Will Vaccines Work Against New Variants Of The Coronavirus?

17:16 minutes

This story is part of Science Friday’s coverage on the novel coronavirus, the agent of the disease COVID-19. Listen to experts discuss the spread, outbreak response, and treatment.

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The rollout of COVID-19 vaccination programs around the world has been anything but smooth. Complicating the effort is the virus itself. The original coronavirus genome that the current vaccines were based on has mutated. Now, there are three virus variants, and experts are somewhat concerned. How will the vaccines scientists have worked so hard to make fare against these three variants, and future ones? 

Stephen Goldstein, post-doctoral researcher in evolutionary virology at the University of Utah joins Ira to talk about what the new numbers on vaccine effectiveness against these variants really mean. 

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Segment Guests

Stephen Goldstein

Stephen Goldstein is a post-doctoral research associate in evolutionary virology at the University of Utah in Salt Lake City, Utah.

Segment Transcript

IRA FLATOW: This is Science Friday. I’m Ira Flatow. The rollout of COVID vaccination programs around the world has been anything but smooth, and complicating the effort is the virus itself. The original coronavirus genome on which our vaccines were based has mutated, resulting in three variants that have experts somewhat concerned. How will the vaccine scientists have worked so hard to make fare against these three variants and even future ones?

Here to tell us everything we want to know about vaccines and variants is Dr. Stephen Goldstein, a post-doctoral researcher in evolutionary virology at the University of Utah.

STEPHEN GOLDSTEIN: Thank you for having me.

IRA FLATOW: I hope I didn’t put you off by saying you’re going to tell us everything we want to know.

STEPHEN GOLDSTEIN: I’ll do my best.

IRA FLATOW: I’m sure you will. OK, let’s talk about what a variant is. Now, the virus is constantly mutating, right? Is that what causes these variants?

STEPHEN GOLDSTEIN: That’s exactly right. So the virus is constantly mutating, and there are many different variants, most of them not of concern. These three that we’ve all become more familiar with are what are termed variants of concern, and that’s because they have particular mutations, or sets of mutations, that do give us concerns that they may be more transmissible or affect vaccine efficacy, as you alluded to.

IRA FLATOW: We have been hearing the word variant and the word strain being used interchangeably. Is that correct? Are they the same?

STEPHEN GOLDSTEIN: We probably shouldn’t use them quite interchangeably. Like I said, there are variants associated with all the different mutations that are happening all the time. We’d probably shift a variant over into the strain category once we’ve confirmed that there is some different biological property about it, so is it more transmissible, is it more or less deadly? And so some of these, probably the B117 variant in particular that’s come out of the UK, we can probably call that a strain at this point. The other two, probably also, but maybe there’s some difference of opinion on whether we’re there or not.

IRA FLATOW: Well, let me talk about the UK variant first that you bring it up. There is a report that the UK virus, the one that is more contagious, has acquired the worrisome mutation seen in the South African virus and the mutation found in the Brazilian virus. Does that double dip make it an extra burden for the vaccines?

STEPHEN GOLDSTEIN: So it just brings it closer to what that South African variant and the Brazilian variant already appear to be. It’s a particular mutation that’s shared by the South African and Brazilian variants that some viruses in this UK lineage appear to have acquired. Most of the virus circulating in the UK doesn’t have that particular mutation right now.

And it’s not clear if that, as you called it, double dipping variant is really going to take over or not. We’ll have to wait and see. It would pose similar concerns that the South African and Brazilian ones pose right now, but I don’t think we’re quite there yet as far as really looking down that barrel.

IRA FLATOW: I’ve heard that some of the mutations in these variants affects, quote unquote, “neutralization.” What does that mean?

STEPHEN GOLDSTEIN: So neutralization is a term looking at what’s going on in the lab. So it basically means how well the serum from somebody who’s either recovered from COVID or been vaccinated with one of the vaccines, you take their blood serum, and you mix it with the virus and look at how much of that serum you need to prevent or reduce the infectivity, the infection, by that virus. And that’s what we call the level of neutralization, the amount you can dilute that person’s serum by and still, say, reduce infection in the lab by 50% or 80%. You can pick whatever number you want.

