MADDIE SOFIA, HOST:
You're listening to SHORT WAVE from NPR.
In the last few months, scientists have moved at an unprecedented speed to learn as much as they can about the coronavirus. And the good news is new information has been coming out really fast. But that also makes it tough to stay on top of.
ED YONG: It's truly incredible. I mean, I'm talking to you now, and every sentence is out of date before I started, probably.
SOFIA: That's Atlantic science reporter Ed Yong, who, these days, is pretty busy.
YONG: I've been pretty much continuously reporting for the last 812 years.
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SOFIA: Ed's been so busy precisely because there is so much to learn about this pandemic. And in his latest story for The Atlantic, he writes about some clues scientists are beginning to uncover that may suggest why this coronavirus has taken off.
YONG: And I think actually, even though there are a huge number of unknowns left, it is astonishing how much we know about this virus considering that literally no one knew that it existed mere months ago.
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SOFIA: This episode will break down what the early science suggests about why this virus has spread so much faster than similar viruses like SARS, where it came from and if it'll slow down here in the U.S. as the weather gets warmer. I'm Maddie Sofia, and this is SHORT WAVE, the daily science podcast from NPR.
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SOFIA: As we say at the top of all of our coronavirus episodes, we are learning a lot about this virus really fast. The information in this episode is what we have learned as of our recording on Monday, March 23, and what we know will probably change.
YONG: Agreed.
SOFIA: OK. So the coronavirus that's causing this pandemic is part of a larger group or family of coronaviruses. So some cause the common cold. There are famous ones like MERS and SARS. But only this one has caused a pandemic. So, Ed, let's talk about why that might be.
YONG: So if we look at the structure of the virus, we see certain clues about why it's behaving in such an extreme way. So like all coronaviruses, this one is basically a ball with some spikes sticking out of it. Those spikes are what the virus uses to launch an infection. They bind to a protein called ACE2, which sits on the surface of our cells. And this binding, like a key fitting into a lock, is the first stage of any infection.
Now, if we compare the shape of the spike protein on this new coronavirus to that of, say, the original SARS virus from 2003, we see that it sticks to the ACE2 protein much more tightly, much more strongly. And that is likely to influence the course of an infection. So in very broad terms, the stronger the stick, the less virus you probably need to actually start an infection.
SOFIA: And that's really important - right? - because if it doesn't take as much virus to start an infection, it's easier to transmit the virus from person to person. It's what we call an infectious dose.
YONG: That's right.
SOFIA: So basically, this virus is stickier than the virus that caused SARS.
YONG: That's right. This virus is better at recognizing and latching on to human cells...
SOFIA: Yeah.
YONG: ...We think.
SOFIA: Ed, in your piece, you suggested that some of the virologists that study these families of viruses have started calling the SARS virus SARS classic...
YONG: (Laughter) Right.
SOFIA: ...Which is (laughter) - it's kind of delightful, in a way.
YONG: It is a moment of, like, light comic relief in the middle of this horrific catastrophe. I think that because this new virus has been called SARS-CoV-2 and the original virus, the SARS from 2003, is technically called SARS-CoV - it's very difficult to talk about the two of them without getting confused and without sort of muddling up which SARS you were talking about. So yeah, virologists have found all kinds of hilariously colloquial work-arounds, calling the first virus original SARS or SARS classic as if it were some kind of soda.
SOFIA: (Laughter) Yeah.
YONG: Could be diet SARS.
SOFIA: Right. And as we know, the sodas get worse and worse as more of them get produced - is how I feel.
YONG: Agreed.
SOFIA: OK.
YONG: It's meant for so many levels jokes.
SOFIA: OK. So those spikes that the viruses use to attach to our cells - those spikes have to be activated. And that activation happens more readily in this coronavirus than the classic SARS, or SARS classic virus.
YONG: It seems that way. So the spike consists of two halves, which must first be split apart for the virus to begin infecting a cell. And that split happens with some difficulty with SARS classic, but it seems to occur more readily with this new virus because the two halves can be separated by an enzyme called furin, which is quite widespread in the human body.
SOFIA: Right. So much like an avocado...
YONG: (Laughter).
SOFIA: ...That spike protein is really only ready to do its job once it's split in half. And this coronavirus can make use of a protein in our body that is - you know, our body's already naturally producing...
YONG: Yes.
SOFIA: ...To make that cut for it.
YONG: Correct. And thanks for ruining avocados for me.
SOFIA: (Laughter) OK.
YONG: (Laughter) You monster.
SOFIA: So basically, that split seems to be happening easier in this coronavirus than in the SARS coronavirus, and that split is really important to activating the infection process.
YONG: Correct.
SOFIA: You also wrote about how this plays into a potential reason why the virus can spread between people before symptoms show up. Talk to me about that.
YONG: Right. So in most respiratory viruses, you either get infections in the upper airways - in which case symptoms are mild, but the virus spreads more easily - or you get infections in the lower airways - in which case symptoms are more severe, like pneumonia, but the virus is harder to transmit. It seems that the new coronavirus can infect both sites. So perhaps it infects the upper airways, causing mild symptoms and spreading easily before moving down into the lower airways and causing some of the more severe illnesses we've seen in the worst COVID-19 cases. And maybe the reason it can do all those things is that it relies on this furin enzyme, which is found in lots of different tissues.
