COVID-19 Mutations & Variants: Everything You Need to Know
This article is part of an ongoing collaboration between the Colorado School of Public Health, the Denver Museum of Nature & Science, and the Institute for Science & Policy. Find all of our previous COVID-19 webinars and recaps here.
As COVID-19 variants emerge across the globe, scientists are racing to understand how dangerous they might be while policymakers try to adjust health guidelines accordingly. Viruses are ever-changing by nature, and each mutated strain poses new and different challenges. What can epidemiology tell us about these new SARS-CoV-2 variants? And how can public health officials stay one step ahead?
Recently, Institute for Science & Policy Director Kristan Uhlenbrock chatted with Dr. Angela Rasmussen, a virologist at Georgetown University's Center for Global Health and Security. Dr. Rasmussen specializes in viruses that are highly pathogenic and/or newly emergent and discussed the fundamentals of mutations as well as what we know so far about vaccine efficacy.
This transcript has been lightly edited for length and clarity. Watch the full recording here.
DR. ANGELA RASMUSSEN: I’m going introduce you to the concept of variants and mutations and what are they are, because I think a lot of times when people hear the word mutation, they think of something like the X-Men, or they might think of cancer. It’s in the context of something that is sort of extraordinary or out of the ordinary — that that mutation always confers some kind of superpower. In reality, especially for RNA viruses like coronaviruses, mutation is actually a completely normal part of the process.
I always start my talks with a territorial acknowledgement and equity statement. Today I'm in Seattle, and I'm presenting from the unseated ancestral homelands of the Duwamish people, and I acknowledge and honor the first people of these territories and their tribal governments, their histories and ancestry and their roles today in caring for these lands. And I'd also like to acknowledge the history of systemic inequity in academic science that has really spanned centuries. My prior institution until November of last year, Columbia University, and my current institution, Georgetown University, were founded using profits from the transatlantic slave trade and the sale of enslaved people. And in addition to that ,they excluded women and people of color from the academic community for more than 200 years. This has left a long and painful legacy of racial and gender-based inequality that continues to this day. So I'm encouraging everybody watching this today: Consider how you can contribute to making scientific research a more equitable enterprise.
And with that, I'm going to get started with this very quick presentation to just describe what mutation and virus evolution is and what we should be thinking about in the context of the variants. SARS coronavirus 2 is an RNA virus. Its genome size is in the range of 1,000 to tens of thousands of base pairs, and in particular, SARS coronavirus 2 has a genome that's 30,000 nucleotides long.
We [humans] are higher eukaryotes and so our mutation rate is much lower than it is for RNA viruses. They mutate all the time. I've shown a little coronavirus here and it's going to do what viruses do: it's going to get into a host and it's going to replicate. When it replicates, it will copy its genome and it will make mistakes. Some of those mistakes are called mutations. Those mutations occur randomly. So you end up with what are called quasi-species, a population of viruses that all have different individual mutations and some of these mutations really do nothing. They won't be selected for in terms of evolution. Some of them will be in a place that is actually harmful to the virus, this is what we call a defective interfering particle. Basically it's a viral particle that has a genome inside that's defective in some way.
And then we might also have some mutants that confer some type of advantage to the virus. As these viruses go out and repeat this cycle of viral replication in a new host, eventually these mutants that have an advantage will take over the population. So you end up seeing a lot of these different mutants that have this genome that's advantageous to the virus compared to the parental virus. And of course the ones with defective genomes don't replicate and they're not preserved, so that’s what's called negative evolutionary selection.
So we've all heard about these variants of concern. And people seem to think sometimes that there's only these new variants and that all the other SARS coronavirus 2 strains that have been circulating are the same and that's not true at all. There are many different variants that have emerged over the course of the pandemic. If you look at this phylogenetic tree, you can mouse over these individual dots and they'll tell you exactly what's different about this from the original parental virus that was collected and isolated a long time ago. It feels like a long time ago, over a year ago in Wuhan, China. All of these are different, and they are different evolutionary lineages that that are related to each other.
So, at some point, for example, this lineage diverged. These variants emerged from that branch and these variants emerged from that branch of it. So, there are many variants. But why are we worried about some of these other ones? This is the one that was discovered in the UK, this is the one that was discovered in South Africa, and this is the one that was discovered in Brazil.