IRA FLATOW: Let’s talk about effective vaccinations. What do we mean when we hear vaccines are less effective against variants? What does less effective mean?

STEPHEN GOLDSTEIN: It’s a good question, because we have to really think about what the vaccine trials are measuring. So most of them are measuring symptomatic COVID, could be mild, moderate, or severe. And so that in many cases, Moderna and Pfizer at least specifically, means any one of the symptoms associated with COVID.

So if you’ve got a cough or a fever, whether alone or together, and that’s the worst that happened, that would be considered an event that’s a vaccine failure. But what we have seen is these vaccines still seem completely effective against the variants at preventing severe disease, hospitalization, and death, which are really the bottom line for most of us. If the vaccines lose some efficacy at preventing you from essentially getting a cold, but your chances of getting really sick or dying are still 0%, that’s a pretty great outcome still.

IRA FLATOW: So if you have a vaccine that’s effective, let’s say, at 50%, that’s still pretty good, because it could prevent you from developing the severe part of complications.

STEPHEN GOLDSTEIN: That’s exactly right. So that Novavax trial where we saw the efficacy in South Africa was 50% instead of the 90% that was seen in other parts of the world, there was still nobody infected with that South African variant who was hospitalized or died. So that’s why we have to be careful about these efficacy numbers. It still looks like you’re in pretty good shape here.

IRA FLATOW: Let’s talk about these vaccines, the Pfizer, the Moderna, Johnson & Johnson, Novavax. They have all tested their vaccines against these variants. And I understand that they each did it a bit differently, right?

STEPHEN GOLDSTEIN: Yeah, they did do it a bit differently, partially just by luck. So Moderna and Pfizer were running their trials months ago, these variants hadn’t even appeared yet. So they couldn’t have tested them against these variants in the real world. Johnson & Johnson and Novavax have been running their trials later, and they happened to be running them in South Africa, which lucked them into the opportunity to directly see how their vaccines work against the South African variant. Moderna and Pfizer are limited to lab studies right now.

IRA FLATOW: And what does that mean about the quality of the testing that’s going on if they’re testing them different ways?

STEPHEN GOLDSTEIN: It means that we certainly have more real-world data about Johnson & Johnson and Novavax, which, of course, is our favorite kind of data to have. What we can do, though, is take serum from people who have gotten the Johnson & Johnson or Novavax vaccines and do the same kind of tests that are being done with serum from people vaccinated with the Moderna or Pfizer vaccines. And given we know what kind of efficacy impact we’ve seen against the two that were trialed in South Africa, if we do those lab experiments in parallel, we can probably make some pretty good inferences about the efficacy of the Moderna and Pfizer vaccines.

IRA FLATOW: Are we equally concerned about the three variants, the UK, the South Africa, and the Brazil one? Or should we be concerned about one more than the other?

STEPHEN GOLDSTEIN: So I think right now we should actually be concerned most about the UK variant, not because it necessarily seems to really impact vaccine efficacy, but because it seems to be the best established already in the US compared to the other two variants, and it clearly does appear to be more transmissible. So as our vaccine rollout is going slowly, there’s a risk that as this UK variant spreads more rapidly that we could have a few more surges to deal with because of this UK variant.

Concerns about vaccine efficacy, I think, are a little farther down the line, because the viruses that are circulating in the US right now are totally susceptible to the vaccines that people are getting in the US right now. And as we discussed, the vaccines are likely to prevent severe disease, even among people infected with the South African or Brazil variant. So I think what we have to worry about now is the virus that’s spreading here the most.

IRA FLATOW: And how could you tweak the vaccine we’re giving out to make it more effective? Is it a simple tweak, or do you have to start all over again?

STEPHEN GOLDSTEIN: From a technical standpoint, it’s a pretty simple tweak. You would just exchange the genetic code, the spike protein genetic code that’s in the vaccines, switch it so you have the genetic code for the spike protein that’s in the South Africa or Brazil variant. And then you’d have to produce that, of course, it takes a bit of time, and go through whatever regulatory steps the FDA says are necessary to approve an updated vaccine. But technically in the lab it’s pretty trivial.

