Deep Dive
Shownotes Transcript
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Hey, shortwavers, Emily Kwong here. So this month marks five years since officials at the World Health Organization declared COVID-19 a pandemic. And we have come a long way since then. Researchers have figured out ways to slow the spread of the SARS-CoV-2 virus with masking and air filtering. They've developed safe treatments and vaccines. And they've tracked hundreds of thousands of different mutations.
And now we know something else, how those mutations evolved. Because if you remember, in March of 2020, a lot of scientists predicted that the coronavirus was not going to evolve very much. It was thought that the coronavirus mutated pretty slowly, like half as fast as the flu or only a quarter as fast as HIV. This is Sarah Zhang, a health writer for The Atlantic.
Back in 2020, some scientists thought that once vaccines arrived, they would offer years of protection. Unfortunately, I think we know what actually happened, which is that in the winter of 2020, we sort of got like this first big variant, what was known as Alpha. And then we just kept getting more and more variants.
Beta, Delta, Omicron. The coronavirus continued to mutate to make these evolutionary jumps that helped it survive. And for a long time, scientists didn't know why. Sarah wrote a piece about this for The Atlantic last month.
Focusing on a series of studies that point to a relatively new idea that the virus could be incubating and mutating further in one specific group of people. When the virus jumps from person to person, it gets about two mutations a month. But sometimes when the virus finds someone who maybe their immune system is a little bit suppressed, it's a little bit more likely to mutate.
they aren't able to fight off the virus. Instead of, you know, being sick for like a week or two weeks, they might be sick for weeks or weeks on end or even months. Meaning that in people who are immunocompromised, the virus may be able to stick around and evolve. And in this process, it's almost like a training camp for the virus to figure out how to evade the human immune system. The virus, during a long, persistent infection, might find just the right combination of mutations that makes it really good at infecting lots and lots of people.
So today on the show, rethinking the rules of viral evolution and how scientists are racing to catch up and predict COVID's next move. I'm Emily Kwong, and you're listening to Shortwave, the science podcast from NPR.
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So just to take a big step back, Sarah, why do viruses mutate? And what does that do to us when we get infected? Yeah, so when a virus infects you, it's basically copying itself millions and billions of times over and over again, right? So it can spread?
Yeah. To different cells. Right. Because like, you know, it infects one cell, then it makes like thousands of copies of itself. And then now you have thousands of copies to infect thousands more cells. It's like basically a numbers game. Like the more of yourself you can make, the more of your progeny out there can continue to infect more people to continue to have more progeny out there.
Most of these mutations, they don't really do anything. But in like a really small number of cases, that mutation or maybe even the whole set of mutations might give the virus some advantage. Maybe it makes it better at entering cells or maybe it makes it better at, you know, infecting the upper airway so you can cough it up and then infect someone else. Okay, so there's almost like one star pupil or a few star pupils who will prove anything.
advantageous against the army of the human immune system. Exactly. The star pupil is going to be one that just has a slight edge. It's a little bit better at copying itself. It's going to keep doing it more and more and more. And it has. It has continued to evolve. But right now, most of the variants that are dominant in the U.S. are descendants of Omicron. Tell us about Omicron's origin story. Like, when did it appear as a variant? And what surprised scientists about it immediately? Yeah, I sort of remember it happening, I think, just before Thanksgiving in 2021. And
I think at that point, vaccines were pretty available. Things were maybe starting to settle back to normal. And then scientists made this big announcement that was really stunning if you knew anything about viral evolution. And I think it was scientists in South Africa who first noticed it. They said, we have this new variant that we found.
It has 50 mutations. Whoa! 30 of them. In bracket, 50 mutations. Yeah, 50, five zero mutations. 30 of those mutations are all in the spike protein. And the spike protein, if you remember, is like kind of the key that viruses use to enter our cells. So it's really important. It's like also what's in our vaccines. So it's how our immune system, once we've been vaccinated,
recognizes a virus. If you think of a vaccine as like giving your immune system a mugshot, lots of changes in the spike protein mean like, you know, the virus is like put on a hat and like changes glasses and it's closed. So it's like not as recognizable to your immune system. Omicron rolled up and was like, I'm going to be something like you've never seen before. Yeah, exactly. And so...
clearly this was going to be a sign of trouble because our immune systems were not really good at recognizing Omicron. Like people, even people who had been vaccinated, even people who had gotten COVID, you know, pre-Omicron, their immune system had this like outdated mugshot of what this virus now looked like. So it was pretty clear that
We were probably going to get reinfected or even if you're vaccinated, you're probably going to get infected. Yeah. I remember this period as the Omicron wave of 2021. And you write that scientists think Omicron's rapid evolution has something to do with the virus incubating and mutating in immunocompromised people.
