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A Medical Doctor Explains What We Know About New Coronavirus Strains

Two new coronavirus strains have been discovered, and experts wonder whether approved vaccines will prove effective against them. (Photo: Tang Ming Tung/Getty Images)

The medical community is reporting two new strains of the virus that causes COVID-19. The first variant of the novel coronavirus was discovered in the United Kingdom in the fall, and the second in South Africa not long after.

Dr. Kevin Pham, a medical doctor and a visiting policy analyst at The Heritage Foundation, joins the show to explain what we know about the variants of the coronavirus, and whether vaccines will prove effective against them. 

We also read your letters to the editor and share a “good news story” about The Los Angeles Dream Center and its successful efforts to support its community during the pandemic through 1.5 million free meals, tutoring help for students, and housing assistance for the needy. 

Listen to the podcast below or read the lightly edited transcript. 

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Virginia Allen: A new strain of the COVID-19 virus has been detected and here to help us break down what we need to know about this new strain of the virus is Kevin Pham, a medical doctor, and a visiting policy analyst at The Heritage Foundation.

Dr. Pham, welcome back to the show.


Dr. Kevin Pham: Oh, thanks so much for having me back.

Allen: So I want to begin first just by thanking you for all of your contributions over the past month. It has been awesome to have you on this show multiple times, to have you writing for The Daily Signal, and really just offering insights and opinions as a medical professional about COVID-19, what’s going on, what we need to know. And obviously right now, as we’re looking at this new strain, once again, thank you for being willing to come on the show and break this down.

So if you could, just tell us a little bit about what we know about the new strain and is this something that we should be concerned about?

Pham: Yeah. So … there are actually two new strains that we’re concerned about right now. One was first detected in the U.K. and that’s the one that’s been making the news. That one’s been identified back in October, and then starting around November, December, it started to really spread. And there’s another strain that was detected a little bit more recently; that one originated in South Africa. They have similar mutations, but they seem to have different characteristics.

The thing about the U.K. strain is that it seems to be highly transmissible. Whatever mutation that it picked up has made it much more … [it] has been able to infect much more people, much more rapidly. And the South Africa strain, it has a similar mutation. It’s in roughly the same spot, but for some reason it doesn’t seem to have picked up that extra infectiousness that the U.K. strain has.

But they’ve both been around for a relatively short amount of time. So we haven’t quite characterized it fully, but these two things are of concern.

What we have not seen yet is these different strains causing more severe disease manifestation. So with regards to the U.K. strain, it infects people a lot more quickly, but it doesn’t seem to be causing worse disease. And so that’s one thing that we can breathe a little bit of relief about. It hasn’t caused worst disease and more infectiousness at the same time.

Allen: OK. So specifically with the U.K. strain that was discovered, you mentioned it’s more contagious. Do we know how much more? Are any percentages being thrown out about that? Do we have a number that we’re confident in landing on?

Pham: Not really. They haven’t quite characterized how much more infectious this is with regards to the “R number,” the reproduction rate, which is a measure of how many people a person will infect with the strain on average. I haven’t seen the numbers for that, but it’s popped up pretty much throughout the entire world by this point. … Oh, I shouldn’t say the entire world, but it’s popped up in very many places since it’s been discovered. So it does seem to be very infectious and people are blaming it for the recurrent lockdown in the U.K.

I think that it’s fair to say that the increased number of cases is likely the result of a more infectious strain. But being that it’s not quite as deadly, I haven’t been too impressed by this new variant. The media, of course, is trying to make a lot of hay about this, and it makes sense. You hear in the media that there’s this new strain that’s going around much faster. It is kind of scary, but as with all things, we should keep an objective perspective on this.

It does seem to be transmitting a lot more quickly, but it does not cause … we have not seen it to cause more severe disease manifestation. And probably the most important thing, the thing that’s on everyone’s minds, is that we don’t know that this thing is going to evade the vaccinations.

Allen: So let’s talk a little bit more about that. You bring up the vaccine. I think that’s the biggest question on everyone’s mind is: OK, there’s a new strain. Do we know if the vaccine will actually be effective in stopping this in its tracks?

Pham:
The vaccine manufacturers of all the ones that have either been authorized or are about to be authorized–so that’s Pfizer, Moderna, and AstraZeneca–they’ve all said that they believe that their vaccines are going to be effective in protecting against these new variants.

And of course, that’s from the manufacturer, so take that with a grain of salt. But virologically, immunologically, it does make sense because the way a virus would evade a vaccine is if it changes its appearance, its outward appearance, enough that the antibodies that we produce don’t recognize it anymore.

So the way that this occurs, if you think of a virus as a Rubik’s Cube, then the antibodies would have to recognize one of the faces of the Rubik’s Cube. In this case, it’s the so-called spike protein, which you may have heard about. The spike protein is what gives the coronavirus the ability to burrow into the receptors in the body and then invade the cells. This has been the target, the vaccine target. For all these vaccines, that’s been the target.