IRA FLATOW: Pfizer and Moderna vaccines were made from the latest technology, the mRNA technology. But some people have called into question whether they’re working as well as traditional vaccines. Are there any clues that the way these vaccines were made is contributing to their ability to neutralize the virus in these new variants?

STEPHEN GOLDSTEIN: As far as I can tell, my read of the data is that these mRNA vaccines are spectacular and that they basically appear to be as effective as any vaccines we have on the market for any viral infection. There’s a question, of course, of how long the immunity will last and how often we may need to update the vaccines based on the virus mutating. And those are questions that just remain to be answered. But as far as the efficacy, at this point they look incredible.

IRA FLATOW: And of course, there’s the question, will we have to keep getting vaccinated to keep up with these variants? And to look for that answer, we spoke with Dr. Adam Lauring, a clinical immunologist at the University of Michigan. And he shared his thoughts on a potential vaccine schedule.

ADAM LAURING: The way I look at it, we’re somewhere along the spectrum between polio, measles, hepatitis B, but then there’s flu. What’s unclear, I think, is where we’re going to end up with SARS-CoV-2 on that spectrum. I guess I would be surprised if it were every year, but I would be surprised if it were every couple years, or every three years, or something like that.

IRA FLATOW: So would you agree, then, we might be taking booster shots every few years for this virus?

STEPHEN GOLDSTEIN: I think that’s probably right. Looking at data from other coronaviruses that generally cause the common cold, so not a huge concern medically, but they do seem to change enough over the course of a few years that our immune systems lose some of their ability to recognize them. And if we expect SARS-CoV-2 to take a fairly similar course, it makes sense that maybe every two, three, four years we might need to get an updated booster shot.

IRA FLATOW: Is there a way to make a vaccine that would work against all the mutations, a universal vaccine? And if theoretically that were possible, where and how would that work?

STEPHEN GOLDSTEIN: This is one of my favorite questions, because this is something that I actually think should be a huge priority for our biomedical research funding agencies. In theory, it should be possible. And people have been working for years on universal influenza vaccines. And I think some of the same principles can be used to guide our research in trying to make universal coronavirus vaccines.

The idea here would be to develop vaccines that would guide the immune system to target parts of the coronavirus spike protein that don’t change very much, the least likely parts of the protein to mutate. And we already know where those are. The question is, how do we shape our immune response to direct it towards those areas? And we just need the research to do that. But I think theoretically it’s possible and needs to be done.

IRA FLATOW: Dr. Goldstein, I’ve been learning from scientists that the vaccines that we have now result from a lot of the work done to try to find an HIV vaccine. Do you think that if we work on this a little bit more, it might push the development of an HIV vaccine?

STEPHEN GOLDSTEIN: Well, I think from a technology standpoint, the pandemic has clearly accelerated the development timelines for mRNA vaccines, and frankly, for the adenovirus vector vaccines as well, like the Oxford vaccine or Johnson & Johnson. HIV is a difficult target, because it mutates so rapidly. And so the reasons why we don’t have an HIV vaccine, I think, go well beyond a technological standpoint. But if these new technologies make it easier to develop an HIV vaccine, then that would be great, and we’ve certainly jumped ahead in our technical achievements with some of these platforms.

IRA FLATOW: I want to go back to the future for a minute and talk about the first vaccines that were made with the virus itself that was inactivated or weakened, going all the way back to Louis Pasteur and then into the polio vaccine. What is wrong with that technology to create vaccines of today?

STEPHEN GOLDSTEIN: So inactivated vaccines, there’s nothing wrong with them. I think that the mRNA and adenovirus vaccines have a bit of an advantage, because our immune response has two different elements to it. So one are the antibodies we’ve all heard so much about, and the development of those is assisted by helper T cells. There’s another part of the immune response called the killer T cells.

