubree Gordon, an epidemiologist at the University of Michigan, said.
Where can I get the new booster shot?
The new vaccine will most likely be available at pharmacies, doctors’ offices and community health centers. Many mass-vaccination clinics across the country have closed, so you may have to seek out a new vaccination site. You can search a directory of sites at vaccines.gov.What is the difference between the Pfizer and Moderna boosters?
Beyond the difference in age criteria, there is no practical difference between shots, said Dr. Peter Chin-Hong, an infectious disease specialist at the University of California, San Francisco. “From your body’s immune system perspective, it doesn’t remember which brand it is,” he said.Will this Omicron-specific booster entirely replace the other boosters?
The new booster shot is a bivalent vaccine, meaning that it targets two versions of the coronavirus: the original strain, and the Omicron subvariants BA.4 and BA.5. The previous booster shot targeted only the original version of the virus.The new shots will most likely become the only available boosters. The F.D.A. no longer authorizes the previous booster doses for people in the approved age groups. People who have not received their first doses of the vaccine will still receive the original vaccines that were rolled out in late 2020.
How long should I wait to get the new booster if I recently had a shot or got Covid?
The F.D.A. authorized the updated boosters for people who were at least two months out from their last shot (whether that was the original vaccine or a booster), but you might want to wait longer. An advisory panel to the C.D.C. voted to recommend the same interval between doses, although several members voiced concerns that two months was too short.Doctors and immunologists said that in general, people should wait around four to six months after immunization or infection.
That’s because your body will probably not generate much of an immune response so soon after a previous encounter with the virus, Dr. Gordon said. “Your immunity level is so high that you’ll just neutralize immediately the antigen that’s being produced — you kind of reach a ceiling,” she said. “You don’t have that much higher to go.”
Does the new booster offer better protection than past ones?
The previous booster shots provided robust protection against severe disease. There were, however, people who had breakthrough infections even shortly after receiving booster shots, including President Biden.Doctors expect the newest iteration of boosters to offer more protection against breakthrough infections, but they won’t be bulletproof. “It’s not a game-changer,” Shane Crotty, a virologist at the La Jolla Institute for Immunology, said. “But it is going to be better.”
There is not yet real-world data on how these bivalent vaccines perform in humans. Infectious disease experts compared the process of creating the new boosters to that of the annual flu shot, which is updated each year and primarily tested on animals, not humans.
“I’m not worried at all,” Dr. Chin-Hong said. “They’re not using any new ingredients. It’s like you’re still making brownies — you’re still using chocolate, sugar, flour. Maybe now you’re using more chocolate.”
Will there be more boosters in the future?
It’s unclear whether this will be the last Covid booster offered, or whether there will be new boosters on a regular basis. The United States could offer the vaccine each year around the fall, similar to the flu vaccine, if the virus surges become predictable, Dr. Chin-Hong said.But the pandemic’s trajectory has been anything but straightforward, and it’s hard to anticipate the state of the virus over the next few months, let alone the next few years. If the virus had not evolved, we probably would not need any new shots now, Dr. Crotty said, adding, “It’s really up to the virus.”
The realities of viral evolution...
Where is Pi?
Last year, the World Health Organization began assigning Greek letters to worrying new variants of the coronavirus. The organization started with Alpha and swiftly worked its way through the Greek alphabet in the months that followed. When Omicron arrived in November, it was the 13th named variant in less than a year.
But 10 months have passed since Omicron’s debut, and the next letter in line, Pi, has yet to arrive.
That does not mean SARS-CoV-2, the coronavirus that causes Covid-19, has stopped evolving. But it may have entered a new stage. Last year, more than a dozen ordinary viruses independently transformed into major new public health threats. But now, all of the virus’s most significant variations are descending from a single lineage: Omicron.
“Based on what’s being detected at the moment, it’s looking like future SARS-CoV-2 will evolve from Omicron,” said David Robertson, a virologist at the University of Glasgow.
It’s also looking like Omicron has a remarkable capacity for more evolution. One of the newest subvariants, called BA.2.75.2, can evade immune responses better than all earlier forms of Omicron.