So long as that spike protein remains relatively consistent, then the vaccines will continue to work. And with the coronaviruses in general, they seem to be fairly stable as far as these spike proteins go. And that’s one of the things that’s been concerning about these two variants in particular, is that they do have a mutation on the spike protein.

So as I was saying about the Rubik’s Cube, if you imagine the virus is like a Rubik’s Cube: If one of the faces stays the same, but all the other five faces continue to change, it doesn’t really matter how much mutation goes on on the other five faces. As long as that sixth face remains fairly constant, then your immune system will recognize it and will be able to attack it. And what we’re seeing with these new strains is that it would be as if you take the sixth face and then change one of the colors of the Rubik’s Cube. So it might not be completely, or it might not be as easily recognized by the immune system, but they [antibodies] will still recognize it enough that they’ll probably still attack it.

Now, the thing with developing an immune response is that when your body starts making antibodies, the antibodies themselves have mutations on them. So then they’ll be able to recognize not just the exact vaccine target, but they’ll also be able to recognize mutations too. So the immune system will have mechanisms to detect variants and strains and mutations and stuff like that.

So that being the case, it is very likely that these relatively minor mutations are still going to be detectable by the antibodies that are developed from these vaccines.

Allen: Dr. Pham, thank you. That’s really helpful to get that image of a Rubik’s Cube and the colors on the sides. That’s just a really great analysis for breaking down how that works with the spike protein. So how long would it take then for medical professionals to determine OK, yes, absolutely, the current vaccines will be effective against either of these two new strains?

Pham:
That really depends on how effective the vaccine is and how much further this virus will spread. And I know that I use the definition, the term in the definition right there, but the more effective the vaccine is, the longer it will take for this virus’s evasive abilities to manifest. So if [the vaccine] is 50% effective against this virus, this new strain, then it’ll take quite a bit of time for 50% of the people who are vaccinated to get this virus. So … there’s no good timeline to determine how well the vaccines will work against this virus.

But what we do know is that even if [the vaccine] is not perfectly protective against the virus strain, it will likely be at least partially protective against severe disease manifestation. And we see that with influenza vaccines. … Even if they get the vaccine completely wrong, then if they vaccinate for the wrong strain of influenza, the people who do get the vaccine tend to have less severe disease with influenza.

And a quick note about influenza: The reason why we have to have a new vaccine for influenza every single year is because there are multiple strains of influenza floating around every single year. And the influenza strains are very different from each other, and the way that they vary is very different from the way that coronavirus mutates. So with the coronavirus, I use the image of one Rubik’s Cube; with influenza, they have two different antigens that can constantly swap out.

That’s what, in H1N1, that’s what the H and the N are, those are the two antigens that the immune system would use to fight against. And the influenza virus is able to take those two antigens, the H’s and the N’s, and just swap those out constantly. So there’s all these different variations that it can present. So rather than having one Rubik’s Cube, the influenza virus has two Rubik’s Cubes and is able to keep changing all six faces on those Rubik’s Cubes.

That’s why it’s so hard for pharmaceutical manufacturers to create a vaccine for this. … Birds typically are the reservoir for influenza, and so they’re able to mutate in the bird populations before they jumped in humans. And so because of that, it’s really difficult to keep track of this thing. And we haven’t been able to eradicate influenza because of this ability for influenza to mutate in animals before they get to humans. Sorry, that’s a lot of information.

Allen: No, that’s helpful, I think, to recognize. Because I do want to ask you: Was the medical community anticipating that there would be this new strain or multiple new strains of [the COVID-19 virus] that would arise, given the fact that we know OK, yes, viruses mutate? But COVID is so different from something like the normal flu that we see every winter that we all know mutates year to year?

Pham: Yeah, as you mentioned, all viruses mutate and they will continue to mutate and the strains that become predominant are chosen by natural selection. We view viruses as this archnemesis, this villain in our daily lives, which they kind of are. But these mutations … they’re not smart mutations. They happen randomly and it just so happens that certain mutations increase the ability of viruses to infect people.

But then many more mutations cause the viruses to become completely inert. And so that’s why we’ll only see the viruses that become more effective at spreading around. And the mutations continue to happen, but the important thing is the mechanism by which it does happen.

So with increased transmissibility, increased contagiousness, infectiousness, what probably happened was that there was a mutation that caused [the virus] to bind better to the human receptors. But the human receptors tend to be fairly constant so long as these proteins are able to attach to the human receptors, and they have to look kind of similar.

If you’re thinking lock-and-key mechanisms, then you can change the key’s appearance [only] so much before it stops working on the particular lock. And that’s one of the things that’s constraining the coronavirus’ ability to evade immunity, is they still have to attached to the ACE [angiotensin-converting enzyme] protein that’s in the humans.

