MADDIE SOFIA, HOST:
Hey, real quick - if you're new to the show, make sure to subscribe or follow us on your podcast app of choice. That way, you get fresh episodes as soon as they're out, first thing every weekday - ah, the smell of fresh baked science in the morning. You love it.
You're listening to SHORT WAVE from NPR.
The words virus and mutating don't sound too good together.
(SOUNDBITE OF NEWS MONTAGE)
UNIDENTIFIED REPORTER #1: Researchers just released a preliminary study that suggests the coronavirus may be mutating.
UNIDENTIFIED REPORTER #2: May be mutating.
UNIDENTIFIED REPORTER #1: Is that true?
UNIDENTIFIED REPORTER #2: The new strain appeared in February in Europe and migrated quickly to the East Coast of the United States...
SOFIA: But while mutations in movies and comic books are always a big deal, in reality, they're really not.
ED YONG: We're always fed this idea that mutations are scary and important and consequential, and most of the time, they're really none of those things. They're just a natural part of viral existence.
SOFIA: This episode, from The Atlantic, science journalist Ed Yong is back on the show for a little reality check on coronavirus mutations. I'm Maddie Sofia, and this is SHORT WAVE, the daily science podcast from NPR.
All right, Ed, so you've got a big piece about this out for The Atlantic. First things first - viruses going to virus.
YONG: Yeah.
SOFIA: And mutations are normal when the virus replicates or makes copies of itself.
YONG: Yeah. So viruses infect other cells and make more copies of themselves. In that process, they have to make duplicates of their genetic material, and that process is sloppy, so the duplicates end up with errors in them, and we call those mutations. They're just like typos in the virus' genes, and they're just completely normal. So whenever viruses infect and reproduce and spread, they'll end up with mutations.
SOFIA: Right. And plenty of mutations do nothing or result in the virus no longer being able to survive. So those strains just die out, basically.
YONG: Yeah, totally. A lot of mutations are detrimental to the virus. The vast majority are completely silent or cosmetic. And it's only a very small minority that we would worry about, that would make the virus, for example, more transmissible or better able to cause disease. Those are pretty rare.
SOFIA: Yeah. So OK - that brings us to this study. It came out a couple weeks ago from Los Alamos National Laboratory. And this was a preliminary study that described the emergence of a more transmissible form of the coronavirus. And that got picked up by the Los Angeles Times and got a ton of attention.
YONG: Right. I think the article was very overblown and presented a very scary perspective to people. I was seeing online people getting really worried, like, really disheartened by this news, the idea that the pandemic was bad enough and now maybe it's going to get even worse. But I think it goes to show that these quite preliminary results can proliferate in a way that really makes a difference to people who are already struggling with a lot of fear and anxiety.
SOFIA: So OK, we'll come back to that study in a little bit. But let's talk about how viruses mutate and how new, you know, strains are formed. You've described it like a family tree. New mutations are like branches and twigs of that tree, but that doesn't necessarily mean a whole new strain of that virus. So let's talk about what constitutes a new strain.
YONG: Right. So when viruses mutate, you get these branches and twigs of the virus family tree that have their own distinctive sets of mutations. And we would call those lineages. But a new lineage is not automatically a new strain. So viruses change all the time, and new strains emerge when those changes really matter. So they might be more transmissible. That's better at spreading. They might be more virulent. That's better at causing disease.
So the distinction - the analogy I used in my piece is that - think of strains as being like breeds of dogs.
SOFIA: Sure.
YONG: So like, a corgi would be clearly very different to a Great Dane or a Chihuahua, but a black-haired corgi is not going to be very different to a brown-haired corgi, for example. So the nature of the differences matter.
SOFIA: Yeah.
YONG: That's what separates a strain from just the lineage.
SOFIA: Are you big a corgi fan there, Ed?
YONG: You know, I'm not saying that this is all an elaborate way of just writing and talking about corgis more, but I'm not not saying that either.
(LAUGHTER)
SOFIA: So it's - I think it's important for us to kind of break down that viruses mutate in different ways. Some of them mutate really frequently, so they're making more mistakes, which could potentially lead to more strains. But it also matters where those changes happen. So, like, our body's immune system recognizes certain parts of the virus. If those parts change, that can be a problem. That's part of why the flu is so tricky.
YONG: Right. So the flu virus changes, mutates very quickly. Some of those mutations change the surface molecules that are recognized by the immune system. And that is why the flu vaccine needs to be updated on a regular basis.
SOFIA: Right.
YONG: Because new strains do emerge that aren't recognized by the immune system in the same way as earlier strains. And this is why flu is such a challenge to deal with.
SOFIA: So how does the coronavirus compare to the flu in, you know, in this mutation rate, for example?
YONG: Right. So obviously, we don't know exactly how fast this new virus mutates because it is new.
SOFIA: Sure.
