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Listen: Coronavirus Mutations   25%

After a new variant of the coronavirus spread throughout the United Kingdom, daily cases hit record levels and the prime minister ordered a national lockdown. Now more mutations from South Africa and Brazil have made headlines. The prospect of a more transmissible virus has many worried, but exactly how bad are these new mutations? And should you change anything you’re doing already?

Vineet Menachery, a virologist at the Galveston National Laboratory who studies coronaviruses, joins staff writer James Hamblin and executive producer Katherine Wells on the podcast Social Distance to explain.

Listen to their conversation here:

Subscribe to Social Distance on Apple Podcasts, Spotify, or another podcast platform to receive new episodes as soon as they’re published.

What follows is a transcript of the episode, edited and condensed for clarity:

Katherine Wells: My understanding is that virus mutations happen all the time. And the lesson I learned in the early days of this pandemic was: Don’t worry about them too much because it’s normal, and it doesn’t mean it’s worse just because it’s mutated. These latest mutations in the news seem different and more worrisome, but I don’t understand why. Are they in fact different and more worrisome than all the previous evolving mutations?

Vineet Menachery: The quickest answer at this point is: We don’t know yet. The mutations that we think about are twofold: There are mutations that allow the virus to replicate or transmit better. These are worrisome because obviously that just changes how fast this virus can spread. And that’s one of the concerns for these variants. There’s the U.K. variant. There’s a South African variant. And, most recently, there’s a variant in Japan that’s been traced back to Brazil. Each of these have a mutation at a position in the spike protein that are associated with, potentially, an increase in transmission.

Wells: Can you help me visualize it? It’s like the spike is spikier and therefore stickier, or something?

Menachery: The analogy I would make is that it’s like a key. And the spike protein has to fit to its key. Now you can think about a key in a lot of different ways, but the better that key fits, the more efficient and transmissible the virus is going to be. These new variants may actually fit that key better. And that allows the virus to replicate or transmit a little bit better than the previous versions. And that’s what’s concerning.

Wells: So this particular mutation wouldn’t mean that it hangs longer in the air or that it is better at sticking to your skin or something. It just means that, once it is in your body, it is better at actually latching on to the cells that it needs to infect you. It’s not actually that it’s easier to get into your body. It just is more likely to infect you once it’s inside.

Menachery: Yeah, I think it gets back to efficiency. Now, we don’t know anything for sure, but the barriers that are in place [such as] masking and social distancing will still be effective against this. The virus hasn’t changed fundamentally. It’s a small difference in a molecular aspect of the virus that gives it a little bit of an advantage. We think, based on the math, that it does have an advantage over the original, but we don’t know the scale at which it has an advantage. Is it 10 times worse or is it two times worse?

Both viruses, the original and this version, are pretty transmissible. And so if it’s two times worse, you may not be able to see the difference. If it’s 10 times worse, you’ll see that in terms of how quickly the virus spreads.

Wells: How do we figure that out?

Menachery: There are a bunch of different ways, and none of them are particularly great. There are experimental ways. Scientists here, and around the world probably, will take the different variants and put them into animals in direct competition. We’ll take the original and the new variant, mix them together, and put them in animals to see how well they transmit [and] how well they replicate.

Wells: Is that what you’re doing now?

Menachery: People in our group are doing that experiment as we speak.

Wells: What animals?

Menachery: We’ll be doing them in hamsters. I imagine groups will try to do it in ferrets, and maybe even in mice. Each of these models are useful in their own way, but none are ideal because none of them are really human.

James Hamblin: When you hear a number, like what was widely reported out of the U.K., like “70 percent more transmissible”—which I believe made it to a push alert from The New York Times and is widely cited—do you think it’s premature to put a number like that on it, or do you think that’s an accurate ballpark [figure]?

Menachery: The number is accurate in the context of the viruses that are spreading in the U.K. So that’s just based on what they’re surveying and the total numbers. You can see that it is becoming a great part of the population very quickly. But it’s hard to gauge. You have the original virus, and you’re comparing it to this other virus. And it’s moving faster, but we can’t control for other aspects. The virus may be moving through a population faster than it was in the summer because of the temperature or the conditions or the lockdowns or how [lax] sick people are with their masking.

