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Coronavirus Variants - What They Mean

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2021 has brought news of emerging SARS-CoV-2 genetic variants that increase transmissibility. Will they diminish vaccine efficacy and lead us to lose pandemic control? University of Michigan's Adam Lauring, MD, PhD, a molecular virologist who uses evolutionary theory to study viral transmission and pathogenesis, joins JAMA's Q&A series to explain the variants and what they mean for public health. Recorded February 4, 2021.

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This transcript is auto generated and unedited.

>> Howard Bauchner: Hello, and welcome to Conversations with Dr. Bauchner. Once again, it is Howard Bauchner, Editor in Chief of JAMA. And I'm joined by Adam Lauring. Adam is a physician, a Ph.D., he's an Associate Professor of Medicine in the Department of Infectious Diseases, Microbiology and Immunology at the University of Michigan. Welcome, Adam.

>> Adam Lauring: Thanks for having me.

>> Howard Bauchner: So, we're going to talk about Coronavirus, evolutionary biology, and these new emergence of variants. I just want to remind people who are watching or who will listen, Adam published a viewpoint with us now almost a month ago entitled Genetic Variants of SARS CoV 2. What do they mean? And then more recently, John Moore and Paul Offit have followed that with an additional viewpoint entitled SARS CoV 2 Vaccines and the Growing Threat of Viral Variants. So, Adam, for my listeners, and maybe to benefit me, let's start with some basic questions. SARS CoV 2 is an RNA virus. What does it mean that it's an RNA virus?

>> Adam Lauring: So, at its basic, it means its genome is made of RNA and not DNA. But functionally, what it means is RNA viruses tend to have higher mutation rates than DNA viruses, and that's because the enzymes, the polymerases that the virus uses to copy its genome, tend to make more mistakes when copying the genome. And those are the mutations. And interestingly, SARS CoV 2, like other Coronaviruses, they're sort of a unique family in that they make fewer mistakes that most other RNA viruses, because they have what's called a proofreading mechanism. They have a protein that recognizes a mistake and corrects it. So, they, at a biochemical level, they make mutations less frequently than other RNA viruses.

>> Howard Bauchner: What would be examples of other RNA viruses and DNA viruses?

>> Adam Lauring: Sure. So, other RNA viruses of note are influenza virus, poliovirus, measles, mumps, hepatitis A, hepatitis C. And then there's the retroviruses which, you know, have RNA genomes, but might behave a little bit differently in how they replicate. And then DNA viruses would be herpes viruses, pox viruses, so cytomegalovirus, Epstein Barr virus, herpes simplex virus, parvovirus, many others.

>> Howard Bauchner: So, has the emergence of these variants surprised you?

>> Adam Lauring: Um, yes and no. I think yes in that I, if you asked me in February or March, would we be where we are today, I wouldn't think so. No in that, you know, if you think about the fundamentals of how these viruses evolve, it shouldn't be surprising that they would, new variants would arise. I think kind of the extent of it all has been a little bit surprising. And I think, you know, that also has to do with the epidemiology and kind of what's going on globally with this virus.

>> Howard Bauchner: So, we'll, we'll get to that in a second. So, you know, the new variant, rather, the SARS CoV 2 was identified a year ago late December. The genome sequence is released, which is remarkable. And there's a genotype. And then there's a report that a variant has been, has developed. We'll get to how that may occur. When they say there's a variant, what do people mean by that?

>> Adam Lauring: Yeah, it's one of those things that, you know, terminology is everything and nothing at once.

>> Howard Bauchner: Right.

>> Adam Lauring: A variant means it's just different. Right? And so, you know, the, if you look at the genome sequence, it's different from that other SARS CoV 2 virus. And so at its base, you can say anything that's different is a variant.

>> Howard Bauchner: Okay.

>> Adam Lauring: And so that's the problem is when do we say something is a variant and when is it just another sequence that's different? And that, you know, has to do with what we're paying attention to. And so right now we're talking about certain variants that have, you know, increased in frequency and may or may not be concerning. And so it's a little bit in the eye of the beholder.

>> Howard Bauchner: And how, how did the, how does your lab or other labs go about identifying that new variants would emerge? And why would they even test for new variants?

