[music]

Matt Katz: While Americans have been worrying about the contagious UK and South African variants of COVID-19 a new study posted on Sunday identified seven different variants that have emerged in the United States. Joining me now to break down what scientists know so far about the COVID-19 variants and to explain what variants are is Paul Bieniasz, virologist and professor of retrovirology at the Rockefeller University in New York City. Welcome to WNYC, Paul.

Paul: Good to be with you.

Matt: We can take some of your variant related questions for Paul Bieniasz, Virologist and Professor at the Rockefeller University. You can give us a call at 646-435-7280. 646-435-7280. Or you can tweet us @BrianLehrer. Paul, let's start with this news of the seven COVID variants that were recently found in the US. The New York Times reports that all have gained a mutation at the exact same spot in their genes. What do scientists think that a mutation in that spot does? What is that all about?

Paul: Well, to be honest, we don't really know at this point what the mutation does. There are really, I think, a couple of main possibilities. One is that it changes the spike protein in some subtle way. That's the protein on the outside of the virus particle that could plausibly, based on where the mutation is, could plausibly make the virus perhaps replicate a little better or perhaps be more infectious.

The other possibility is that the mutation marks a spot where antibodies or some other component of the immune system actually recognizes the virus. As more and more people have experienced infection and immunity in the community builds up, then it can be sometimes advantageous for the virus team to make mutations in spots that are recognized by the immune system. Those are really, I think, two key possibilities here.

Matt: Does this continue? Do the mutations-- Will this just continue to happen?

Paul: Absolutely, viruses evolve. They evolve like any other biologically replicating entity. They are constantly making mutations. In the case of viruses, many more mutations than you can possibly imagine. We only really get to see them and appreciate their importance when they confer some selective advantage on the virus. As in this case where you see the same mutation cropping up in sort of independent lineages of the virus, then we begin to suspect that particular mutations might confer some advantage to the virus.

Matt: Some advantage to the virus, which means a disadvantage to us?

Paul: In principle, that can be a disadvantage to us. Obviously, a virus that is more transmissible is not good. Obviously, a virus that has learned to defeat some aspects of the immune response by making a mutation, that can't be a good thing. In general though, individual mutations such as this-- The size of the effect-- This is a single amino acid change, the size of the effect of those mutations is sufficiently small that it really shouldn't and doesn't affect how we interact with or behave in terms of understanding how the virus infects and replicates in us.

Matt: We've known about the UK and the South African variants for a little while, but these American variants, are they new or is the US just slow to uncover them?

Paul: The actual variant itself isn't new, the mutation that sort of ties these lineages together that isn't new, that's been around for some time. What's new is an understanding that the prevalence of viruses that have this mutation appears to be increasing. That along with the fact that we now see it multiple times suggest that there's some advantage to the virus. There have been similar clusters of this appear in the other countries around the world, for example, in Egypt, which adds weight to the theory that this particular mutation that's been found in the US recently, can be advantageous to the virus.

Matt: If you're just joining us, you're listening to the Brian Lehrer how. I'm WNYC reporter, Matt Katz, and I'm filling in for Brian. We're speaking with Paul Bieniasz, Virologist and Professor of retrovirology at the Rockefeller University in New York City. We're taking your calls. If you have questions about what all of this means, I certainly do, give us a call at 646-435-7280. Let's go right to the phone lines, Pat from Peekskill. How are you, Pat?

Pat: Yes. Hi, Matt. Thanks so much. I'm still confused about what more contagious means. Does that mean we keep further distance from each other? Does it mean when I go out and walk in this weather and the warmer weather-- When I rode my bike, you didn't have to keep your mask on because it was so quickly, you were walking quickly, you might not necessarily-- Anyway, my point is does this mean I keep my mask on when I walk or ride my bike all the time? What does more contagious actually mean in terms of practical daily living?

Matt: Thanks, Pat.