We can look at a schematic of the coronavirus genome. This is how the virus is organized in terms of what the virus particles look like. It is an envelope RNA virus in which the RNA genome which is single stranded and positive and is complexed with an N protein and nucleocapsid protein, and it's stored inside this shell that's bounded by a lipid envelope. In that envelope is the E envelope protein, the M matrix protein, and of course, the spike protein that the vaccines are designed toward. When this gets into a cell, the genome will go into the cytoplasm of the inside of that cell and the genome will be translated into a polyprotein that's encoded by the ORF1a or ORF1b sometimes called ORF1a-b, because we like to make names difficult and confusing.
There are also these sub genomic RNA. These are transcribed and then translated after the virus gets into the cytoplasm during replication, so there's individual RNAs for all of these. This includes spike proteins and E and M protein — these are the structural proteins — as well as all of these other accessory proteins, some of which we kind of know what they do and some of which we don't. But that is where the mutations go. They go into all of these different proteins or genes encoding proteins, and they can have an impact on what the virus is actually doing, particularly mutations in these structural proteins such as the S protein, as we'll probably talk about later.
So these are the three different variants of concern. And you can see here that of interest are these mutations in the spike protein. All three of these variants have these 501Y mutations, which is in what's called the receptor binding domain of the spike protein, and the receptor binding domain is a part of this spike protein that interacts with ACE2, which is the virus's host cellular receptor. So when the spike interacts with ACE2, that essentially is the signal. It's like a locking key that the virus needs to enter and infect your cells, so these mutations are thought to be very important, both in terms of the virus being able to infect cells, as well as antibodies since antibodies directed at the receptor binding domain are thought to be very important for neutralization.
There are a variety of other mutations that are also in the spike protein. Some of them are shared between these mutations and some of them are not. And we're still really looking into what they're all doing. But we know that the three variants are concerning because they're more transmissible, but we don't know how they're more transmissible.
With all of these mutations it's great to know what they are. It's great to know where they are in the genome. But that's a different story than actually knowing what they're doing to contribute to the increased transmissibility that's been observed. So there's a couple different possible mechanisms of increased transmissibility and that's what people are working on right now to figure this out. One possibility is that these mutations increase viral fitness which means they make the virus able to replicate better. This could lead to increased viral shedding. And you can imagine how that might make person more contagious: if they're shedding more virus from their nasal passages, it also could be a longer interval of contagiousness, meaning that a person is contagious for a longer period of time than they would be if they were infected with one of the “old” variants.
Another possibility is that they could increase receptor binding affinity and we already know that the N501Y mutation that I just mentioned does, in fact, increase receptor binding affinity to ACE2. So that could cause increased infectivity, meaning that you don't need to be exposed to as many virus particles to be infected. Basically, the virus is more efficient at infecting cells than it otherwise would normally be. And we know that not only does N501Y increase binding affinity to ACE2, but some of the other mutations that have been found specifically in the B1351 and P1 variants have first discovered in South Africa and Brazil, respectively, have other mutations that amplify this effect so that they're capable of binding even more tightly to ACE2.
And then another possibility is that this could actually increase virus particle stability or virion stability (that's what we call a virus particle). Mutations and all of these structural proteins that I was just mentioning — S, E, M, and nucleocapsid — could make the virus capable of being stable in the environment for a longer period of time. So if you’re in an enclosed space with somebody who's infected with one of these variants, maybe you don't need to be in there for as long to be exposed to a sufficient dose of infectious virus to become actually infected.
KRISTAN UHLENBROCK: We really appreciate that level of detail and I want to try to unpack some of that. Do we know if that mutation pathway would turn it into a less effective or more contagious virus?
AR: We don’t, and that's one of the troubles with working with a virus that is brand new. We know of course that the spike protein is important. So any type of deletion of the entire protein in the receptor binding domain is not going to result in an infectious virus. But individual point mutations are very short deletions. We don't really know what kind of effects that will have. The best we can do is compare it to other related coronaviruses that we have studied in more details such as SARS coronavirus classic. The problem with that is that SARS coronavirus 2 has some features genetically that SARS coronavirus classic does not have. And obviously it's a different virus that causes a very different disease.
