StarTalk Radio - The Omicron Variant with President of Regeneron, George Yancopoulos

Episode Date: December 7, 2021

What is the Omicron Variant? On this episode, Neil deGrasse Tyson and comic co-host Chuck Nice discuss the emergence of the new Omicron Variant of COVID-19 with biomedical scientist and president of Regeneron, George Yancopoulos. NOTE: StarTalk+ Patrons can watch or listen to this entire episode commercial-free here: https://www.startalkradio.net/show/the-omicron-variant-with-president-of-regeneron-george-yancopoulos/Thanks to our Patrons Vincent Krohn, Eu, Valeritte (Chuck, just call me Val), Austin McCauley, Avneesh Joshi, Timothy Lew, and Nikki Amberg for supporting us this week.Photo Credit: Linda Bartlett (Photographer), Public domain, via Wikimedia Commons Subscribe to SiriusXM Podcasts+ on Apple Podcasts to listen to new episodes ad-free and a whole week early.

Welcome to StarTalk. Your place in the universe where science and pop culture collide. StarTalk begins right now. This is StarTalk. Neil deGrasse Tyson here, your personal astrophysicist. We've got a special installment today. It's sort of an update on the COVID-19 virus. In particular, Omicron. Oh my God, we got Omicron.

I got Chuck Nice, co-host here. Chuck, how you doing, man? Hey, Neil. All right. Omicron, I mean, I know it's very serious, but I know it's a letter of the Greek alphabet. But the only thing I know about Omicron is Omicron Persei 8, which is... Oh, is that from Star Trek? Okay. Some planet in Star Trek.

Well, neither you nor I have expertise in this subject. And so we found someone who does. And it is Dr. George Yonkompolis, who is president and chief scientist of Regeneron. Regeneron, a biomedical company, actually right up the street here in Tarrytown, New York. And we don't normally invite CEOs onto the show because we just don't. Because why? Why would we? Right. show because we just don't. Because why? Why would we? But in this particular case, George Yonkopoulos is a classmate of mine from high school. And so that's why we have him on. So that legitimizes it, I think. Doesn't it, Chuck? Yeah, without a doubt. That's the reason. There

you go. So George, where are you? There you go. Welcome to StarTalk, George. Thank you, George. Thank you, George. Thank you, Neil. Sorry about that. Listen, that is a sign of true confidence right there when you enter a show and thank yourself. It's hard for me because, you know, as you guys just heard, I'm a classmate in high school of Neil deGrasse Tyson. So, I'm living in the shadow forever. Well, yeah, I don't know what that shadow looks like because we come out of high school,

you are my valedictorian, right, of our graduating year. I graduated something like 300th or something. You're a valedictorian. And so now you're sort of a billionaire co-founder of Regeneron. You are a biomedical scientist, immunology expert. You're an expert. And some of the items on your resume or in your company's resume is that you developed the most valuable mice ever. These are mice that have the exact immune system of human beings so that one can test antiviral treatments on these mice and know it's going to work with humans.

I didn't know you could do that. That's a thing you could do? Invent a mouse? Except for Walt Disney. Except for Walt Disney, yes. Mickey Mouse might actually be more valuable if you take that into account. But, you know, for movie fans, if you saw I Am Legend or so forth, you remember that Will Smith was in the basement and he was, you know, working with these rats and he was injecting them with the... Well, just to catch everybody up, he's a biologist, I guess an immunologist,

and there's a virus that basically turned everybody into zombies who they didn't otherwise kill. And he's trying to find the magic serum for this. And he thinks he's at one point the last person alive on Earth to do so. So pick it up from there. And he's testing at night while he's fighting the zombies during the day. At night, he's in the basement laboratory injecting, you know, rodents with test serums and so forth. Our basic theory was a long ago, was if you had any disease, any epidemic, and the example I used to give was Ebola. disease, any epidemic. And the example I used to give was Ebola. And as we know, unfortunately,

if most people get Ebola, they're going to die. And rarely, as Will Smith was in the movie, one in a million might survive. And that one in a million would then have the magic serum that their body made, which was really antibodies, to keep them alive. And that was Will Smith, the hero in the movie. His was the one in a million person who had beaten the virus because of his own antibodies. And what he was trying to do was clone them out of himself. But cloning antibodies out of a human is really hard. So we had the idea. Why?