Paul: Yes. That's a very good question. Really what it means it's really a statistical phenomenon. There's no bright line between the virus that's more contagious than a virus that's less contagious. The chances of becoming infected when you encounter an individual, it's a very probabilistic type of event. What I would say is I don't think you have to take extra precautions, but I would advise everyone to redouble their efforts in maintaining the precautions they're already taking.

That means having fewer social contacts, keeping a safe distance, wearing a mask wherever appropriate. You don't have to wear a mask if you're 100 feet away from somebody outside, this is not a virus that has dramatically different properties. These are subtle changes, but those subtle changes are enough for that virus to basically out-compete the other variants, talking specifically about the UK variant now. The US variants that have been described recently, we really do not know at this point, whether they are any more or less transmissible than other strains.

Matt: We don't know about the current vaccines that we have and how they can protect us against these new variants, right? It's too early to know?

Paul: With respect to the US variants that have just been described, there's really no reason to think that they will be any less susceptible to immunity that's induced by the current generation of vaccines. They appear to be quite different to, for example, the South African strain that has been described, where we're now beginning to accumulate evidence that that particular variant is less susceptible to immune responses that have been induced either by prior infection or by vaccination. That evidence just simply isn't there at present today for the variants that have just been described in the United States. My prediction would be just based on what the variant is, that it's really not going to be a major factor.

Matt: We're going to go back to the phone lines. Paul, you're very popular. Everybody has questions for you. I'm sure everybody in your family and friend circle has questions for you these days too. Let's go to Rich. Rich, you're on the line. Rich from Manhattan. Hi, there.

Rich: Thank you for taking my call. I actually had the same question you just asked about the vaccines, the effectiveness of the vaccines based on the variants that are appearing. Do you think in the future that-- I had read somewhere that some of the companies might have to offer a booster shot, if that's the case, would you have to then have the original vaccine in order to get the booster and how much do you think that the variants will change over the next let's say six months or so, and how long the vaccines might last, be effective?

Matt: Good questions. Thanks, Rich.

Paul: All right, that's actually a somewhat complicated question. Simply asked, but complex to answer. We're pretty sure that the current generation of vaccines will provide robust immunity to the strains of the virus that are currently circulating in the US. There is some evidence from other parts of the world that there are strains that are hardly resistant to the immunity that's induced by vaccines.

Now, when answering these questions, we have to think about what we're trying to achieve with a vaccine. Really the most important thing is to stop people from dying and to stop them from ending up in hospital and even though there are these variants that seem to have learned a little bit how to get around immune response, it's nevertheless true to say and I'm pretty sure this is true, it was true yesterday, I think it's true today. Nobody who has been vaccinated as yet died from COVID-19.

That's the key thing to bear in mind. Now, if the variants do erode vaccine efficacy a little bit, what one would start to see is perhaps, an increase in the number of people who have been vaccinated, but have mild infections. Of course, the other thing that one would want vaccines to do is not just to protect the person that's been vaccinated, but also protect other people with whom they come into contact.

If I'm vaccinated and I'm vaccinated to the extent that I cannot be infected, that's not just me that's protected, in principle all my family as well with whom I spend a lot of time. If vaccine efficacy is eroded to the extent that let's say the virus that's circulating is not sufficiently well matched to the vaccine, so the vaccine doesn't give complete protection, then in principle, people who have been vaccinated while not dying or becoming seriously ill themselves, they could potentially become vectors for asymptomatic transmission of the virus.

That's obviously not great, but of course, it's not as bad as the vaccines, using complete efficacy so that the death rate in people who are vaccinated matches in those that haven't. That almost certainly isn't going to happen, what's likely to happen over time is that we'll be monitoring the sequences of viruses that are circulating. The companies that are making the vaccines will, in general, attempt to match the genetic sequence of their vaccine to the predominant strain and that circulating.

That'll give more robust immunity. Now, the fact that if you've had a vaccine in the past that matches the current circulating strain, in no way precludes you from in future having boosts of say an updated or modified vaccine. I think with this virus, it's quite likely that we're going to get into a scenario where we have periodic boosters and that's, I think likely to be the case, irrespective of how the variants play out.