One of the reasons why COVID-19 has become a pandemic and SARS classic did not is that it can be transmitted pre symptomatically. With SARS coronavirus classic, if you had SARS, that's when you became contagious. So if you were getting a fever, if you were developing respiratory illness and became symptomatic, you could be isolated without requiring a test. With SARS coronavirus 2, you know, you can be transmitting virus without having any idea that you're actually sick. So there are a lot of big differences between both the viruses, even though they're closely related, which makes it very difficult to just use SARS and what we know about that to make conclusions about what's functionally important for SARS coronavirus 2.
Unfortunately, the way that that we figured this out is by basically making mutant viruses, infecting cells and animal models with that and seeing what mutations have an effect and which don't. To further complicate this, sometimes there's a phenomenon called epistasis in which multiple mutations will have a synergistic effect. So you have to get them in the right combination when you test them to actually see that effect in the lab. So it really is very challenging and that's really why we can't just look at the sequence and say why we know that that's important, because many parts of the genome we just don't know what's functionally relevant and what not, for the virus or for the host.
KU: What do we know about the more noteworthy mutations? Are they causing more severity in the disease?
AR: There has been very limited data from the U.K. — and I'm pretty skeptical of it actually —that says that the B.1.1.7 variant actually increases disease severity or increases mortality risk. I'm not sure about that, just because that's based on a pretty small subset of patients that they analyzed to determine that. But the real thing that all three of these variants have in common is that they're more transmissible and the reason why this was even on anybody's radar is that these variants became the predominant circulating variants in the regions where they emerged very quickly.
So, by contrast, there's another mutation that was characterized back in May called D614G. And because that was becoming dominant in the US and in Europe, people suggested that it was more transmissible. And honestly, there may be a slight transmission advantage after months of doing experiments on that particular variant, but it's not it's not as clear as that and it took months to become the dominant circulating strain. The B.1.1.7 variant, for example, became dominant in one and a half months in southeast England. So that's unusual. That suggests that the virus is able to outcompete effectively all the other viruses that are circulating around there. So we know that all of these are more transmissible and the reason why that's a concern is that with COVID, really, the hospitalizations and deaths are kind of a numbers game. The vast majority of people who get COVID will not end up going to the hospital because of it. And as many people who want to downplay the severity of the pandemic will point out, there is a fairly low case fatality rate of SARS coronavirus.
But if you get enough people infected with it, then you are going to start seeing those numbers skyrocket, which we've actually seen here without these variants. And then you'll see a coincident burden on the healthcare system that can lead to other morbidity and mortality because healthcare resources are strained or used up and healthcare rationing has to be implemented. So that increased transmissibility and the potential for additional surges is really what's of concern with regard to these variants, much more so than increased virulence.
KU: How difficult is it to detect these emerging variants?
AR: So, the UK is very good at detecting them which is why they detected the B.1.1.7 sequence. In the US, not so much, which is why it took us a little longer to figure out that these variants were actually already here, because we were sequencing less than 0.5% of all of the sequences. Genomic surveillance is really important, and I'm glad to see that now the CDC is under leadership that recognizes the importance of that and there is starting to be more dedicated funding for that. But prior to this sort of wake up call about these variants, the genomic surveillance that was occurring in the US was mostly people using their own grant funds, their own research funds to do a little sequencing here and there. There are a couple surveillance programs that work with influenza that had been somewhat repurposed. But we were not doing nearly enough genomic surveillance. So I'm glad to see that at least we're learning that lesson that we need to be doing more of that.
KU: There’s some talk about being reinfected from COVID-19. What do you know about reinfection rates and how does that tie in?
AR: Yeah, so this is a pretty good segue actually into antibodies and vaccines, because the short answer is we still don't know that much about reinfection. We think that in general, reinfection is fairly rare. There would be epidemiological indications as people were getting COVID and then months later coming back and being put in the hospital again with COVID. And that's not happening all the time, but it has happened. So we know that reinfection does occur and this reinfection has been confirmed, in some of these cases with sequencing confirming that they were actually infected with a different variant of SARS coronavirus 2.
And people have been very alarmed at the finding that in South Africa, where there were a high percentage of people participating in a clinical trial, who previously had COVID-19 then tested positive, suggesting that they were reinfected with the variants at a rate of close to 4%. Now that's alarming. But we don't know that much about what those people's immune status was. We don't know if maybe some of them had lower levels of antibodies, if they didn't have good immune responses to their first infection. We don't know that that's going to be the case with vaccines because this rate of reinfection was reported in the placebo group.