Why is it really hard? Because essentially, you have to almost kill the human to get all the antibodies out of the human. So we had this idea a long time ago now was, well, what if we put the human immune system into a mouse and we gave a thousand or 10,000 mice Ebola? If one in a thousand or one in 10,000 mice survived from Ebola, they would have beaten it with a human antibody. But we could literally harvest all the antibodies out of that one human mouse. We wouldn't have to do these one-at-a-time experiments

that Will Smith was doing. We could literally take all the antibodies, harvest them all out of that mouse, and essentially come up with a cure for Ebola, which we actually did. We came up with a cure from Ebola by essentially infecting mice with the equivalent of Ebola. One of the mice survived.

We pulled out the fully human antibody that that mouse was making because it had a fully human immune system, grew it up in these bioreactors outside the body, purified it, gave it back to humans. And we did a trial with the World Health Organization, the NIH in the Congo during the depths of the epidemic there. And it was a cure for Ebola. And so that's why people were so excited in the early days of the pandemic before there was anything else about our approach and the antibody approach in particular, that we might be able to come up with antibodies that could attack the virus and kill it and cure people. Wow. All I can say to that is, I just want to say two things. One, that is genius, absolute genius.

And two, mice hate you. Okay. Actually, mice in the wild would just get swallowed by a bird, an owl or something. So maybe the mice in the lab, they're seeing that as a- They lived a good life. They lived a good life. They're well fed. They lived a good life.

You guys want to hear something that's totally crazy? Okay. You know, many humans are allergic to cats, right? You all know that. So why are they allergic to cats? Because cats make an allergen, something that we're all allergic to. an allergen, something that we're all allergic to. So we actually took a couple thousand mice and attacked them and made them allergic to cats. And we got a couple mice that actually were now resistant. They had beaten the cat allergen. Essentially, they had cured themselves

of cat allergy, and we've now purified and given it to humans and actually works against cat allergy in humans. So think about it. We first made mice allergic to cats, and then we used the mice to come up with the cure for cat allergy. So somehow, I don't know, that's somehow related to the war between the animals and mice and cats and Tom and Jerry. You actually negotiated the first peace treaty between Tom and Jerry. So this fact that we get one in a thousand or one in a million, that goes beyond clinical trials.

You can't test a million people typically in a clinical trial. But we know, am I correct, that there were some people who were found to have a natural immunity to the HIV virus. The HIV, is that correct? Yes, that is true. So were those people collected and do a sort of, you know, an I Am Legend scenario with them? Yeah, so that's a really interesting point. So with HIV, there's two ways that rare people can become resistant. And one way is because their bodies are genetically missing the receptor for HIV. So HIV, in order to enter cells, has to bind to

something on human cells. And some human beings are missing that receptor. And these are people who are rarely resistant. They don't get any infection at all. Other people got infected, but their bodies very rarely made what they call a broadly neutralizing antibody that was effective. And both of those approaches are being used going forward and have already, in some cases, helped people. They actually took the stem cells out of a human being

because the stem cells, what they call the blood stem cells or the hemopoietic stem cells out of a human being because the stem cells, what they call the blood stem cells or the hemopoietic stem cells, they make your blood cells, including your T cells. We all know that HIV attacks your T cells. So what they did, they took out their stem cells, they knocked out the HIV receptor, and then they gave them the stem cells back and now this person's own stem cells were now engineered genetically engineered to be resistant to HIV because they no longer had the receptor and they repopulated themselves and they were cured of HIV now that's a very hard treatment to do to thousands or hundreds of thousands of people because that's a genetic

manipulation and a stem cell transplant but it actually works so you're to do to thousands or hundreds of thousands of people because that's a genetic manipulation and a stem cell transplant, but it actually works. So you're absolutely right. Just like I am legend, there are the rare HIV people who are immune via these two different approaches. One is antibodies, which is related to what we're doing for COVID.

And the other is, you know, missing the receptor. And they've taken both approaches and they're trying to use them to help in the HIV situation. But if I don't have a receptor, it doesn't mean I'm warding off HIV. It means I'm not affected by it, but does that mean I can still carry it? No, well, the beauty is the way we all get infected

is just a few viruses enter into our body. And if the virus sticks to our cells, enters into them through the receptor, and then replicates, makes many, many copies of itself, that's how it continues to survive in our body. If it has nothing to stick to, it floats around for a little while, and then it just dies.

