#151: Richard Michelmore and Brad Pollock on COVID-19 Variants
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Our host Kira Dineen is joined by Dr. Richard Michelmore and Dr. Brad Pollock to discuss genotyping for COVID-19 variants surveillance.
Brad Pollock, PhD, MPH, FACE, is Professor of Epidemiology, Chairman of the Department of Public Health Sciences, and Associate Dean for Public Health Sciences at the University of California (UC) Davis School of Medicine. He received his B.S. in biological sciences from UC Irvine, and his MPH and PhD degrees in epidemiology from the UCLA School of Public Health. Dr. Pollock is a leading researcher on the epidemiology and control of childhood and adolescent cancers.Throughout his career, he has focused on developing research infrastructure integrating diverse disciplines such as epidemiology, biostatistics, and informatics with clinical and translational approaches to address important health issues. In March 2020, Dr. Pollock was appointed Chair of the University of California (UC) Systemwide Public Health COVID-19 Workgroup. This group has guided system wide efforts to reduce SARS-CoV-2 transmission on the UC campuses. Dr. Pollock is also the Director of Healthy Davis Together a large demonstration project involving the City of Davis and UC Davis in partnership.
After studying Natural Sciences at Cambridge University, Richard Michelmore joined the faculty of University of California at Davis in 1982. Richard was the founding Director of the Genome Center at UC Davis in 2003. He is currently a Distinguished Professor in the Departments of Plant Sciences, Molecular & Cellular Biology, and Medical Microbiology & Immunology. His multidisciplinary research utilizes molecular, genetic, and evolutionary approaches to plant genomics and he has published over 200 scientific papers. In particular, he aims to exploit such approaches for information-driven deployment of resistance genes in crop plants to provide more durable disease resistance. His interests also include applications of DNA sequencing to all areas of biology and its increasing impact on society. In response to the current pandemic, he has been a major contributor to the team providing rapid, high throughput testing for SARS-CoV-2 to the UC Davis campus and the City of Davis and is now deploying rapid genotyping to monitor for variants of concern.
On This Episode We Discuss:
Testing for COVID-19
COVID-19 variants including L452R and E484K
Variant genotyping
Public health implications of genotyping data
Vaccinations protection against COVID-19 variants
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Transcript
[Advertisement] I’m Mary Parker, and I hope you will join us for Eureka's Sounds of Science, a podcast from Charles River. We tell the stories of how - how chicken eggs impact vaccine development, how a single parent can change the FDA, how a Horseshoe crab saves lives. Listen to Eureka's Sounds of Science on Apple Podcasts, Spotify or wherever you download your podcast.
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[Intro Music] How is it that we find ourselves surrounded by such elegance, such complexity? The genes of you and me, they're all made of DNA. We're all made of the same DNA...
Hello. You're listening or watching DNA Today, we are a genetics podcast and radio show. I'm your host here, Kira Dineen. I'm a prenatal genetic counselor. And on this show, we explore genetics’ impact on our health through conversations with leaders in the field. So we're talking to other genetic counselors, researchers, doctors, patient advocates. Today we are talking about the genetics side of COVID-19.
Before we start out, Dr Michael Moore, it would be great to hear from you in terms of giving us background information on what type of virus COVID-19 is, because, as we were talking before, we started recording, a lot of our audience is genetic counselors and people that may not specialize in Virology. So if you could provide us a little bit of background there in terms of the type of virus we're talking about.
So SARS-CoV-2 is a coronavirus. It's a member of RN positive strand RNA viruses. It has a fairly large genome for a human virus. It's got about 300 bases. And Fortunately, actually, it isn't one of those really robust protein encode viruses. It's in a coating of lipid with four structural proteins. So it's relatively easy to disinfect talking about variation. Viruses vary all the time, and the replication of viruses tends to be error prone. Now, most of those changes are inconsequential or maybe even deleterious, so they don't propagate. But occasionally, some of those changes will actually confer an advantage to the virus. And one of the things, of course, a virus wants to do is to be more infectious. So when SARS-CoV-2 moved into humans, it wasn't really tremendously well adapted. It is actually remarkably, fairly well adapted. But some of these changes that have occurred have resulted in strains that will be more infectious. And so when we're looking at COVID testing, when people are like, Oh, I got a COVID test. It's negative or it's positive. Are there different types of COVID test that maybe the public isn't as aware of in terms of? There's not just one, there's multiple, definitely. Can you tell me the answer that I was asking? That's a good prompt, broadly, that kind of two types of tests, one of which is it tests for the presence of the RNA. And they tend to be PCR based so that they amplify up. And they will specifically ask, can I detect a particular part of the virus? And different tests. Different PCR tests will detect different parts of the virus.