>> Adam Lauring: Sure. I think what my lab and many others do, we do sequencing, you know, samples of viruses from people. And in the case of SARS CoV 2, you get the sample and you sequence it, and then we compare it to other sequences and see how they're different. And initially we were doing that a lot to kind of inform the epidemiology, because the sequences and how they change can tell you where the virus is transmitting and who's spreading the virus to whom. And that has been something we've been interested in for a long time, and so we started working in that area. But now you the sequences that my lab and many, many other labs around the world generate allow you to see how variants are arising and either arising in parallel in different locations, which provide clues, or in the case of the tremendous amount of sequencing in the United Kingdom, you know, people have been able to follow how these variants come to dominate, and, you know, across regions, or across the entire country, that's very informative. And now we're trying to learn how variants are moving from one country to another using this sequence data.

>> Howard Bauchner: So, when you first detect a variant, does it immediately raise concerns that it could be more infectious, more transmittable, lead to more mortality, or do you have to combine that then with epidemiologic data to know that?

>> Adam Lauring: Sure. I think more the latter. I think it's always sequence data on its own can tell you things. But it's much richer with the epidemiologic data. And I think another point that I think is critical is you're only as good as your data. And one thing that has stood out in terms of the B117 story, which we'll probably get to, is the United Kingdom has done a tremendous amount of sequencing, so I think it's something like 10% of the viruses in the country are sequenced, and so that allows you, that degree of sampling allows you to really understand things, where in the U.S. we might, we don't sequence as much, so you might see a virus increasing, but you're not sure if that's really reflecting its change or if it's something to do with your sampling, that maybe you're sampling a certain area, and it's prevalent in that area. But, so it's hard to, you know, infer what's going on unless your sampling is, you know, unbiased and broad [inaudible].

>> Howard Bauchner: And then you have to marry epidemiologic data with the emergence say of the variant in the UK to understand if it's changed, the epidemiology of the disease. Right? As a standalone, it's not very helpful.

>> Adam Lauring: Exactly. As a standalone, you can get a lot of clues. But, yeah, it's definitely much richer with the epidemiologic, or even in some cases the clinical data that go along with it, to really paint a picture of what's, what's happening.

>> Howard Bauchner: Okay, so now let's take a step back. You're a virus in the word, and you're floating around, and then you begin to see people who are immunized, people who got some Remdesivir, people who got some steroids, people who recovered and have antibodies. What's the virus doing to mutate so that a variant occurs? So, make believe you're a Disney movie and you're the virus. What are you doing to protect yourself?

>> Adam Lauring: Right. So, if we're going to think of viruses as, you know, anthropomorphizing them, right, if you're thinking, well, what does a virus want to do? The virus wants to be able to get to the next host and be able to make more of itself. That's all a virus cares about. And so viruses are mutating all the time. Every time they copy themselves, they're making mutations. And you can think of it as trying out new solutions, trying to, you know, either that mutation is either going to make you a better virus or a worse virus. And then what you have is selection. So, survival of the fittest, for lack of a better term. And, you know, the viruses that have a mutation, it allows it to do something better, are going to win out over time. And what we see is, well, as things change on the ground, you know, viruses might be better at growing within, you know, certain hosts, or it might be better at transmitting from one host to another, or, as you suggested, you know, that's going to, then there's going to be an overlay of people who have immunity. And so the virus, you know, may find itself in someone new in a more hostile environment because they've got immunity, and so it's going to make mutations, and that's going to change which mutations are going to be better or worse for the better in that, you know, little microcosm, in that one host. And writ large, that's going to really change things over time.

>> Howard Bauchner: So, then obviously just the last two or three weeks, it's really quite amazing, it finally seems like much of the world is catching up with vaccines, you know, Moderna, Pfizer, J&J, Sputnik, Novavax, the Oxford vaccine, mRNA adenovirus. And then all of a sudden we hear you have a UK variant, South African variant. Now there's a Los Angeles variant that we'll shortly be reporting on. And immediately raises the concern that is the vaccine effective against this new variant. So, I've made you CEO of Pfizer. You're also an MD and a microbiologist. So, how do you go about trying to understand if your vaccine is still effective against a new variant of the virus?