There are so many factors that contribute to that. It does appear, based on just the pure mathematical numbers, that the strain is moving faster and is more transmissible. But again, we don’t have a relative scale to know how much more transmissible it is than the original.

Wells: How do I, as a person trying to just get through this, internalize this news? There are two concerns: Do I have to change my behavior? And should I be worried about vaccines?

I’ve developed an understanding of how this transmits, a way of behaving, a risk tolerance that involves mostly being very worried about being not masked with people close and kind of being aware of surfaces, but everyone tells me surfaces aren’t really how it transmits. Does this raise the stakes of any of my day-to-day behaviors?

Menachery: I don’t believe so. The precautions you’re taking should still keep you safe. The virus is not structurally different. It’s these small changes at the molecular level. But it is a situation where, if you’re unmasked, you may be at a greater risk of getting infected from that same person. We don’t know how much more, but if you’re in contact and don’t have the same level of precaution as before, you’re going to be at a greater risk with these new variants.

Hamblin: As I understand it, viruses can become more transmissible by either being more efficient—that key being better able to enter a cell—and/or increasing the viral load within a person. So when you are carrying this virus, you just have more within you and you therefore have more that’s able to infect other people. Are there possibly other effects of that? [If it causes] a higher viral load, people might develop symptoms differently or the disease might manifest differently. Could that have other good or bad consequences that would change the course of the pandemic?

Menachery: The worry would be: If you’re increasing the viral load, the virus is replicating better and that might cause more severe disease. We haven’t had any evidence that these new variants cause more severe disease. And this gets to a weird aspect of disease and transmissibility. If you get really sick, you actually don’t transmit the virus all that well because you’re really sick and you don’t interact with the same number of people, whereas a virus that causes less disease might actually be more transmissible in a sense, because, since you don’t feel as bad, you’re more likely to transmit it to other people.

So there’s a bit of a dichotomy in how viruses spread. This particular COVID-19 is kind of this Goldilocks of viruses. If it was a little bit more severe, it would be easier to control. If it was a little bit less severe, it wouldn’t be as disruptive. And so, in the same sense, these variants could push in one direction or the other. So far, we haven’t had any evidence from the human data that there’s more severe disease associated with it. But often it takes three or four weeks for that data to come in. Coronavirus doesn’t kill in three or four days. It takes three or four weeks. And so, we may be just getting some of that information now. And then the studies we’re doing in hamsters and in mice will also give us some insight. When we compare the variant to the original, we’ll see how sick those animals get and really look at how much disease and how much damage the new variant causes, relative to the original viruses.

Wells: What is your level of worry right now?

Menachery: On a scale of one to 10, I’m probably at a three or a four at this point. There are certain mutations that are more important than others. Some are related to transmission. And these variants are coming up in a population of people [where] the vast majority of people don’t have any immunity. These variants we’re seeing haven’t been pushed to evolve away from antibodies yet.

Your antibodies may be not as effective, but they’re still going to be effective. If you have 10 times the amount of antibody that you need and you lose half of that, you’re still going to be well protected. And I think that’s where these variants are. Most people will be well protected from the worst aspects of disease.

Hamblin: Is the virus going to become more transmissible and eventually infect us all but cause less severe disease? Do we have any idea of the overall arc of this narrative that’s just starting to unfold?

Menachery: It’s hard to say, obviously. What you’ve described is something that may have already happened in the natural world with common coronaviruses. There are four or five common-cold coronaviruses. Many of them have their roots in animals, whether they be bats or cows or other animal species, and then jumped into humans. None of those viruses cause severe disease. They’re all relatively transmissible, and you can get infected every two or three years with them.

There is some possibility [SARS-CoV-2] will go along that route. Once we’ve all gotten some level of baseline immunity—we’ve seen a virus like this or very similar to this—the next time you have it, it [may cause] a mild infection but, for the most part, you won’t end up in a hospital or on a respirator. That’s kind of the trajectory that you could expect, but again, we don’t know.

This event could have happened in 2002 with [SARS-CoV-1], but that virus was effectively stopped through quarantining and other procedures. We have an event now where most of the world will have seen this virus, either through a vaccine or through natural immunity, and so its trajectory in a few years is really hard to predict. I’m hopeful that it’s going to be more like a common-cold coronavirus. The best outcome would be that it’s like SARS 1 and it just disappears from the Earth.

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