So the people who don't have the HIV receptor are not only resistant for themselves, but the virus just naturally, the few viruses that will get into you die out and you don't make any more. The way you infect somebody else, the way viruses work is they use us as a host to make many copies of themselves and then spread themselves out, often through our secretions, through our cough and so forth. So if you're not making much virus, you're not going to spread it. So those people are resistant to the virus and they will never spread it. So this is what they talk about when they talk about viral load, when it comes to the spread of COVID and there are people who have more viral load at a certain time, and so they're more prone to give the disease to somebody else. Exactly right.

So what happens is we all catch it from an aerosolized particle, a little droplet of moisture in the air that somebody has coughed up, for example, or by touching a surface that somebody recently might have rubbed their eyeball and touched and now you touched it. So a tiny particle of moisture that has a few viruses in it, we then touch and we touch one of our own mucous membranes. That one or a few viruses enter into us. That will not do us any harm normally, except that if one of those viruses sticks to a receptor inside of our body, it invades that cell. It takes over the cell. That's all she wrote.

It makes millions of copies. That's all she wrote. Those millions of viruses then flow out, away from that first cell, and they now affect a million cells. And soon enough, a million times a million becomes a billion. And all of a sudden, you are way out of control. And that's viral load. Actually, a million times a million is a trillion. And all of a sudden you are way out of control and that's viral load. Actually a million times a million, a million times a million is a trillion, just to be clear.

It's an astronomically, astronomically large number. So tell me the difference between, I think I know this, but I want to hear it out of the horse's mouth. Sorry to call you a horse in this example, but the other companies made vaccines against COVID and you made what we call monoclonal antibodies against COVID. So as I understand it correctly, your treatment is if you got COVID, you take your treatment and that helps you fight it and might even prevent you from having a hospital visit. So you're not preventing COVID in the first place. You're attacking it after it is manifested. Do I understand that correctly?

Well, yes, you do. But there's other ways to use antibodies. So let's step back for a second. So this is why we need all these weapons, because they do different things, like you just said. So let's step back for a second. So this is why we need all these weapons, because they do different things, like you just said. So let's step back for a second. Let's get back to this concept of viral load. A few virus particles attack your body, and they soon take over one cell and then a million cells, and now there's an astronomical amount of virus in your body. What happens? Astronomical. In the case of Ebola, unfortunately, the body can't react fast enough, okay? Because the Ebola replicates so fast and so destroys so many cells that

unfortunately, invariably, as we know, almost all people with Ebola will die, okay? Luckily, in the case of COVID, it's not as lethal, which means the virus is replicating more slowly. So you get to these astronomical levels more slowly and allows, in most cases, the body to respond. What does that mean? The body responds by making antibodies. And unlike the Will Smith movie, I Am Legend, where one in a million people made the response, or unlike HIV, where only one in a million make the right response, to COVID, most humans do make that response. Okay. And that's why most people do well. And what is that response? Most people make their own antibodies that will cover their antibodies specific to sticking to the virus. They stick to the surface of the virus, neutralize it, keep it

from sticking to anything else itself, and the body just naturally clears it and you're cured. So most people, the virus comes on, achieves high levels, but it does it relatively slowly over the course of a week or so. The body responds by making antibodies that coat the virus, neutralize the virus, and resolve the infection. And that's why, unlike Ebola or unlike the zombie virus that Will Smith was trying to beat, most humans beat it. And so you say it's a race, basically. Your ability to respond to it and its ability to multiply. That's exactly right.

And unfortunately, some people, and we know, the people who have risk factors, if you're older, your immune response is not as fast, just like, you know, we don't run as fast as we did when we were, you know, in high school. Okay. If you've got certain diseases, if you, if you're diabetic, if you're immunocompromised, the definition of immunocompromised is you can't make antibodies. So it's a race. Some people are just slower and the slower you are, the more dangerous the virus becomes for you because it races to higher numbers before you control it. So you're exactly right. It's a race between your antibody immune system and the virus

to who takes over. So what does a vaccine do? This is why vaccines are so important. to who takes over. So what does a vaccine do? This is why vaccines are so important. They prepare you. They are like a fake infection. The only thing that the vaccine is doing is it fools your body to think that you actually have a viral infection,

but all you're making through these mRNA vaccines is you make the so-called spike protein. The body reacts to the spike protein by making antibodies against it, which are neutralizing to the spike, which is body reacts to the spike protein by making antibodies against it, which are neutralizing to the spike, which is neutralizing to the virus. So the vaccine fools your body into making in advance before you need them, the very antibodies that would normally make to defeat the virus. But now you're prepared. It's like you've already beaten the virus. So the vaccine will protect the vast majority of people who get it because now you've made the antibodies.