It's a super interesting idea. Can you explain why scientists suspect that? Yeah. So we don't like have, we haven't traced Omicron back to like one person. And I just want to be clear about that. There's been a lot of sort of indirect evidence to suggest like this is what happened. So, you know, I mentioned Omicron has 50 different mutations, but 30 of them are all in spike. Over time, as scientists have been studying these persistent infections, immunocompromised people, they see this very clear pattern that you
you not only get a lot of mutations, but you get them concentrated in spike. And the reason is probably because, you know, as the virus is infecting someone for weeks or months at a time, the immune system, even as someone who's immunocompromised, still like can do a little bit, right? Not enough to entirely clear the virus, but maybe enough to like suppress it a little bit. And it's still like recognizing the virus, right?
But if the virus is able to change its spike, then it gets a little bit harder. They're kind of in this back and forth cat and mouse game. It's really about the length of infection. You know, just like basically the more time you have, the more even random mutations you can accumulate. And some of these mutations will probably give it some sort of edge. And in most cases, it's not enough of an edge for the virus to then spread from that initial person. But in
Really rare cases, like probably Omicron, it does. What kinds of immunocompromised patients are we talking about? Do they include folks with long COVID? Yeah, that's a really good question. You know, the researchers I talked to who've studied this are really clear that these persistent infections aren't necessarily the same thing as long COVID.
But with long COVID, it's not like necessary that you are shedding viruses the entire time you're sick. With someone with one of these persistent infections, like you are shedding virus. So it's not the same thing as long COVID. It's possible that some people who have long COVID actually have one of these persistent infections. But I don't want to say that. I want to be pretty clear that they're not thought of as the same thing. So.
When it comes to just the rapid mutation capability of SARS-CoV-2, is it simply that it's just more powerful than other viruses? It's just better somehow? That's such a good question. And I think really one of the open questions of what's going on here, right? It's definitely true. We have not seen this with any other virus. You know, is this dynamic something specific to
SARS-CoV-2 or is it just like when you have a new virus jumping into new species for the first time it just has like so many opportunities to mutate that it's just had all these chances because it's new or is there something that is gives it some sort of ability that other viruses don't and I don't think we entirely know yet
This phenomenon where a virus mutates more in immunocompromised patients, can that happen with any virus like HIV or bird flu? Yeah, we haven't seen this exact pattern in other viruses. But a few years ago, before COVID, one of the scientists I talked to had studied viruses.
flu in patients who were immunocompromised and had the flu for weeks and weeks. And he did find that you could see some of the same mutations over weeks inside these immunocompromised patients as you would then see the seasonal flu next year. Wow, that's really interesting. Though the thing that's different is that he didn't find any evidence that the flu viruses from immunocompromised patients was actually seeding next year's seasonal flu, right? He just thought they were happening in parallel.
With SARS-CoV-2, it seems like one actually is seeding the other. These persistent infections are seeding the viruses that then infect all of us over the next few years. So I think this is somewhat new. That's why it was so surprising that this could happen. Yeah, but
But part of what's cool about COVID is it's been sequenced in such depth. Like we've really been tracking its every move. Yeah, we've never sequenced any other virus to the extent that we sequence COVID. So there's probably a lot of stuff going on in viral evolution that we are just entirely not aware of because we are not sequencing other viruses, right? There are like
At least dozens, maybe even hundreds of viruses that cause the common cold. We don't really have a great grasp of how they evolve from year to year or mutate from year to year. Man, so COVID really is changing how virology is done. It could change our understanding of viruses. If this tracking were to especially focus on infections within those who are immunocompromised, what would that do to disease surveillance?
Yeah, something really interesting is that when scientists, even back in 2020, were looking at how viruses change in persistent infections, they were seeing some of the same mutations that ended up showing up in these variants months and even sometimes years later. Oh, so almost like a crystal ball? Yeah, exactly. What's happening inside one infection is...
basically like a sped up version of what might happen out in the world. So, you know, there's some thought that like, hey, if we could just keep a closer eye on these persistent infections, maybe that will give us a sense of what the virus is going to look like, you know, a month from now or maybe a year from now. And I think it's important to sort of keep an eye on these things to make sure you
We see them early enough that we can start to take action. But also, I think we have to keep an open mind and, you know, we might not know what's going to happen in the future. Well, in the meantime, you are following as closely as you can. Sarah Zhang, thank you so much for talking to me. Thank you for having me.
This episode was produced by Hannah Chin and edited by our showrunner, Rebecca Ramirez. Tyler Jones checked the facts. Robert Rodriguez was the audio engineer. Beth Donovan is our senior director. And Colin Campbell is our senior vice president of podcasting strategy. I'm Emily Kwong. Thanks for listening to ShoreWave, the science podcast from NPR.
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