There's no way to tell how vaccine induced immunity would protect against that variant, but there's no indication that they were very sick from their reinfections. So that may suggest that while the variant is capable of evading some immune responses, it's not capable of evading all of them and people who've previously been infected are still protected against severe disease, even though they may be susceptible to reinfection. But it's an important area that there's just a lot of knowledge gaps in right now. So we definitely need to look into it more. But I'm not as worried about it as some of the headlines have suggested we should be. Just because it doesn't seem like all those reinfection cases were ending up in the hospital with their reinfection case of COVID.
KU: There’s been reporting about countries considering spreading out the dosages of vaccines to try to get more people at least a first shot. What are your thoughts on that strategy for vaccine implementation?
AR: So, I'm opposed to that strategy without data to support it. With the AstraZeneca vaccine, there is data to support it, there's data that suggests that that spacing out the shots by up to two weeks longer actually can result in more protection. So for that vaccine, sure, go ahead. 12 weeks is great for the second shot. For the Pfizer vaccine, there's just no data to support that. And I know that in the UK, they said, you can do 12 weeks between shots for both AstraZeneca and Pfizer. Those are two very different vaccine platforms. The Pfizer vaccine is an mRNA vaccine. They work pretty differently in terms of how they express SARS coronavirus 2. I'd be very reluctant personally to suggest that anybody getting the Pfizer or Moderna vaccines space it out beyond six weeks, which is the limit to which those dosing intervals have been tested.
There is some data suggesting that you can go up to 42 days after your first shot and still have equivalent protection for Moderna and Pfizer. But 12 weeks, I'm not sure. And the reason I think that that could be dangerous is because a lot of people may be like, we have other vaccines, we sometimes wait years before giving a booster shot for those. What's the harm? The harm is not that I think that a second shot given 12 weeks after the first shot would mean that the vaccine wouldn’t work. It's that people might not be protected for that entire period of time from the first shot alone, and there is some data that suggests that for both of Moderna and Pfizer vaccines. You really do need that second shot to induce high levels of neutralizing antibodies which are the antibodies that will render the virus non infectious. So for that reason, without any data suggesting otherwise, I recommend that people get their second shot on time at least within six weeks of the first shot.
KU: Is there anyone working on a vaccine that is potentially going to protect against all these variants, or a kind of a pan-vaccine?
AR: Yeah, I think in the future certainly there is the possibility of developing a more universal COVID vaccine. And the reason we can't do that right now is that we don't know what mutations are going to be important or advantageous for the virus so it's really hard for us to predict how the virus is going to change, and specifically how the spike protein is going to change. The spike protein is the antigen, or the target that antibodies are elicited to during vaccination. And we just don't know how the antigen is going to change. As the pandemic goes on and as we start to control this, we will be able to see the variants that are going to emerge and then we can develop boosters and potentially a universal vaccine. I think that it's very wise, even though there's no evidence that the vaccines for the most part are completely non protective against these variants. There may be reduced efficacy for some of them but it's not completely shot.
So I think that it is wise to start making boosters and the good thing about these vaccines is that it is actually very technically easy to change them, especially the mRNA vaccines. If you think of mRNA as a message, it's a matter of changing the spelling of a few words effectively. So there is a more complicated regulatory process that we'll have to go through, but I'm not sure how that is going to work, but we do this every year for influenza vaccines. We change them based on what strains are circulating. So I'm confident that we can do this as well for the SARS coronavirus 2 vaccines, and it may mean for most people realistically that you're just getting a booster.
KU: Are there potential avenues of research besides vaccines to change the course of viruses and how they interact with their DNA?
AR: Well, so RNA viruses don't really interact with our DNA. And maybe I should have explained this a little better in the beginning. When the RNA viruses go into the cytoplasm, that's not the total inside of the cell. The inside of the cell where our DNA is is the nucleus of the cell and most RNA viruses including coronaviruses don't get in there. mRNA doesn't get in there either.
Going forward though, this is a really broadly interesting question that I could probably spend the entire time talking about because this is actually what I study, and that's the host response to viral infection. Viruses have to interact with our proteins and those cells in many different ways. And it's actually not well understood for any virus. You know, some of those interactions are well understood, but not all. So when we say the viruses hijack cells to get into them and to replicate, that basically means that they're appropriating different types of cellular machinery to replicate themselves. They're also usually messing with the host immune system, including the innate cellular immune systems, so that the cell basically isn't trying to defend itself against them. So there's all these different interactions and they're really important in terms of pathogenesis as well as susceptibility and long term immune protection, but like I said, that's my entire area of research.