For now, BA.2.75.2 is extremely rare, making up just .05 percent of the coronaviruses that have been sequenced worldwide in the past three months. But that was once true of other Omicron subvariants that later came to dominate the world. If BA.2.75.2 becomes widespread this winter, it may blunt the effectiveness of the newly authorized boosters from Moderna and Pfizer.
Every time SARS-CoV-2 replicates inside of a cell, it might mutate. On rare occasions, a mutation might help SARS-CoV-2 replicate faster. Or it might help the virus evade antibodies from previous bouts of Covid.
Such a beneficial mutation might become more common in a single country before fading away. Or it might take over the world.
At first, SARS-CoV-2 followed the slow and steady course that scientists had expected based on other coronaviruses. Its evolutionary tree gradually split into branches, each gaining a few mutations. Evolutionary biologists kept track of them with codes that were useful but obscure. No one else paid much attention to the codes, because they made little difference to how sick the viruses made people.
But then one lineage, initially known as B.1.1.7, defied expectations. When British scientists discovered it, in December 2020, they were surprised to find it bore a unique sequence of 23 mutations. Those mutations allowed it to spread much faster than other versions of the virus.
Within a few months, several other worrying variants came to light around the world — each with its own combination of mutations, each with the potential to spread quickly and cause a surge of deaths. To make it easier to communicate about them, the W.H.O. came up with its Greek system. B.1.1.7 became Alpha.
Different variants experienced varying levels of success. Alpha came to dominate the world, whereas Beta took over only in South Africa and a few other countries before petering out.
What made the variants even more puzzling was that they arose independently. Beta did not descend from Alpha. Instead, it arose with its own set of new mutations from a different branch of the SARS-CoV-2 tree. The same held true for all the Greek-named variants, up to Omicron.
It’s likely that most of these variants got their mutations by going into hiding. Instead of jumping from one host to another, they created chronic infections in people with weakened immune systems.
https://www.nytimes.com/2022/09/22/...3226&surface=home-featured&variant=0_identity
Unable to mount a strong attack, these victims harbored the virus for months, allowing it to accumulate mutations. When it eventually emerged from its host, the virus had a startling range of new abilities — finding new ways to invade cells, weaken the immune system and evade antibodies.
“When it gets out, it’s like an invasive species,” said Ben Murrell, a computational biologist at the Karolinska Institute in Stockholm.
Omicron did particularly well in this genetic lottery, gaining more than 50 new mutations that helped it find new routes into cells and to infect people who had been vaccinated or previously infected. As it spread around the world and caused an unprecedented spike in cases, it drove most other variants to extinction.
“The genetic innovations seen in Omicron were far more profound, as if it was a new species rather than just a new strain,” said Darren Martin, a virologist at the University of Cape Town.
But it soon became clear that the name “Omicron” hid a complex reality. After the original Omicron virus evolved in the fall of 2022, its descendants split into at least five branches, known as BA.1 through BA.5.
Over the next few months, the subvariants took turns rising to dominance. BA.1 went first, but it was soon outcompeted by BA.2. Each one was distinct enough from the others to evade some of the immunity of its predecessors. By this summer, BA.5 was on the rise.
The U.S. Food and Drug Administration responded by inviting vaccine makers to produce booster shots that included a BA.5 protein along with one from the original version of the virus. Those boosters are now rolling out to the public, at a time when BA.5 is causing 85 percent of all Covid cases in the United States.
But BA.5 could be fading in the rearview mirror by winter, scientists said. Omicron has continued to evolve — likely by sometimes jumping among hosts, and sometimes hiding for months in one of them.
Since these new lineages belong to Omicron, they haven’t gotten a Greek letter of their own. But that doesn’t mean they’re just a slight twist on the original. Antibodies that could latch onto earlier forms of Omicron fare poorly against the newer ones.
“They could arguably have been given different Greek letters,” Dr. Robertson said.
BA.2.75.2 is among the newest of Omicron’s grandchildren, identified just last month. It’s also the most evasive Omicron yet, according to Dr. Murrell. In lab experiments, he and his colleagues tested BA.2.75.2 against 13 monoclonal antibodies that are either in clinical use or in development. It evaded all but one of them, bebtelovimab, made by Eli Lilly.
They also tested the antibodies from recent blood donors in Sweden. BA.2.75.2 did substantially better at escaping those defenses than other Omicron subvariants did.