>> Adam Lauring: Sure. I think that's, that's whatever, the 64,000 dollar, or maybe 64 million dollar question. I think there's two, there's two parts to that as I think about it. One is what does it mean for a vaccine to be effective? What are we, what are we measuring, right? Are we thinking about vaccine effectiveness in terms of protecting the most people in the population, protecting against severe disease or not severe disease, protecting against infection or transmission? All those, all those are different ways of thinking about how a vaccine works and whether it works or not. And then you've got what are called correlates of protection. And that is probably the early warning sign that a lot of vaccine makers will probably look at to see, okay, what's coming down, do we need to worry about this. The correlate of protection that people use the most are looking at serum, looking at antibodies and seeing in vitro in the lab, mixing it with virus and seeing if it blocks the virus from infecting cells. It's easy. Even I can do it. And it's also, it's pretty easy to get serum from people. And so what we see is a lot of studies where you take serum, you test it with virus one, virus two, and see if there's a difference. And that provides you a clue of whether the antibodies that are stimulated by the vaccine protect you or not. But then there's also the factor of, well, that's just one part of immunity. And, you know, you may not have a lot of antibodies in your blood, but you may have cells that produce antibodies, and so you may still be protected, you may have T cells, there's a lot going on. And so what you're looking for are clues with these [inaudible]. And, you know, sometimes they're reliable and sometimes they're not. But what we don't know is kind of what's that threshold. So, if you see in your in vitro assay that you can only neutralize the virus half as well, or one tenth as well, you know, if it's a variant. How does that translate to whether someone is protected? And that's not clear right now. And I think we need to learn more about that as well.

>> Howard Bauchner: If you have serum for me, say disease or I was vaccinated, so that serum is going to have IGG and IGM in it. But it will not have my T memory cells, correct?

>> Adam Lauring: Right, right.

>> Howard Bauchner: And so that's what you were talking about in some regards to partial test of is that accurate?

>> Adam Lauring: Yeah. Yeah, I mean, it not only will, you know, unless, you know, in serum, you won't have your T cells, you won't even have your memory B cells or plasma cells that might, you know, be important, just for the antibody response. So, there's a lot we're missing. It's important work, bullet it's important to recognize that it's a correlate, it's correlated with protection. And we don't, we still don't know in many cases how it translates to where the rubber meets the road. And is that person or is that population protected?

>> Howard Bauchner: There's, there's quite a few questions, but I have one or two more, and then, and then we'll get to the questions, Adam. So, we thought of, I have, I've called it the great pandemic of 2020. Obviously people call it many other others; SARS CoV 2 and COVID 19, COVID ID 19. Is this, is this just going to become a chronic Coronavirus pandemic at some low level? That is the fear that people are beginning to develop, that we will appropriately vaccinate about, against the current variants. I've said yesterday I had a chance to talk with Tony. Variants aside, I'm guardedly optimistic for March and April. You know? We're vaccinating a million, we're supplying 1.3 million vaccines plus a day. There's 55 million people older than the age of 65. Theoretically, at the current rate, everyone in that age group could be vaccinated by April 1 if they want the vaccine, or at least get the first dose. That will dramatically reduce the rate of death, which is still 80% in that age, or 80% of the deaths are in that age group. But that obviously is taking this variant, and whether or not the Moderna, Pfizer vaccines, ultimately the J&J vaccine are effective against it. Are we is that what you anticipate, chronic SARS CoV 2 Coronavirus disease?

>> Adam Lauring: I don't anticipate I think the Super Bowl is this weekend. It's where is the goal posts, right? What do we do? Are we eradicating or eliminating SARS CoV 2? I don't think so. You know, can we get to a place where we're not, you know, you know, confined to homes and not able to go out to eat and not have our kids at school? I don't think that's going to last, you know, a super long time, months. And I think what we may get to a place where, you know, we have annual, you know, just like we have flu epidemics every, every year, we might have, you know, wind up in a place where, you know, every year there's, you know, a time of year when we have a lot of SARS CoV 2 around, and some people get sick, some people get very sick, some people die, but it won't be where we're at now. That's I think where we're headed.

>> Howard Bauchner: Now virtually all of the vaccines, adenovirus vector vaccines, mRNA have focused on the spike protein. For the few vaccines that are more traditional heat killed or manipulation of the virus, that would be less, less true. Do we need to think about vaccine development that's broader in its target than the spike protein?

>> Adam Lauring: I think that's a really good question. I mean, I have worked in the influenza field for a while, and everyone there has been focused on HA or hemagglutinin, which is kind of a corresponding protein to spike on the surface, because it's thought that that, you know, protein is really important in terms of providing immunity or targeting that for immunity. But in recent years, people have learned that this other protein on the surface called neuraminidase, or NA, is also important. And so vaccines that, you know, direct a response to that can also provide some protection. And so I think it is something that I'm sure many are looking at now in terms of, you know, other, other, other ways of combining antigens and vaccines or different spikes in vaccines, or different ways of updating vaccines, that, as you said earlier, if I were the head of Pfizer, I would be thinking about those, and I'm sure they are.