And what those can do is if the virus slips past your first line of defense, even if you’ve been vaccinated, those can swoop in and kill the cells that have been infected and nip the infection in the bud. Inactivated vaccines only produce that first part, that helper T cell and antibody response, which when it works is great, but it doesn’t really give you that last line of defense that you get from, say, these mRNA or adenovirus technology vaccines. And so that’s why I really like those.

IRA FLATOW: It’s always good to have a backup, right?

STEPHEN GOLDSTEIN: Exactly. It’s always good to have a backup. The live attenuated or weakened vaccines do this too. The issue is they can’t often be given to people who are immunocompromised, because even a weakened version of a virus could cause disease in someone who’s immunocompromised, whether through some sort of disease or medical treatment. Often they’re not given to women in pregnancy. So these new technologies have a lot of the benefits of those without the downsides.

IRA FLATOW: This is Science Friday from WNYC Studios talking about COVID-19 mutations and vaccines with Dr. Stephen Goldstein, a post-doctoral researcher in evolutionary virology at the University of Utah. Do all three vaccines do the same thing, have this backup system to boost the efficacy of the vaccines?

STEPHEN GOLDSTEIN: So the Moderna, Pfizer, Johnson & Johnson, and Oxford vaccines all produce the antibody helper T cells side and the killer T cells, and that’s because the spike protein is made in your body. We’re injecting the genetic information, but then your own cells actually make the spike protein. And that’s the key difference. That kind of mimics natural infection.

The Novavax are just injecting the spike protein in, and so your body sees it outside of your cells and makes antibodies and those helper T cells, but that’s it. And this is just like a technical point of immunology. To get that killer T cell response, you need that protein that’s provoking the immune response to be made inside your cells.

IRA FLATOW: Well, so if I could choose which vaccine to get, I’d want to get that extra one.

STEPHEN GOLDSTEIN: I would as well. I would say right now while we’re supply limited, if you have a chance to get a COVID vaccine, get that COVID vaccine. They all work. And it’s worth pointing out that even the Novavax vaccine protected very well against severe disease, even from the variant. But yeah, if you could go to the doctor’s office and choose from a menu, I would personally choose one of the vaccines that is going to get those killer T cells cranking as well.

IRA FLATOW: Would it be fair to say that over time the vaccines, the number, their high efficacy number, is going to drop and drop as these variants come out? And at what point do we need to actually tweak them? And who makes that decision about tweaking them?

STEPHEN GOLDSTEIN: So I think it’s fair to say that over time some of those efficacy numbers may start to come down a bit. Again, though, that may not mean that people are becoming more susceptible to severe disease or death. But of course, we’d like to keep people completely healthy if we can.

To figure out exactly when we need to tweak them, I think that’s a question we don’t really have an exact answer to yet. We need to figure out what are known as correlates of protection, which means we need to figure out what level of antibodies you need to have to be protected. And then if people’s antibody levels against a particular strain start to decrease towards that level, that minimum level of correlative protection, we’d probably talk about updating the vaccine.

But they’re going to make these formulations in advance, the updated formulations, and then we’ll be able to pick whichever one seems to be most urgent to actually put into production. The timeline for that actually happening, of course, depends on both manufacturing and regulatory questions. And the manufacturing, hopefully with more money we can develop the capacity to maybe in parallel, as we continue to manufacture the current vaccine formulations, start manufacturing the updated one.

And I can imagine that we’d be ready to start boosting people towards the end of this year, which seems sufficiently quick to me. If we do start boosting people towards the end of this year, I don’t think that means we’re going to need boosters every year. It may mean we need a relatively quick booster this first year or two of the pandemic, and then I think it’s more likely we’re on to something like a two to three to four-year schedule.

IRA FLATOW: Well, the timeline could then depend on how much money we have to spend on getting those new vaccines out, would they not?

STEPHEN GOLDSTEIN: Money always helps in science, always makes things move faster.

IRA FLATOW: [LAUGHS] It certainly does. Well, we’ll all hope for that. And I want to thank you very much, Dr. Goldstein, for taking time to talk with us.

STEPHEN GOLDSTEIN: Thank you for having me.

IRA FLATOW: Stephen Goldstein, a post-doctoral researcher in evolutionary virology at the University of Utah.

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