So you'll see the different kits from the different companies, they'll say it's the gene, the gene, different letters for the protein genes that are being detected. The good test will detect two or 3 different targets. So they're not affected necessarily by a chip. One change. Then you have another group of tests that try and detect the presence of the protein. So these are antigen tests. So is distinguished from antibody tests that detect whether you've been infected two or 3 weeks ago. So the antigen tests tend to be more rapid, but tend to be a little less accurate, though. The whole field of diagnostics will never be the same again. So many technologies and so much money and so much ingenuity has been poured into diagnostics that the whole field of diagnostics, and I'm sure it's going to impact genetic counseling tremendously, as I say, it's never going to be the same again. You have these quick point of care tests and then the speed of the PCR tests and the scale, a number that we can conduct is definitely going up. I just had, I think, and Richard put his finger on it. So the antigen tests have really been evolved to give you rapid results. And those are the sorts of things you'll see when you have a 15 minute test. They tend to be not quite as accurate, of course, compared to the PCR methods, which require more laboratory work and a turnaround time of many, many hours, usually, if not a day or two.
The other tests which we really have poopooed a lot, are the serology test. And that is the antibody test. In epidemiology. Those have often been used to get a snapshot of a population to have some idea of what the prior exposure to the virus was. In other words, if people have developed antibodies in many cases for some viruses, you'll get antibodies that are very persistent. They could detect that the fact that you were diagnosed or you were infected two or 3 years ago. Right. So we do look at those sorts of things. And in fact, when the pandemic began here, you saw a number of population surveys being done. For example, in Santa Clara County, California, Stanford did a study where they were trying to assess how many people had been exposed or infected. With a virus historically, and they came up with estimates, and they're much less useful, though, for active planning and moving forward because they don't tell you who is infected. Now, you could have had an infection six months ago, developed antibodies to it. Maybe they were persistent, maybe not. In fact, there's some evidence that they're not very persistent. And then you test zero today. So they're not as informative, but each of these different testing modalities can be used in different of contacts to give you slightly complementary information.
Another useful distinction is clinical testing versus public health testing. And one of the characteristics, actually, of SARS CoV two is that many, many infected individuals are, asymptomatic the whole medical clinical industry is set up to take to diagnose symptomatic individuals. But given that 50 or 60% of the infected individuals will not be symptomatic, that puts it outside the normal clinical workflow. So this is something we did at Davis was you have the clinical all testing in the hospital where you really need to know if someone's infected, but then you need high throughput inexpensive testing for a public health context, evasive tomatic individuals. So you kind of have these parallel universities, and they are complementary if you use the right way. I'll just point out one of the flaws we've had to deal with was the federal government didn't know how to regulate these the right way. They're really only regulating in the context. And a lot of your listeners will know from genetic testing are these clear, certified tests. And when you're dealing with population testing, where your intent is to try to catch somebody who's got an acute infection, and you don't necessarily want to rely on having something that's going to be as convoluted. In fact, at the beginning, you remember, many of the academic medical centers were given 20 test kits a day to use on the original medical test, and that was clearly insufficient to do anything. So I think what we've seen, the difficulties we faced are that the regulatory agencies, the FDA in particular, really wasn't thinking about this second track, which is the population based testing, which really is a different intent. And I think Rich and I both agree, a you don't have one without the other. You do need to have the medical testing as part of this, but it's not sufficient to try to roll that out on a population basis the way that things were structured. And what role did the UC Davis Genome Center play in the pandemic response and just how you handle things and how you developed testing, right. So we just mentioned that the clinical folks were taking care of the hospital, they had supply chain issues, and they thought you're running 300 tests a day. 500 tests a day was high throughput. I come from a So AG biotech background, and I knew there was technology out there that could generate millions of data points a day, million orders of magnitude more than what the clinical folks were thinking about. And the Genome Center is set up to provide high throughput high complexity tests of different types. So we repurposed the Genome Center. We had skill personnel there. We weren't really used to doing quite the high throughput. But I reached out to contacts in the AG biotech industry, and we then collaborated with LGC to move their technology into running. And it's no sweat for us to run 5,000 tests a day. We could push it up to 8,000 if we wanted to. In fact, in theory, we could do 24,000 tests a day. But the challenge is not the molecular biology is actually the sample acquisition, the human side of just processing that many samples, getting them into systems, acquiring those samples. Yes. The acquisition is much more challenging once the sample gets to the lab. No problem. We can handle thousands and thousands of samples today.