>> Howard Bauchner: One last question for me there, then I'll go through the questions. The holy grail in influenza has been kind of the broadly neutralizing vaccine, or broadly neutralizing antibody vaccine. Are we any closer to that? Because it may have then clues for what we could do around Coronavirus. I mean, that's been pursued for a decade or more.

>> Adam Lauring: Sure. And I think the universal flu vaccine is, I think we're getting closer. I think the strategies for that might be a little bit different than what we're probably going to be dealing with with SARS CoV 2. But, you know, I think, you know, thinking about, you know, these, these ways of targeting a virus that, you know, is always changing in the ways of finding something unifying, the tricky, the tricky thing with influenza that might also affect SARS CoV 2 is it's, it's hard to find that one antigen that will rule them all and provide protection, often because it's hard to direct the immune response against those very conserved regions of the virus, those universal targets are sometimes elusive. And I don't, I don't know if we know how it will play out with SARS CoV 2 yet.

>> Howard Bauchner: Let's go through some of the questions. And I always tell the people who I'm talking with, you have the right to say you can't answer that question or you don't know. Okay?

>> Adam Lauring: You'll hear that a lot.

>> Howard Bauchner: Yeah, it's not like, it's not like Jeopardy that you've got to answer the question. So, how do you explain that children seem more vulnerable to some of the new variants?

>> Adam Lauring: I don't, you know, I've seen mixed data on, you know, certainly from the UK early on, it was thought that there was a lot more spread of the new variant, of the B117, the quote UK variant. A lot of the, a lot of those things have been rethought as data comes in. And so I say we're still not sure, or at least I'm not sure, given my knowledge of, you know, the differential between kids and adults. So, I think we'll learn more as the weeks and months pass.

>> Howard Bauchner: We have published a research letter very early on about the amount of ACE receptors in the nose of children versus adults. And it does seem to vary, because certainly children have been much, much less prone to serious disease. And that's very different than flu, which is very interesting. I mean, the question has always been do children spread disease, spread COVID 19 more effectively than adults, but they certainly get less serious disease, at least prepubertal children. I'm always hesitant, I'm a pediatrician, so when we say children, I think we really need to talk about prepubertal versus postpubertal.

>> Adam Lauring: Right. And I'm an internist, so I say, oh, I don't do kids.

>> Howard Bauchner: Right, you

>> Adam Lauring: So, ask your pediatrician.

>> Howard Bauchner: Are there any studies being done on viral shedding from people infected with different variants, or are those studies being ongoing?

>> Adam Lauring: Yeah, I think, I think they're ongoing. There have been, you know, whiffs with data that suggest that there are differences in shedding. Those studies are very hard to do because you have to control for the time varying nature, you know, when you sample someone in the course of their disease can affect the amount of virus you detect. And so, but those studies are ongoing, and some do suggest that there's different levels of shedding with the B117 variant versus, you know, what was before.

>> Howard Bauchner: I don't know if you had a chance to read Paul's viewpoint in JAMA, but the question is, do frameworks for the proposed surveillance systems and repositories proposed in Paul Offit viewpoint exists in the U.S., so what Paul and I discussed before he wrote it was that there would be a, you know, a single place. Obviously we would favor the Centers for Disease Control that could collect sera and the variants and then report out what was occurring at the national level. Does that make sense to you, Adam?

>> Adam Lauring: I think it makes sense. It's what, it's what's largely done with influenza virus for years. The CDC has surveillance networks and collect viruses and sera from all over the country with academic and hospital partners. The NIH also has parallel efforts, and so I think those sorts of and I think those sorts of plans are underway. And so I think it will probably be, you know, certainly an organizational structure from the federal government, but probably in partnership with, you know, you know, research institutes and universities across the country as well.

>> Howard Bauchner: Is there any reason to be hopeful or to think that the South African variant, the UK variant, I know people are using the numbers, and Rachelle Valinsky [phonetic] asked me to use the numbers and not the names of countries, because it can be stigmatizing, so I do apologize. It's hard for me to remember all the numbers. Is there any reason to think that all those variants won't make it to the United States at some point?

>> Adam Lauring: Well, they all have.

>> Howard Bauchner: Okay.

>> Adam Lauring: So, B117 is, I think there's at least been close to 500 sequences now.

>> Howard Bauchner: In the United States.

>> Adam Lauring: Yep.