The antibodies that we know can beat many viruses, including this virus. That's why vaccines are so important. This accounts for the ranking of who got the vaccine first. Because when we only had limited supplies, you gave it to the people who are most at risk because they would need the best help. Otherwise, the virus takes them out and they've got no chance. So if I may, just to recap for me, okay? So basically, you have this thing that happens to you and the vaccine is not necessarily fighting the thing. It's kind of like an emergency fund that when you save money for an emergency fund, if you lose your job, you're prepared for the loss of your job. You got this money in the bank. And so now you can actually ride this thing out because you're prepared for it.

And so that's what the vaccine is really doing. That's antibodies in the bank. Yes. It's really like soldiers in the bank. Okay. This virus is ready to invade, you know, the fortress. Okay. And the doors are open. If there's no soldiers who are going to shoot, you know, the virus that's trying to invade, the virus is going to come in and the battle is going to be in the fortress. If you man the walls of the fortress

with soldiers who are shooting the virus before it comes in, you're prepared. So essentially it's preparing you to ward off the virus so we will never enter into your body. Wow. George, I have an idea for you. So a new Regeneron,

when you have a slow year for business, introduce the Regeneron video game. The virus attacking video games. It's not bad, actually. Here come the antibodies. Here come the viruses. Here come the... So monoclonal means what? Because you came up with monoclonal antibodies. What does that mean? So what monoclonal means is that your body normally, in response to a vaccine, your body makes thousands and thousands of different antibodies. They're all different. Only some of them are powerful neutralizers that stick and kill the virus. Only a small percentage of all of those antibodies.

But the vaccine is good as making so many antibodies that on average, most people will make good amounts of neutralizing antibodies. What we did, and in this case, we use our special mouse, our magic mouse, to make antibodies when you can't make them in humans. Like for example, humans don't really, it's very hard to get antibodies against Ebola in humans, so you have to do it in a mice. In the case of COVID, we used our mice to make these powerful neutralizing

antibodies, but we also took them out of some humans who had beaten the virus already. And we looked both in mice and man for the most powerful neutralizing antibodies. So we all make many, many antibodies. It's called polyclonal, poly for many, clones for individual antibody clones. So in response to the virus, both mice and man make thousands and thousands of different antibodies. We go into the mice and men and we find the single best antibody. That's a clone of an antibody. And our cocktail is a mixture of actually just by accident, could have been both from mice or both from human, but we got a spectacular antibody from a mouse and we got another spectacular antibody from human. And until recently, when we put them together, those two monoclonal antibodies,

or monoclonal antibody cocktail is a mix of two monoclonal antibodies, was considered the most powerful approach for the last year, year and a half now to fight the virus. So it's the best. It's the Lenny and George antibodies. Exactly. The Lenny and George antibody. Exactly. The Lenny and George antibody. Of mice and men. There you go. Oh, sorry. Lenny, Lenny, I'm sorry. Sorry. John Steinbeck. Okay. As you guys may or may not know, I think, Neil, you actually met him once, but my co-founder and the other president of Regeneron is Len Schleifer. So it is sort of like the book.

It's the Lenny and George show. He is Lenny. Gosh, gosh. So we've got to take a quick break. But, George, when we come back, we want to talk about Omicron and why that represents a new challenge to your entire industry in terms of what methods and tools you might use to protect us. So right when we return, let's talk. Hi, I'm Chris Cohen from Hallward, New Jersey, and I support StarTalk on Patreon. Please enjoy this episode of StarTalk Radio with your and my favorite personal astrophysicist,

Neil deGrasse Tyson. We're back. StarTalk. Yet another installment of our discussions about the coronavirus, COVID-19. And in particular, we're concerned about Omicron. And in this installment, we've got actually an old friend who happens to be president of Regeneron, Dr. George Yancopoulos. And of course, we got Chuck there. And we left off trying to distinguish between why one would get a vaccine and when one would get a monoclonal antibody treatment, which was the specialty of Regeneron. So I would get a vaccine before I'm even exposed to COVID, but I get a monoclonal antibody

treatment afterwards. So why don't I get the monoclonal antibody treatment even in advance? What's the difference? Well, that's a great question. So the whole point of the vaccine is to make your body make antibodies to protect you against the virus.