And then how does Healthy Davis Together fit into all of this?
Sure. And that's a really nice segue, because, as Richard said, it's the acquisition. That's the challenge, right. Of course, the technology side was challenging, but the issue is, how do you actually get samples? How do you actually get people to volunteer to be part of something where they're going to be tested, especially in the context of asymptomatic individuals? Right. So that means people they feel healthy, there's no reason for them to get tested. Right. You're asking him, could you please submit to getting tested? Now, one of the things I think was, again, very clever. Richard and his crew, and we did talk a lot about this, but it made no sense to try to do nasal fringe swabbing for a large number of people in the general population. And I know if any of you had the test done is you feel like your brains are going to be rubbed out when they do that. So that's not a very viable way of doing this on a mass scale. So we did move to a saliva based platform to make the acquisition a lot easier, much more acceptable. You spit into a small tube. But the Healthy Davis Together project, it's actually fairly comprehensive. And the intent of it was really to look and see whether or not we could control COVID-19 in the Davis community. So it was really taking a lot of what we had put in place already for the campus control, with students moving back last fall, making sure we had the appropriate non pharmaceutical interventions for public health measures as well as the testing, and then expanding our bubble from the campus to the whole community. And it's actually a fairly large project at its core.
There are really two major approaches that are being used to control COVID. One of them is the epidemiology infectious disease control. And so that's where testing is the central piece for that. It's testing it's, identifying positives, quickly, doing case identification, contact tracing. And then for those individuals that need to be separated out, that is positive cases or high risk contacts, it's providing isolation and quarantine. So the idea there the testing is critical to get people out of circulation, so they're not infecting others. So that's really the infectious disease control component of Healthy Davis together, along with wastewater monitoring. So we're looking at trace levels of virus in the wastewater, and there's some other things that are involved, too, including vaccination, which really comes under the same heading. But back in June of 2020, we didn't have a vaccine available. So that was a future project to be expanded out. Half of the Healthy David Gather project is really focusing on health behavior change. So as you've maybe heard some Epidemiol just say, you can't test your way out of an epidemic. So all the testing in the world is not going to fix you from having this population explosion. So you have to incorporate in behavior change where people are going to separate out. Masking was part of that social distancing, obviously, learning indoor outdoor use of spaces, and so on. So the other half, a Healthy Davis together was to put together a package of mass communications and interventions, including incentivizing individual behavior, getting business partners involved to try to move the needle forward in terms of the health behavior change. So when you combine epidemiology with help behavior change, you result in real positive effect. And we're now seeing that now we're looking at the numbers of cases we've had in the Davis community, and they're much lower than control areas, including in the same County as well as other cities around the state. So I think that's important. But I want to point out here that it's really the combination of the technology platform, along with the sort of the people side of things. How do you get people in to get tested? And that has not been any small feat. We've had probably a little over half the population of Davis that have submitted and had at least one test on. But getting people to do this on a frequent basis when they don't have to. Theoretically, it's taken a lot of communications, a lot of messaging to try to do that. And even now, more. So when the CDC has come out with guidelines for a fully vaccinated individuals, and they said, Oh, you don't need to test unless you're symptomatic. We're really not happy with that advice because of the issue of variance creeping up now and break through cases. So anyway, I think these the platform, the testing platform, is critical, and then having the affected arm of being able to get people into the system, that combination there has really been very powerful.
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And you brought up a good point of the next phase, maybe of this pandemic, of looking at the variance. I think when we started with a pandemic or like COVID 19, is that there or not? But now we've gotten so much more information as we're recording this in June 2021. Looking at this. I mean, what is COVID 19 variant? How are we tracking this?
Good question. So as we mentioned earlier, the virus is changing all the time, but most of those changes in consequential, but if they confer an advantage, you're going to see them increase. People don't believe in evolution. Just tell them to look at what's happening with SAS Kobe, too. I mean, it's evolution in real time here, guys. What you see is there'll be a response to a selection pressure. And the major selection pressure up to this point has been for increased infectivity. If you have a strange virus, it's more infectious is obviously going to become prevalent. And that tends to occur when you have better binding of the So called S protein to the receptor on the human cell. And there's a limited number of amino acids on that interface between the S protein and the receptor. And so what we've seen actually is the same changes. Same mutations have occurred in multiple locations in the world. Wow. So it's not just one place we've seen. It solely evolves. We're seeing this evolved differently in places, but in parallel.