YONG: But based on other coronaviruses that scientists have studied, they seem to mutate much less quickly than the flu does - about 10 times less quickly. And this new coronavirus, SARS-CoV-2, does seem to be mutating at the same kind of slow pace that you would expect based on other coronaviruses. So it's not going to be changing as rapidly as flu does.
SOFIA: Right. Right. So I think it's worth trying to explain the Los Alamos study a little bit more. It gets kind of technical, so we'll go slow. But it reveals something interesting about how viruses spread. So they were looking at two versions or lineages of the coronavirus called lineage D and lineage G.
YONG: Yeah.
SOFIA: Tell me the difference between those two versions.
YONG: So D is the original, and that's the group of viruses that first emerged in Wuhan, China. And at some point, they developed one mutation that changes one tiny part of a molecule that the virus uses to interact with cells. And that gives rise to the so-called G viruses.
SOFIA: And so for a while, the early version, the D version, was more common. Like, that was infecting more people. But over the last few months, researchers detected more of this G version.
YONG: Yes. The G viruses became more common in some parts of the world, including Europe, parts of the U.S., Australia and so on.
SOFIA: And so why do we think that is?
YONG: So there are two possible reasons. One is what was suggested in the paper and in the LA Times coverage, which is that the G viruses are more transmissible, that they spread more easily. But the other is that the G viruses just got lucky because we know that a lot of the spread of these viruses around the world happened through just chance events.
SOFIA: Right.
YONG: It's just, like, one - or a small number of people moving from - first from China to Italy and sparking off epidemics in Europe, then people moving from Europe to the U.S. So if the G viruses get into the right people at exactly the right time, they get to be the ones that start off the epidemic in Europe and then in the U.S. and in other parts of the world. So their success might have nothing to do with the viruses themselves and everything to do with the people in whom they happen to sit.
SOFIA: Right. Because all of this concern is based on the fact that this one virus is circulating more widely now. But it's not like the different versions of this virus have been tested side by side. Like, we don't have any data as of this point that actually shows that one of these viruses passes from one human more quickly to another.
YONG: Yeah. That's absolutely right. And that's why all the virologists I've spoken to are really skeptical, for the moment, about these claims about some new transmissible strain. We cannot say that, based on current evidence. We would need the kind of experiments you're talking about. And that just hasn't happened yet and might not happen for a while because people with the right facilities to do those experiments are too busy trying to do things like find drugs or vaccines.
SOFIA: Yeah. And I think the point that you made in your piece is that this probably won't really change what we need to do right now. And so these scientists, although they're interested in this, they're like, this isn't going to change that we need to socially distance. This isn't going to change that we need a ton of testing right now. So this is kind of, honestly, not a priority.
YONG: Yeah. And that was a bit surprising to me because I wasn't expecting people to say that, especially people whose entire careers are built on studying exactly these kinds of issues, like the rise of new mutations and the evolution of viruses. Those folks did say very clearly that this is going to be a really interesting thing to study about a year from now or, you know, two years from now. For the moment, whether there is a new strain or not - and they still think that there is not - it doesn't change the fact that we need better testing, that we need more contact tracing, that the public health stuff is what's important right now. And that isn't materially altered by this debate.
SOFIA: Yeah. So you recently wrote about how this pandemic is really confusing for people. You know, I think we all want these big answers, and the media kind of jumps in to try and fill that void, and that can actually make things more confusing.
YONG: Yeah. I think here is a classic example of those dynamics at work. You have a preliminary study that has not been formally published that gets released. Scientists discuss it, and then someone writes a piece taking it at face value. And then it, well, goes viral.
And, you know, I think that it's almost easier to believe that we're in the situation that we're currently facing because of something to do with the virus itself, that this already difficult antagonist has become even more difficult to control, rather than grappling with how bad our response has been, rather than to really deal with failures in leadership, in federal coordination, the failure of rolling out widespread testing. All of these have severely compromised America's ability to control the pandemic, and they have made far more of an impact than anything the virus has or hasn't done in the past months. And I think those are the things we need to be focusing on.
(SOUNDBITE OF MUSIC)
SOFIA: OK, Ed Yong, I appreciate you. Thank you for coming on.
YONG: Thanks, Maddie.
SOFIA: There are links in our episode notes where you can read Ed's recent article about all this and follow his reporting on the coronavirus for The Atlantic. This episode was produced by Brent Baughman, fact-checked by Emily Vaughn and edited by Geoff Brumfiel. I'm Maddie Sofia. Thanks for listening to SHORT WAVE from NPR.
Copyright © 2020 NPR. All rights reserved. Visit our website terms of use and permissions pages at www.npr.org for further information.
NPR transcripts are created on a rush deadline by an NPR contractor. This text may not be in its final form and may be updated or revised in the future. Accuracy and availability may vary. The authoritative record of NPR’s programming is the audio record.