The researchers posted their study online on Friday. Researchers at Peking University reached similar conclusions in a study posted the same day. Both have yet to be published in a scientific journal.
Dr. Murrell cautioned that scientists have yet to run experiments that will show the effectiveness of BA.5 booster shots against BA.2.75.2. He suspected that getting a big supply of BA.5 antibodies would provide some protection, especially against severe disease.
“It’s still important, but we’ll have to wait for the data to come out to see exactly what the magnitude of the boosting effect is,” Dr. Murrell said.
There’s no reason to expect that BA.2.75.2 will be the end of the evolutionary line. As immunity builds to previous versions of Omicron, new versions will be able to evolve that can evade it.
“I don’t think it’s going to hit a wall in the mutational space,” said Daniel Sheward, a postdoctoral researcher at the Karolinska Institute and co-author on the new study.
Lorenzo Subissi, an infectious disease expert with the W.H.O., said that the organization was not giving Greek letters to lineages like BA.2.75.2 because they are much like the original Omicron viruses. For example, it appears that all Omicron lineages use a distinctive route to get into cells. As a result, it is less likely to lead to severe infections but possibly better able to spread than previous variants.
“W.H.O. only names a variant when it is concerned that additional risks are being created that require new public health action,” Dr. Subissi said. But he did not rule out a Pi in our future.
“This virus still remains largely unpredictable,” he said.
Why Omicron Might Stick Around
Omicron, the 13th named variant of the coronavirus, seems to have a remarkable capacity to evolve new tricks.Where is Pi?
Last year, the World Health Organization began assigning Greek letters to worrying new variants of the coronavirus. The organization started with Alpha and swiftly worked its way through the Greek alphabet in the months that followed. When Omicron arrived in November, it was the 13th named variant in less than a year.
But 10 months have passed since Omicron’s debut, and the next letter in line, Pi, has yet to arrive.
That does not mean SARS-CoV-2, the coronavirus that causes Covid-19, has stopped evolving. But it may have entered a new stage. Last year, more than a dozen ordinary viruses independently transformed into major new public health threats. But now, all of the virus’s most significant variations are descending from a single lineage: Omicron.
“Based on what’s being detected at the moment, it’s looking like future SARS-CoV-2 will evolve from Omicron,” said David Robertson, a virologist at the University of Glasgow.
It’s also looking like Omicron has a remarkable capacity for more evolution. One of the newest subvariants, called BA.2.75.2, can evade immune responses better than all earlier forms of Omicron.
For now, BA.2.75.2 is extremely rare, making up just .05 percent of the coronaviruses that have been sequenced worldwide in the past three months. But that was once true of other Omicron subvariants that later came to dominate the world. If BA.2.75.2 becomes widespread this winter, it may blunt the effectiveness of the newly authorized boosters from Moderna and Pfizer.
Every time SARS-CoV-2 replicates inside of a cell, it might mutate. On rare occasions, a mutation might help SARS-CoV-2 replicate faster. Or it might help the virus evade antibodies from previous bouts of Covid.
Such a beneficial mutation might become more common in a single country before fading away. Or it might take over the world.
At first, SARS-CoV-2 followed the slow and steady course that scientists had expected based on other coronaviruses. Its evolutionary tree gradually split into branches, each gaining a few mutations. Evolutionary biologists kept track of them with codes that were useful but obscure. No one else paid much attention to the codes, because they made little difference to how sick the viruses made people.
But then one lineage, initially known as B.1.1.7, defied expectations. When British scientists discovered it, in December 2020, they were surprised to find it bore a unique sequence of 23 mutations. Those mutations allowed it to spread much faster than other versions of the virus.
Within a few months, several other worrying variants came to light around the world — each with its own combination of mutations, each with the potential to spread quickly and cause a surge of deaths. To make it easier to communicate about them, the W.H.O. came up with its Greek system. B.1.1.7 became Alpha.
Different variants experienced varying levels of success. Alpha came to dominate the world, whereas Beta took over only in South Africa and a few other countries before petering out.
What made the variants even more puzzling was that they arose independently. Beta did not descend from Alpha. Instead, it arose with its own set of new mutations from a different branch of the SARS-CoV-2 tree. The same held true for all the Greek-named variants, up to Omicron.