So there's a mutation L-4-5-2-R, otherwise known as Larry, right. And another one, the E-4-8-4-K. These mutations have occurred multiple times. So L 4 52 R, it occurred in the UK. First the So called B 107, or now the Alpha strain. It occurred in the South African strain. It occurred in the Brazilian strain completely independently. Is this something we would have expected? Because you're blowing my mind a little bit now. I mean, this isn't my area, but that's shocking to it's. So called convergent evolution. So what you've got to realize is that because the replication of virus is error prone, it is essentially exploring all sorts of evolutionary space. Right. As I say, most of that space is not advantageous to the virus, but a few times, it will be. And if it's a big advantage, it's going to you're going to see it over and over and over again. And the technology that we developed, we took him from the biotech sector was actually set up to detect DNA changes in plant breathing materials, sniff at a so called single nucleotide polymorphisms. So it was a complete no brainer that we just said, okay, we know how to do this is to develop assays in the collaboration with LGC that will detect these changes that you see over and over again. And then with a relatively few number of changes, I can tell whether, in fact, it's the Alpha variant, the Beta variant, the gamma variant, or the Delta variant, because they have a different pattern of these advantageous reoccurring mutations. And so we now test 100% of our positives. So we run our tests, and it's fast. So we're returning many of the results close to 40% of our results. We return the same day and over of the results go back within the next day. And then we take those at all the positives and run them on our so called SNP assay. And therefore, within a few days of someone sitting in a tube, we know what the variant is. Now. It isn't a hundred percent of the time because you need a certain amount of virus in your tube. And so we actually run the test on a positive. We don't necessarily get data back, but it's the same with sequencing. Sequencing also can't give you a sequence on 100% of samples, and the sensitivity is about the same.
But a point I would make with the genotyping or the SNP genotyping is it's complementary to sequencing? It doesn't replace sequencing. It Blatantly stands on the shoulders of sequencing. So you need to sequence a certain percentage all the time to look for those new variants. But then when you know what variants are circulating, you can develop your sniff assay very quickly. Within a few days, you know what variant. And so the point about the problem with sequencing is it's expensive, tensely, more demanding, and it's a lot slower. So a lot of the sequence information you're seeing, though, it's getting better. But I exhaust in four to 6 weeks after the sample was collected. That's no good for realtime interventions, right? But we need that sequencing to design the Snip assays to know what we've got. So the two complimentary.
Is it those two variants that you mentioned specifically that Davis and maybe other places are looking for? Is that just two examples of a list of many variants?
You can pretty much tell what you've got for the major variants right now by running half a dozen sniff assays, but you'd like to have a little bit of redundancy in your calls. So we run about 12 to 14 steps, which is probably overkill. But I'll have three changes that will tell me whether I've got the Alpha variant, I'll have three or 4 chain. Now two or 3 changes will tell me whether I've got the Delta variant. Right. And actually, there's a new version of the Delta variant that has one of the other changes 144 that we've seen in some of the other strains that hadn't actually been seen in initial Delta variant. So the Delta variant is acquiring more of these advantageous mutations because the same assay is informative over and over again. We can pick that up.
And with that, then is there you're talking about the Alpha beta? The different really almost types of COVID 19. Are there one that is more infectious or one that were a little bit more scared of for lack of a better word that we're really having our eye on in terms of it getting worse and more contagious?
Yeah. So the B one and 7 or the Alpha variant was the first one that really came up. That was about 40 to 60% more infectious than the standard strain that was going around at the time. Now the new Delta variant is 40 to 60% more infectious than the Alpha variant. So it's really quite infectious, building upon each other. It's selection. Right. If it's an advantageous to be more infectious, you're going to be more infectious. Now, another thing about viruses is it isn't actually in the best interest to kill you. Right. They're reliant on you. In fact, the ideal virus will propagate be highly infectious, but a symptomatic. We have individuals walking around with some of these variants that have incredible high numbers of for the office. No, we have a symptomatic individuals with the CT value of 12 or 14. That will mean something to some of them. And that is true mind blowing. Right. But there is some time I finished. I'll lose it. Now we talk about selection pressures. Right. So the selection pressure at the moment has been for increased infectivity, but I could not design a better selection experiment that's currently happening in the U S, where you have a steep selection pressure called vaccinated individuals, and you have a large number of infected infectious individuals that are not vaccinated. That approach feed presenting variance all the time against his selection barrier. Up to this point, we really haven't had a steep selection pressure for there is at scale to overcome the vaccine, but it's now there. So there are I don't want to be alarmist for their eye. And others basically think it's just a matter of when not if there will be variants that overcome the vaccine or to varying extents, it may not happen all at once. It may be gradual. Some of the strains on the vaccines are effective against it, but not quite as effective. So you could see step wise in terms of selection, it doesn't need to be all or nothing. Right. So you'll see this step wise thing. So this talk preparing for the next pandemic is it another virus that blows in from animals, bats, whatever. I personally think the next pandemic is going to be variance of SARS-CoV-2 that overcome a vaccine. And what we're doing in terms of monitoring is essentially practice when that happens.