KU: What is the easiest way to get an antibody test and how accurate are they these days?
AR: That depends on the antibody test. But you should be able to get an antibody test just by asking your provider to order one for you. I know in New York, they were offering antibody tests last summer to people who wanted to come there and see if they had gotten COVID during the spring surge last year when PCR tests were very unavailable for people and people didn't know if they'd had COVID or not.
So, you should be able to request an antibody test. The problem there is that there are a lot of different antibody tests and not all of them are created equal. So you're going to want to ask your provider when they're ordering that test for you to order one that is both highly sensitive and highly specific, and that should be in the package insert. The major manufacturers of antibody tests are pretty good from what I've seen.
One thing to think about too is what you want the antibody test for. If you want to see that you're having a good response to the vaccine, you also need to ask your provider to make sure they're ordering an antibody test that's looking specifically for antibodies against the spike protein. And that's actually really good because you can distinguish in a vaccinated person, for example, if they've actually been exposed or infected with coronavirus after vaccination. If they haven't, they won't have antibodies, and if they have, they will, because the vaccines are only directed against the spike protein. If you wanted to see if you had COVID in the past, any antibody test will do. If you want to see that you're having a good reaction to the vaccines, then you want to make sure that you're asking for an antibody test that specifically looks at antibodies to the spike protein.
KU: How is our interconnected nature shaping this pandemic, and will COVID stay with us long term?
AR: Another version of this question is, do you think the virus is going to become endemic? I think that there's a good chance that it will. I think it's very difficult to forecast because of a couple different things. One is, how quickly can we vaccinate as many people as possible? Another is, how many people are willing to actually be vaccinated once we do have those supplies? A third is, are people going to continue to take precautions right now in the short term to reduce community transmission?
And a lot of people have been discussing this, that we need to get vaccines done faster, and we do. But right now we're still having supply shortages. We also need to really double down on our efforts to reduce transmission in the community. That means increased adherence to masking, physical distancing, ventilation, avoiding gatherings and enclosed spaces, hand washing and disinfecting high touch surfaces, staying home if possible. We’re acknowledging that this is not possible for everybody but the more people can apply any of these measures, whenever they are interacting with other people in the world, the more they're going to reduce their own exposure risk, the more they're going to bring community transmission down.
If we can bring community transmission down while we simultaneously ramp up vaccination, I think that we have a very good chance of really getting this under control sooner rather than later. That doesn't mean that it won't become endemic because the larger problem is that as we go back to international travel and as we sort of go back to “normal life,” we're gonna have to contend with the fact that that even if we get to herd immunity in the US, there's not going to be that globally. We need to really think about how we're rolling out vaccines globally in an equitable way because until all of us are safe, none of us are.
I think that I would really encourage people to think about the long term endgame. This is not going to be something that's going to just go away overnight. The end of this pandemic is going to be more gradual. And I know that's tough. This sucks. I hate it. I hate being stuck in my house. I love doing stuff like this. Normally I'd go to conferences in person and give a lecture like this. I hate having to do this over Zoom and I'm tired of it just like everybody else is. But I really do encourage people to just hang in there a little bit longer. As we get more and more vaccines out to people, we will be able to start sort of easing back into a more “normal” life.
KU: We have a story, and I'm not going to read the whole story, shared by one of our guests. In essence, this person has received two doses of the Moderna vaccine and has had some side effects and is worried about how that will affect the rollout. What are some of your thoughts on that and do you have any tips for communicating with people about this?
AR: Yeah, absolutely. And that that is a very legitimate concern because many people have reported that the side effects — while again, not lethal and not permanent — are difficult for many people and more difficult than your annual flu shot. Some people have reported being knocked out for 24 to 48 hours, especially after the second shot and understandably that makes people reluctant to take the vaccine.