>> Howard Bauchner: Because that's one of the questions. And B117, sorry, is B117 from the UK or South Africa?

>> Adam Lauring: Yeah, that's the UK variant.

>> Howard Bauchner: Okay.

>> Adam Lauring: We've had, I think, 30 documented in Michigan where I live. And then P1, which is the Brazilian variant.

>> Howard Bauchner: Ah, Brazil, right, thank you.

>> Adam Lauring: Was I believe identified recently by the state health lab in Minnesota. And then I believe the South African variant, which is B1351, there were two cases that I know of in South Carolina. And then as we kind of discussed earlier, the concern is we don't do as much sequencing in the U.S. relative to the UK. And so we may be just seeing the tip of the iceberg. It might be reminiscent of earlier in the pandemic when there wasn't as much testing. And that there was, you know, circulation that we didn't know about until later. So, I think that's the concern, you know, certainly I think B117 is here for sure, the UK variant. The other ones, it's unclear whether we're containing them or not, and so we don't know how widespread.

>> Howard Bauchner: Is the, is the testing for the variant, I mean, you know, before we started, you said you were at the University of Washington UCSF. I'm more familiar with much of Boston medicine. Does every city, every major hospital academic medical center have the capacity to test for variants? Is it too complicated, or are there enough centers that could do it so that you could easily have 20, 30, 40, 50 centers that are testing for variants if they had the resources?

>> Adam Lauring: I think, I think that model would work. There is this, CDC has a sphere, it's called the spheres network. It's kind of a network of state labs, as well as academic labs. My lab is part of it. Many other academic labs are. And I think there's the problem I think to date has been it's patchy, right, you know, we do a ton of sequencing in Ann Arbor, Michigan. But, you know, that's great in Ann Arbor, Michigan, but it's not telling you what's going on in Chattanooga, Tennessee. And so, and so what we need is, you know, probably more widespread, and I think, yeah, I think these kind of federal, state, you know, research institute partnerships would be great. And you could easily see how we could, you know, with a fair bit of organization and logistics get this done. And then funding, of course. And a lot of it is figuring out how to get the samples from the labs to the place where they're going to get sequenced and how that's linked to the data that you need to start making sense out of it.

>> Howard Bauchner: Can you imagine, given the emergence of variants, that someone is going to get a Moderna vaccine and a Pfizer vaccine, or a Moderna vaccine and a J&J vaccine? You know, at the moment in the U.S. we're committed to Moderna times two, Pfizer times two, and a very, very specific time sequence, give or take a few days. But, you know, Pfizer's three weeks later, Moderna's four weeks later. J&J is likely to be approved in the coming months, given the press releases. It could be within a few weeks. But can you imagine that there would be a mixing and matching that may evolve over the next six months or a year or not likely?

>> Adam Lauring: I don't, I can see it at some point. I mean, this is kind of where we reside with influenza these days, that there is, you know, the egg, the various egg based vaccines, there's cell based, there's, you know, a subunit vaccine. There's all these different ways that people make flu vaccines. And we can, I can see us getting to that place. Whether that's going to be driven by the variants or not, I'm not sure yet, because right now they're all kind of targeting the same protein. The genetics are the same. But, you know, we may get to a point where, yeah, maybe some of them are updated sooner than others, and it's a real complicated both public health and regulatory problem to think, to think through.

>> Howard Bauchner: A couple more questions, many more questions have come in. Would it be better for immunocompetent adults, people, to get live attenuated vaccine as it will expose the body to the whole virus rather than single proteins? I mean, you know, we've been focused on adenovirus, adenovector and mRNA. But there are, there have been other developments. I'm not entirely sure what both vaccines from China are. But would a live attenuated vaccine likely provide broader protection?

>> Adam Lauring: Yeah, it certainly might, or it might potentially stimulate more immunity kind of at mucosal sites, which is, you know, perhaps of it interest for a respiratory virus like SARS CoV 2. Obviously, you know, there are always, you know, kind of regulatory concerns with a live attenuated vaccine. And boy are you sure it's attenuated, are you sure it's stable, those sorts of things I think would give people pause, but it's certainly something that people are investigating, and it's worthy of investigation.

>> Howard Bauchner: Where are we when it comes to modeling possible escape mutations in the spike protein?

>> Adam Lauring: Sure. So

>> Howard Bauchner: Can you explain that question for our listeners?