I just going to add, and I think the interesting thing here is that the other element where we might reduce the chance of having this huge challenge is really the speed at which we vaccinate, and it's the pool of unvaccinated that are left in the population. So I want to just emphasize and amplify what Richard said, which is we're going to see this big battle happen. There's going to be something coming along. It's going to challenge the current are vaccines we have available in terms of their efficacy, but that is much less likely to happen if we used a blitzkrieg lightning approach and really got everybody vaccinated all at once, because if you do that, you reduce the pool of individuals who are infected, and that's where the mutations occur. So you want to try to eliminate a pool. So it's not just a constant time issue here. It's really this issue of trying to hit it hard, fast upfront. And what you're seeing, Unfortunately, globally is you're seeing rates that are highly, very different across the globe. My son's moving back from Columbia, South America on Friday. But South America now has one quarter of the Cove deaths and only about 5% of the world's population.
So it just rampant down there, even in the United States here. We've got these pockets of parts of States where you've got highly large numbers of unvaccinated individuals. So I think that this battle that's brewing here, and I would agree with Richard that we may see this Megan battle happen. We really want to try to put out all the fuel ahead of time, get rid of the fuel before that fire gets let, because we don't want to see that happen. And, of course, the vaccine manufacturers are trying to stay on top of this. This is where the role of boosters will come in, where we can reformulate. And Unfortunately, what the Messenger RNA vaccines. These are much easier to reformulate to add in the additional response for these new mutant types than you had in the old conventional vaccine development world. So that's good. It's very difficult. And we don't know. The problem is we don't know when that battle is actually starting to get one in certain areas. And we may be reverting back to a lot of these horrible lockdown measures and outbreak things that we've had to endure for the last year and a quarter.
And when it comes to talking about, like the booster vaccinations, I mean, obviously hard to say. We're speculating, but coming from your research and what you've been seeing, when do you expect that we may be needing those booster vaccinations? I know for me, I was vaccinated by the end of December 2020 because I'm a healthcare provider in person, so I was one of the first to get it so well, people that were on that front end of getting it first be getting the first to get the boosters. Is that how you expect it to work? Is that going to be years down the road? Months?
Those are great questions. And I think the manufacturers who already have boosters in early trials are trying to sort through that. One thing I will say from the regulatory hurdle standpoint is the boosters will not require the same level of FDA review and the scrutiny that you had and getting the FRA emerges outhouse authorizations. So they've been kind of granted in the influenza vaccine that they're not going to have to go through the same level of regulatory review, and they have them in prototype right now. But the questions you asked have not really been answered yet.
Which order do you go in? And it may be much less a function of when you were vaccinated. Right. Because we're all getting the same vaccines. It's what viruses are present, what variants are present now, not how long you've been vaccinated. There are questions about vaccine longevity and so on. But I think even Doctor Fauci said we're probably looking at 2 or 3 years at a minimum. That's not the problem. The problem is that's for the wild type that the vaccines were all developed for. So it's an interesting situation for us to be in with this race against time and where boosters will come in and how they may be able to thwart this. But again, I fear Richard's battle scene scenario here, which is the boosters aren't going to be around fast enough to necessarily deal with that outbreak when the battle is being won in some local areas. That's my fear.
Yeah. I think that's a really good point. And we'll just have to see as it plays out, as we've been doing for the last year and a half or so. But thank you both for coming on the show and sharing your expertise with this. It is very, very needed. And people can head over to HealthyDavisTogether.org to learn more. And obviously the CDC is going to be the best resource in terms of anywhere you are in America.
So thank you so much for coming on and sharing this perspective on just where we are and where we're headed. I think that's where a lot of people are focused. So thank you both so much.
Thanks, Kira.
You're Welcome.
Good chatting with you.
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[Outro Music] We’re all made of DNA, we’re all made of the same chemicals.