It’s likely that most of these variants got their mutations by going into hiding. Instead of jumping from one host to another, they created chronic infections in people with weakened immune systems.
https://www.nytimes.com/2022/09/22/...3226&surface=home-featured&variant=0_identity
Unable to mount a strong attack, these victims harbored the virus for months, allowing it to accumulate mutations. When it eventually emerged from its host, the virus had a startling range of new abilities — finding new ways to invade cells, weaken the immune system and evade antibodies.
“When it gets out, it’s like an invasive species,” said Ben Murrell, a computational biologist at the Karolinska Institute in Stockholm.
Omicron did particularly well in this genetic lottery, gaining more than 50 new mutations that helped it find new routes into cells and to infect people who had been vaccinated or previously infected. As it spread around the world and caused an unprecedented spike in cases, it drove most other variants to extinction.
“The genetic innovations seen in Omicron were far more profound, as if it was a new species rather than just a new strain,” said Darren Martin, a virologist at the University of Cape Town.
But it soon became clear that the name “Omicron” hid a complex reality. After the original Omicron virus evolved in the fall of 2022, its descendants split into at least five branches, known as BA.1 through BA.5.
Over the next few months, the subvariants took turns rising to dominance. BA.1 went first, but it was soon outcompeted by BA.2. Each one was distinct enough from the others to evade some of the immunity of its predecessors. By this summer, BA.5 was on the rise.
The U.S. Food and Drug Administration responded by inviting vaccine makers to produce booster shots that included a BA.5 protein along with one from the original version of the virus. Those boosters are now rolling out to the public, at a time when BA.5 is causing 85 percent of all Covid cases in the United States.
But BA.5 could be fading in the rearview mirror by winter, scientists said. Omicron has continued to evolve — likely by sometimes jumping among hosts, and sometimes hiding for months in one of them.
Since these new lineages belong to Omicron, they haven’t gotten a Greek letter of their own. But that doesn’t mean they’re just a slight twist on the original. Antibodies that could latch onto earlier forms of Omicron fare poorly against the newer ones.
“They could arguably have been given different Greek letters,” Dr. Robertson said.
BA.2.75.2 is among the newest of Omicron’s grandchildren, identified just last month. It’s also the most evasive Omicron yet, according to Dr. Murrell. In lab experiments, he and his colleagues tested BA.2.75.2 against 13 monoclonal antibodies that are either in clinical use or in development. It evaded all but one of them, bebtelovimab, made by Eli Lilly.
They also tested the antibodies from recent blood donors in Sweden. BA.2.75.2 did substantially better at escaping those defenses than other Omicron subvariants did.
The researchers posted their study online on Friday. Researchers at Peking University reached similar conclusions in a study posted the same day. Both have yet to be published in a scientific journal.
Dr. Murrell cautioned that scientists have yet to run experiments that will show the effectiveness of BA.5 booster shots against BA.2.75.2. He suspected that getting a big supply of BA.5 antibodies would provide some protection, especially against severe disease.
“It’s still important, but we’ll have to wait for the data to come out to see exactly what the magnitude of the boosting effect is,” Dr. Murrell said.
There’s no reason to expect that BA.2.75.2 will be the end of the evolutionary line. As immunity builds to previous versions of Omicron, new versions will be able to evolve that can evade it.
“I don’t think it’s going to hit a wall in the mutational space,” said Daniel Sheward, a postdoctoral researcher at the Karolinska Institute and co-author on the new study.
Lorenzo Subissi, an infectious disease expert with the W.H.O., said that the organization was not giving Greek letters to lineages like BA.2.75.2 because they are much like the original Omicron viruses. For example, it appears that all Omicron lineages use a distinctive route to get into cells. As a result, it is less likely to lead to severe infections but possibly better able to spread than previous variants.
“W.H.O. only names a variant when it is concerned that additional risks are being created that require new public health action,” Dr. Subissi said. But he did not rule out a Pi in our future.
“This virus still remains largely unpredictable,” he said.
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The next U.S. COVID wave is coming. Why it will be 'much weirder than before.'
It has become pretty much impossible to keep up with all of the latest coronavirus variants, but there's most likely a new wave on the way.
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