SOFIA: Right.
YONG: Now, of course, this is still conjecture. It's kind of a - if you look at it, it's a plausible story. It makes sense, and it checks out.
SOFIA: Yeah.
YONG: But it could also be completely wrong.
SOFIA: Yeah. This is actually kind of, you know, newer data. That's kind of interesting because I think initially, we thought, you know, the majority of that infection is in the lower respiratory system, right? That's very similar to SARS or the classic SARS. And now we're starting to get, maybe, some data that shows that that upper respiratory tract can be infected, too. But like you said, this is pretty preliminary stuff.
YONG: Right. You know, I keep reminding myself that this is a virus that no one knew about.
SOFIA: Yeah.
YONG: So we're really racing to understand it even while we're also trying to control it.
SOFIA: Absolutely. Absolutely. OK, so let's talk about the animal origins of this virus.
YONG: Sure.
SOFIA: What we know now is potentially that the closest wild relative of this virus is found in bats. Is that right, Ed?
YONG: Yeah, that's right. So there are millions, perhaps billions of coronaviruses out there in other animals. And of all the ones that scientists have found so far, the one that most closely resembles SARS-CoV-2 is one that is found in bats. So it's likely that the virus originated in some kind of bat and eventually hopped into humans either directly or via another intermediate species.
SOFIA: Right. And so that jump from an animal to us - there's a difference in what happened with this virus, we think, versus what happened with the original SARS virus. Is that correct?
YONG: That's right, yeah. When a virus enters a new host, there's often a brief period of acclimation, a little span of time when it's mutating a bit and finding ways of better existing within that new type of body. And that's what we saw with SARS classic. It took a little while before the virus became very good at infecting humans, and it doesn't seem to be the case with this new coronavirus. It seems to have been a really good human pathogen right off the bat...
SOFIA: Yeah.
YONG: ...So to speak.
SOFIA: Yeah. So basically, SARS had to take another step before it was good at infecting us. And regardless of where this virus came from, as soon as it got into us, it seems to be just kind of great at infecting humans.
YONG: Right. Yeah. It just seems like it was good to go from the off.
SOFIA: OK. So let's talk a little bit about, you know, the seasonality, potentially, of this virus.
YONG: Sure.
SOFIA: So what did the experts that you talked to say about whether or not this outbreak will let up soon with the change of the seasons?
YONG: So it's really hard to say. And there are actually several papers out there now that seem to come to differing conclusions about the seasonality question. So in general, coronaviruses do tend to infect people in the winter, and they disappear in the summer because it's hotter and more humid. Now, it's possible that this new coronavirus will also behave in the same way. And a lot of the people I spoke to felt that seasonality was likely. The problem is that the virus is now spreading through a global population of people who have no pre-existing immunity to it.
SOFIA: Right.
YONG: And it's just moving really easily from one person to another. The speed at which it's moving might be a little slower come the spring or summer but not enough to curtail the spread of the pandemic on its own. One epidemiologist explained it to me like this. It's as if the world is just full of tinder, and you've got this gigantic wildfire that's blazing through it. And hoping that seasonality will help is a bit like hoping that a light rain is going to douse it. It might make it a little weaker.
SOFIA: Sure.
YONG: But that fire is still going to blaze.
SOFIA: So one thing that I found really interesting in your article was the state of coronavirus research in general and how that plays into how prepared we are right now. Like, this is a big group of viruses that cause a decent bit of disease throughout the world. But one researcher you talked to said that until recently, not that many people were studying coronaviruses.
YONG: Right. So a very small group of people - maybe, you know, several dozens of researchers - have focused on coronaviruses for a few decades now. But it really has been a very, very niche field, even among virologists. When SARS classic first emerged, I think coronavirus researchers were really shocked that the things that they were studying were suddenly of public health importance.
SOFIA: Right.
YONG: And they are even more flabbergasted now.
SOFIA: And so because of that - because even after SARS, there wasn't a huge uptake in how many people were studying this, we don't necessarily have surveillance networks in place for coronavirus like we do for the flu.
YONG: Right. A lot of our preparedness measures in general have been focused on flu as the most likely next pandemic - and for good reason - because flu actually is the most likely next pandemic. It just so happened that this time, it was a coronavirus. And we don't have surveillance for coronaviruses. We know, actually, surprisingly little about coronavirus biology. And all of those deficiencies have contributed to this dire situation that we're facing when we don't know enough but we're forced to act as quickly as possible.
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SOFIA: OK, Mr. Ed Yong. Thank you for coming by and talking about the science of this virus with us.
YONG: Thanks, Maddie.
SOFIA: Ed Yong. We have a link to his piece in The Atlantic in the notes of this episode, which was produced by Brent Baughman, fact-checked by Emily Vaughn and edited by Viet Le. I'm Maddie Sofia back tomorrow with more SHORT WAVE from NPR.
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