>> Adam Lauring: Right. And so the idea would be that, you know, these variants, or, you know, have, a lot of them have mutations in the spike protein, which is what's predominantly targeted by our immune system, and it's what's in the vaccines. And so the idea is if a virus has an escape mutation, a mutation and spike that allows it to escape antibodies, right, what we were talking about earlier, that virus may escape our immune system and still cause infection despite vaccination. And so a large part of what we are talking about with sequencing is trying to see if we're seeing hints of that and seeing if in a vaccinated population, are you starting to see more of viruses with certain mutations, because that might provide a clue that those viruses are having advantage in escaping.

>> Howard Bauchner: Adam, you're so knowledgeable about this. So, I really want to thank you for joining me. But a birdie has told me, I have to ask one final question. Could you tell me a little bit about your birthday cake from September? Apparently we have an image of it. And I have been told it was quite interesting. So, could you say a little bit about what that, what we're going to see if we're going to hopefully we're going to see it.

>> Adam Lauring: This is kind of a surprise. I guess I got clued in a little bit earlier. But, yeah, we had a Coronavirus birthday cake. And so, you know, I guess it's making the best, I have a September birthday, so before a lot of the variants emerged, making the best of a pandemic.

>> Howard Bauchner: Who made it for you?

>> Adam Lauring: I would need to see the picture, because there were, there were several cakes around.

>> Howard Bauchner: Okay.

>> Adam Lauring: And so, yeah, so there was also a former post doc in my laboratory who, who was a fantastic baker and would make a lot of cakes. And so that, you know, that was always a treat for our laboratory birthdays.

>> Howard Bauchner: Did, did your kids and family, did your kids and your wife love it?

>> Adam Lauring: Yeah, my kids are, they are, of course, indoctrinated into virology, and so they know, they know more Corona virology than most adults at this point, for better or worse.

>> Howard Bauchner: One last question. So, Tony wrote a viewpoint for us almost three years ago about the speed at which vaccines were being developed. And he has this wonderful table in 20 years, 15 years, 10 years, 8 years. I think he finally gets it down to like three years. And this was three years ago. You know, you're, you know, 10 or 15 years into your career. Did you ever imagine that you would see a virus sequenced in January and there would be testing of a vaccine in June or July?

>> Adam Lauring: It's bonkers. Yeah, it's amazing. And I think it's one of the things you can lose sight of in the moment we're in, you know, because there's so much concerning and bad news and things are hard. But then you're just like, wow, I mean, it's remarkable, from the sequence to two EUA vaccines that are highly effective within a year, that's just amazing. And the other thing to think about is people are concerned about the variants, and, you know, are the vaccines going to work as well. There was data last week, you know, from Novavax, and then some data from the Yonson vaccine that [inaudible] 50 to 70% against the variant perhaps. Boy, if we got 50 to 70% vaccine effectiveness for influenza every year, we'd be ecstatic.

>> Howard Bauchner: It's so interesting, you say, because I think the struggle has been, you know, the bar, I think when people saw 95% first, I think Pfizer was first, I can't remember, and then 95% from the other, one, it was so nice that the mR, that the same vector or platform mRNA came up with the same. I don't think people, they were disbelieving. And so now the problem is when you have new vaccines and they say 70% or 60%, people are going to go, oh, my Lord, it's only 60 or 70%. There are very few vaccines against viruses that are, that approach 95%. It was an extraordinary achievement. And the bar has been set so high.

>> Adam Lauring: Right. Or the, to the Super Bowl analogy, the goal post had been moved, you know, our expectations, you know, because it was just amazing how well those first two reported vaccines worked. And so, you know, it's, you know, that's, when I started getting concerned and kind of getting down on this, that's kind of what I come back to. And we'll see how it plays out.

>> Howard Bauchner: This is Howard Bauchner, Editor in Chief of JAMA. I've been talking with Adam Lauring. Adam is an Associate Professor of Internal Medicine at University of Michigan. He has a position in a division of infectious diseases microbiology and immunology and ecology and evolutionary biology. And almost a month ago, anticipating sadly anticipating the struggles that we may have with variants. Adam, along with Emma Hodcroft, wrote a viewpoint for us entitled Genetic Variants of SARS CoV 2, What Do They Mean. Adam, thanks so much for joining me today. And I didn't get a chance to see the picture of your cake. So, now I have to go watch the video so I can see a picture of these cakes.

>> Adam Lauring: Indeed. Indeed. Well, thanks for having me.

>> Howard Bauchner: Thanks, Adam. Take care.

>> Adam Lauring: You too.

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