When the original Omicron swept across the country this winter, it launched America into a new COVID era, one that almost everyone shares –95 percent of adults, according to one estimate by the Centers for Disease Control and Prevention, have some immunity to the virus through vaccinations, infection, or both. Since then, however, Omicron subvariants are still capable of causing large waves of infection. They achieved this by eroding our current immunity.
This will keep happening. says Jesse Bloom, an evolutionary virologist at the Fred Hutchinson Cancer Center. Experts are cautiously optimistic that the changing pace of resurgence will eventually slow, and for many people, cases are already more benign and hospitals are not overcrowded. But as the virus continues to change, the only real guarantee is that it will be different — and that its changes won’t necessarily affect everyone uniformly.
The evolution of SARS-CoV-2 follows a well-understood dynamic: When a variant sweeps around the world, it leaves behind a lot of immunity to itself. This puts severe evolutionary pressure on the virus to turn things around; Any subsequent variant must somehow avoid immunity to earlier variants to continue finding new hosts. There are no limits to how long the coronavirus can continue to do this. The well-established respiratory viruses that cause the flu and the common cold are still evolving to keep re-infecting us over and over again.
But immune escape is not an intrinsic characteristic of any new variant. SARS-CoV-2 does not go up a ladder with each variant, but rather becomes more and more immune escape over time. Instead, think of the coronavirus as a tireless rabbit chased by our immune system, a tireless dog. The rabbit always runs away from the dog, and the dog always tries to catch up. The space in which they have to chase each other is so large that it might be infinite on human time scales. as bloom He told me earlierthe number of potential mutations in SARS-CoV-2 far exceeds the number of atoms in the known universe.
Occasionally, a rabbit might make a dramatic omicron-like leap and shoot forward for a while until our immunity becomes aware. How often this will happen is hard to predict. “It probably depends on how much the ‘Omicron’ black swan event happened,” says Adam Loring, a virologist at the University of Michigan. “The Omicron was very different and very unusual compared to everything that happened before.” Could it happen again? Most people probably think no but… you don’t want to burn twice.” Whether an Omicron-like event occurs every two years, 20 or 200 years could mean different paths to the future of COVID. But at this point, we only have two and a half years of data to follow, So expect the prediction at your own risk.
More predictably, though, SARS-CoV-2 is likely to make fewer gains over time, accumulating mutations that make it progressively better at re-infection. Virologists call this “antigenic evolution”. (antigen It refers to the parts of pathogens that our immune system recognizes. For SARS-CoV-2, this is mostly a spike protein.) Different viruses appear to be capable of different rates of antigen development. Of the four seasonal coronaviruses that cause the common cold, for example, OC43 and 229E evolve at a rate 0.3 to 0.5 adaptive mutations in their spike proteins every year. Kathryn Kistler, also a virologist at Fred Hatch, who has studied the evolution of seasonal coronaviruses, says a third ingredient, NL63, doesn’t seem to change much at all. She is currently trying to confirm this with blood serum samples collected in the 1980s and 1990s. And there are so few samples of the fourth coronavirus, HKU1, that we don’t have enough to tell which trend.
Influenza is much better studied, and different types of influenza show different rates of development from one another. Among the most common, influenza B is the slowest, roughly on a par with the OC43 and 229E coronaviruses. H1N1 flu is faster, and H3N2, the dominant flu strain in the world right now, is the fastest. The differences may be due, at least in part, to the form of the antigen that our immune system recognizes. For example, the thorny protein in coronaviruses needs to be altered enough to trick the immune system, but not so much that it stops working completely. H3N2 can throw off a smaller change in its counterpart of the spiky protein: “Often one mutation—sometimes two—[that] “The virus can give me a huge advantage,” Kistler told me.
Contrast that with measles, a virus that has barely evolved over decades. Our antibodies recognize multiple parts of their core protein. A recent study found that At least five out of the eight major sites of this protein need to be changed immediately to undermine our immune defenses. Having a mutation in just one or two of these sites does not give much advantage, but to have all five of these sites at once is very unlikely. So any potential new variants fade away, and the dominant measles variant remains quite stable.
However, SARS-CoV-2 evolves antigenically faster than any of these viruses, even faster than H3N2. This could be due to the uniqueness of the Spike protein, but some of this unusually fast pace over the past two years may also have to do with the virus being new. When a new strain of H1N1 “swine flu” emerged in 2009, Kistler noted, it, too, had a blast at first before slowing down. The alpha and delta variants of the coronavirus emerged during a time when many naïve people were immune to infection, and the first variants often succeeded in becoming intrinsically more transmissible. Bloom says the virus can only increase its transmissibility so much, so SARS-CoV-2 will have less and less room for improvement. However, it could go on to find new ways to circumvent immunity, as Omicron sub-variants do.
However, the nature of the immunity against which SARS-CoV-2 develops is also changing. Currently, some people are immune to the original, alpha or delta coronavirus, others are immune to the Omicron family, and others have both. As more variables emerge, our individual exposure history will be more diverse; Depending on our previous immunity, some of us may be more susceptible than others to a new variant. The effect will be less consistent. We’ve already seen this with the Omicron sub-variants, where the countries with smaller previous waves are Experiencing larger BA.5 waves. Some people may also have weaker immunity than others; Older adults, for example, tend to have less persistent immune responses to SARS-CoV-2, which is why this group has always prioritized boosters. Powerful vaccine updates and booster campaigns can help everyone’s immune system keep going.
Instead of always trying to catch up with the virus, can we expand our immunity and beat it? Although our current vaccines are still very good at protecting against severe disease, they are not capable of doing so. The The White House is now promoting– Although not really funded –Next Generation Vaccines That could be better: mass coronavirus vaccines that scientists hope will elicit antibodies against parts of the spike protein that don’t change much, or nasal vaccines to elicit antibodies in the nose and mouth where the virus replicates first, possibly stopping infection altogether.
But these ideas are not new to SARS-CoV-2 – researchers have tried these methods of dealing with influenza for many years. Universal influenza vaccine Still elusive. The flu vaccine, FluMist, does exist, but its effectiveness is quite mixed: It was originally thought to be more effective than the vaccine, and then is thought to be less effective — so much so that The CDC withdrew the vaccine from 2016 to 2018– So reformulate it. In any case, FluMist clearly does not come close to preventing all cases of mild flu infections. Barring any major innovations in vaccine technology, our immune systems may be the dog that has been chasing the coronavirus rabbit for the long haul.
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