So what I've what I've suggested are a couple things, and I suggested this to my parents who got their first shot of Moderna a few weeks ago and are getting their second shot next week. I asked them how was the first shot, they said, oh well, you know, we have pain but otherwise not too bad, but they've heard it's a lot worse after the second shot. For some people, that has been true. I think that early on, when the phase three clinical trial started to read out, one thing that that could have been done better was communicating with the public about those side effects upfront. I think that it has been more difficult than it needed to be because that wasn't really disclosed
Alongside the very encouraging and awesome topline efficacy data. And I think that it is really important to be honest and open with people about some of the things that might make this difficult, so people can prepare themselves. I think that nationwide, there should be some policy changes to support this as well. And this actually makes it easier for people to do non pharmaceutical interventions. For example, paid sick leave. If people could take a day or two off after getting the vaccine, plan ahead for it and not worry about their jobs and not worry about not getting paid, I think that would make it a lot easier for people I think it's a tough ask to say that okay, you might basically have flu like symptoms where you feel like crap for a couple days after you get the vaccine but guess what, you still have to go to work.
I think there are things we could do to prepare people for it better and make it easier. And going forward in the future, if there was a need for boosters — we don't know anything about like if a third shot would be even worse, in terms of the side effects. So that's definitely something that needs to be looked at. We also need to start thinking about doing what's called heterologous boosting, and that is when you use a different vaccine platform to boost. Now, I don't know if that would have any effect on side effects. But the side effects reported for the Novavax vaccine, for example which is a protein subunit vaccine, different than mRNA, that's actually giving you the spike protein has been associated with fewer side effects and same with Johnson and Johnson. So it may be possible that if you can sort of mix and match booster shots, that we may be able to help people get away from some of these side effects.
I think that it's a combination of just being honest with people about the side effects. Also, there is one encouraging think about the side effects, and that is that when you get sick with the flu or with a cold, the symptoms activate your body's immune system, responding to that infection and that's what the side effects are. For this virus too, if you do have bad side effects, it actually just means that your antiviral machinery is pumping out a ton of interferon which is an important molecule for recruiting antiviral immune defenses. It means that the vaccine is working. And I think that that that does give people a little bit of comfort that, you know, okay I feel terrible but it's a lot better than having COVID, and it's a sign that this vaccine is eliciting real robust immune responses and it's going to protect me. So I try to cover all those points when talking to people who are concerned about the side effects and what they might need.
Ultimately, to drive one more point home, having those side effects for 24 to 48 hours is much better than having COVID, because even if you have mild COVID, you know, as many as 30% of people have reported having some symptoms of long COVID. It's something that doesn't necessarily go away. It's not transient like the side effects. So get the vaccine, tough it out through the side effects if you can, and know that you're not going to have a much longer term problem because you're protected from COVID.
KU: As a final word, what's your greatest hope for the rest of 2021?
AR: So, my greatest hope is that people actually just hang in there for just a little bit longer, long enough for us to increase the supplies of vaccines so that people can be vaccinated on demand. As I was saying earlier, I'm really concerned with the idea that just because we have the vaccines that we're completely in the homestretch and we're free and clear. We're not, and these variants are just a real red flag about that.
I think that if people can just hunker down for a couple more months — this is not eternal lockdown. This is not eternal restriction. But if people can hunker down, hang in there for a couple more months, get community transmission down while we simultaneously get vaccination up, we will be able to go back to a more normal life. We will be able to go indoor dining. We will be able to go to bars. We'll be able to hug our parents. We’ll be able to hug our kids and see our kids and grandkids and do all those things that we've been missing out on doing through a combination of both elimination through targeted interventions, and vaccination.
Vaccines are, you know, certainly the greatest public health triumph of the modern era, although I've argued with people as to whether sanitation and water are equally good. They're also good. But vaccines have prevented hundreds of millions of deaths worldwide. Not just the COVID vaccine, but all vaccines. Vaccines are just a triumph of public health I love them, but they're not the only thing that's going to get us through this. I really hope that these variants are a wake up call for people because if we don't get transmission down, new variants might also emerge. As I said at the very beginning of my talk, mutation is a normal thing that happens when viruses replicate. If you give the virus more opportunity to replicate, new variants will emerge. So we need to take away those opportunities for the virus to replicate while simultaneously protecting ourselves against it.
And if we can just, again, for a little while longer, find that extra burst of energy to make it across the finish line, I think that we're going to have a very nice, summer, fall, winter 2021. So that's my greatest hope: that people will stop looking at this as a sort of one sided thing. Non- pharmaceutical interventions are a part of that bigger picture.
The Institute for Science & Policy is committed to publishing diverse perspectives in order to advance civil discourse and productive dialogue. Views expressed by contributors do not necessarily reflect those of the Institute, the Denver Museum of Nature & Science, or its affiliates.