Matt: Did you imagine a scenario where we're getting boosters every year for the next three, four, five years?

Paul: That is one possible scenario, whether it'll be necessary every year or every two years or whatever the period is, it's very difficult to say at the moment, it's a new virus in humans, it could be that we get to a state where everybody's vaccinated and then everybody can be infected, but not get seriously sick.

In which case immunity might be maintained by periodic reinfection. That's the situation that we have with common cold coronaviruses that circulate in humans, we're often reinfected by these viruses, but we build up sufficient immunities such that they do not cause serious disease.

Matt: Let's go back to the phones, George in the upper West side. Hi there, George?

George: Good morning, Dr. Bieniasz, I've had the pleasure of hearing you speak two times on a Zoom line, the Rockefeller University Sponsors, you even spoke about a week ago on this similar topic. I simply want to congratulate you, your associates and the other labs with whom you work, on what you've done, and how you present your science it's extraordinary.

I had to scramble to try and take notes and go back and read them, but I got a good sense of it. The first question I want to ask you is you described something in that is called trimeric proteins, are those the items that you showed that are talking about how they work on the hook for the virus itself which you've identified as being common among South African, Brazilian, British, et cetera, in terms of the variance?

My second question is in terms of auto-immunity, it seems that I, for example, have had two Moderna vaccines, I've had the two of them. I called Moderna because I said afterward, "Well, am I supposed to know in a month the level of my autoimmune antibodies?" Apparently, nobody is testing for autoimmune antibodies that are produced by the vaccines themselves.

I'm wondering, first of all, why that is? Secondly, if there is ever going to be deemed the need to do it? Or is the fact that as you said since nobody's died from having the vaccines, that it's not worth the trouble of going and trying to test for the auto-immunity antibodies.

Matt: Thanks, George. Thanks for the questions.

Paul: Okay, let's take the first question first. The trimeric protein that we're talking about here, this is what's called the spike protein, it's the protein on the outside of the virus and it's composed of three identical components that assemble together to make this spike-like structure and that's the protein that attaches to cells and enables the virus to infect the cells.

It's also the protein that's included in essentially all of the vaccines that are in current clinical trial. It's the protein to which antibodies bind and the antibodies in so binding to that spike protein, confer protection from infection. Some of the antibodies physically block the ability of the virus to attach to cells and infect cells.

Now, I think I should clarify something here, you misused the term autoimmune antibodies, that is not what the vaccine elicits. When you are vaccinated, given the injection of RNA or in some cases, protein, if you have Novavax, but in your particular case, Moderna is an RNA. If the RNA enters into the cells, the muscle cells, and causes those cells to make the spike protein, that is the component of the virus that the antibodies recognize.

We know already from clinical trials that provided you've had two shots of say the Moderna vaccine 21 or 28 days apart, that just about everybody makes high levels of antibodies, antibodies that recognize the spike protein and neutralize. For now, we don't really need to test everybody for the levels of those antibodies.

Now, these are new vaccines and we don't have really have a particularly good idea at this point how long that immunity is going to last. It's possible that a year, two years from now that a regular test that one might take at the doctor is to measure the levels of antibodies against the first Covid-2 spike protein.

It's something that we monitor for hepatitis B vaccine, for example. The levels of antibodies can give a pretty good prediction of how protected you are. At this point though, we're much more concerned with actually getting the vaccine out to as many people as possible. Later we'll be monitoring immunity.

Matt: My guest has been Paul Bieniasz, Virologist and Professor of retrovirology at the Rockefeller University in New York City. Paul, thank you so much for giving us an education on what's going on with these variants, really appreciate it.

Paul: No problem good to be with you.

Matt: I'm Matt Katz and I've been filling in for Brian Lehrer today. Brian will be back tomorrow.

Copyright © 2020 New York Public Radio. All rights reserved. Visit our website terms of use at www.wnyc.org for further information.

New York Public Radio transcripts are created on a rush deadline, often by contractors. 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 New York Public Radio’s programming is the audio record.