Allen: OK. And the medical community as a whole, do you feel like they’ve been thrown for a loop? Or was this really expected? Like OK, we knew the other strains were going to come and at the end of the day, most medical professionals are probably not too concerned about this because it was anticipated?

Pham:
It was certainly anticipated. A lot of medical professionals are probably concerned, because one of the [virus] variants did come that became more infectious. But no, we always knew that new variants would eventually emerge. This is what happens with all viruses.

Allen: And do you know about how many cases we’ve seen in the U.S. of either of these two new strains?

Pham:
I don’t know the exact number, but there were a couple of cases I believe in Colorado, where these new strains were identified in people with no history of travel. And when that happens, when you have a community case that did not originate from elsewhere, then you know that that virus strain has established itself in the community.

Allen: So are there any new precautions that we should be taking for ourselves or our loved ones to protect ourselves from these new strains, or is it still all the same of, OK, we need to keep wearing masks and social distancing and all of those things?

Pham:
It’s all the same. They’re still respiratory viruses and they transmit on our respirations. And being that these are more infectious, then it becomes more important to take these precautions.

But a lot of what we’ve done, a lot of what we tried to do, hasn’t had a major impact. The nonpharmaceutical interventions haven’t had a real impact on the spread of these viruses. The early lockdowns seem to have done a lot to crimp the ability of the virus to stop spreading. But … after the original 15 days and the 30 days to 45 days total, after that happened, people sort of burned out on these measures, because they were very harsh measures.

So what really is important now is just taking personal responsibility, taking a look at who is at risk in your own life and trying to maintain as much physical distance either from them or isolating yourself before you go see them.

For instance, I know we’re past the holiday season, but before I traveled home, I isolated as best I [could] for at least two weeks before I went home to see my parents. These are the kinds of precautions that we need to continue to take.

And as I said before, … the disease manifestation is not greater. It doesn’t seem like it’s more severe. But the fact that it spreads much more quickly, then it will be able to reach more people who are susceptible to severe disease, though: the elderly, people with preexisting conditions. So it just becomes that much more important to try to protect them as much as possible.

Allen: And as far as testing goes, do the tests that we are broadly using right now to diagnose COVID-19, will those work on the new [virus] strain? So in other words, if I start having COVID symptoms and I go get tested, but I actually have one of these new strains, will that test come back positive?

Pham:
Yeah, they should, because the tests, the PCR [polymerase chain reaction] tests are a little bit different from what you would expect from a vaccine. The PCR tests, which is what most people are doing, and even the antigen test, should be able to detect these.

But what the tests do is they detect certain, more consistent segments of the viral genetic material. And so some of these have to remain fairly constant within the virus’ genome [or] genetic sequence. Because if there’s too much mutation, too much variation, then either A, you’d have a different virus entirely, or B, the virus would just self-destruct. You can’t have too many mutations in any kind of microorganisms. So the current tests should continue to work.

Allen: Dr. Pham, before we let you go, can you just give us, in your opinion, the worst-case scenario and the best-case scenario for the next few months as we tackle these new strains of the virus?

Pham:
Sure. I’ll start with the worst-case scenario. The worst-case scenario is that these variants or an emerging variant will end up becoming more virulent, that is, become … more severe in disease and are more transmissible. We’re already having a very difficult time trying to contain the spread of this virus. All the things that we’ve done so far [have] not staunched the rise in cases that we’ve been seeing.

And if there’s enough variation that they’re able to evade the vaccines to a significant degree, then you’ll see massive transmission. Because it’s more and more usage of health care resources, because it’s causing more severe disease, and it’s spreading without being stopped by the vaccine.

That’s going to be the worst-case scenario. We’re going to see a spike in both cases and deaths, like we saw early spring of 2020, and it will be as if we have a new pandemic. That is the absolute worst-case scenario. It’s also pretty unlikely, because of the things I said.

And also when viruses become more virulent, they tend to be more constrained because a virus needs to spread through people who are relatively healthy enough to walk around and talk to other people. If a virus kills people too quickly, then it’s not going to have a chance to spread. And that’s sort of why Ebola didn’t become this massive pandemic the way COVID has, because Ebola was very deadly but it killed people faster than the virus could spread. So that’s the absolute worst-case scenario.

The best-case scenario of this is that these mutations … don’t prove to be quite as infectious as the impression that they’ve left. We’ve identified a lot of these of the strain in the U.K. We’ve identified it throughout the world, but … because of the way international travel works these days–you just get on a plane and you’re in a different part of the world entirely–it’s very easy for these viruses to get around. So there could be a false impression of how contagious this is.

So the best-case scenario is that this is just another mutation that’s happened, another strain. There have been thousands of strains that have been able to be isolated. Most of them function just the same as your average COVID, your everyday COVID strain.

Allen: Well, Dr. Pham, we really appreciate your time today and just breaking down what we need to know. Thanks so much for coming on the show.

Pham:
Absolutely. I’m always happy to be on.

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