Some people aren't vaccinated, unfortunately. Or some people, even if they are vaccinated, their body hasn't made good enough antibodies. Or some people who are immunocompromised haven't made, unfortunately. Or some people, even if they are vaccinated, their body hasn't made good enough antibodies. Or some people who are immunocompromised haven't made any antibodies. So some people, either because they're not vaccinated or they didn't respond well enough to the vaccine, will still get sick.

For those people, we can give them the monoclonal antibody treatment. Because what that does is it's like loading them up literally with a thousand times more antibodies than you would make in response to a vaccine. And it helps you beat and control the virus. So what we showed, and in the highest risk people who have a high chance, somewhere on the order of 10% of having to be hospitalized or dying, these are the elderly who suffer from an assortment of problems, that we reduced the rate of hospitalization and death by around 70 to 80 percent. That is huge because it's keeping people out of the hospital

and it's saving their lives. So you can use this to treat the people who are getting sick if they're at high risk, whether they got vaccinated and didn't respond or whether they never got vaccinated. So as the know, the White House just announced there were more than a couple million people dosed with this. And this has, if you do the math, it saved countless lives. Oh yeah, you just factor into that. Yeah, it's what is it, 20,000? No, no, 200,000. 10% of 2 million is 200,000. And if we save, we save 70 to 80% of those, that's a big number. We should have.

Logistics have prevented us from really, we could have treated more. We should have as a society. Just like we should be vaccinating more people, we should have treated more people with monoclonal antibodies. And so this is what the FDA has authorized our antibody treatment for, but also a couple of other antibody treatments that are also very impressive for this purpose

of taking people who are already sick and keeping them out of hospitals and keeping them from dying. And all of the monoclonal antibody treatments are very impressively effective. Ours has been sort of up until now the most widely used of these treatments. It even was used by the president. Exactly. Yes, if I remember correctly.

The other important thing that we've shown in clinical trials, and we have vied for authorization with the FDA, and we think it's very important that they act quickly on this and allow it is as we all know now, and there's been, you know, stories on 60 Minutes and CNN and so forth. Okay. That despite vaccination, the immunocompromised are not protected. If anything, they get a false sense of security. What does immunocompromised mean is you're not making antibodies to a disease, but also to a vaccine. So those people are unprotected, even if they've been boosted, boosted twice. It doesn't matter. Your body is not making antibodies. You get no protection from the vaccine. Unfortunately, there's five to 10 million Americans like that. And so what we've shown is that for people who don't have their own antibodies,

we can protect you. We can do exactly what you said, Neil. We can give you the antibody beforehand. In fact, we can give it to you maybe twice a year or four times a year. And now the antibodies last in your body for months and they keep you protected. You're as good, if not better protected than a vaccinated person. So for the people, the small percentage, I mean, you'd wanna, because it's much harder to make monoclonal antibodies than it is to make a vaccine. So you wanna vaccinate as many people as you can,

but there will always be that five to 10 million Americans, about 5% of the population, three to 5% of the population that will just not respond to the vaccine. For them, they are 5% of the population, 3% to 5% of the population that will just not respond to the vaccine. For them, they are true prisoners of the pandemic because they can't go out and resume their lives. And many of them, these are people who've had lymphoma or multiple sclerosis or other of these diseases, other cancers that are keeping their immune system down. Many of them know it. They're very sophisticated.

You know, medically speaking, they know that they're not protected. And so they're trapped. Okay. So for these people, we have applied for the FDA for authorization that we could give ours as what's called a passive vaccine. You made a joke about a horse before. a horse before. The first Nobel Prize was awarded in 1896 because some genius guy, von Bering, realized that if you took a horse that was immune to diphtheria or to tetanus,

you could take out the horse serum and you could inject it into humans. And now the humans would be protected from what were at that time scourges and epidemics of diphtheria and tennis and so forth. What was in the horse serum? It was antibodies. So this was called for years, for over a century now, it's been called the passive vaccination. It protects people who don't have their own antibodies. So there's two purposes of monoclonal antibodies.

To treat those who are already infected, load them up with monoclonal antibodies, which will bind, kill the virus, and help cure them, keep 70 to 80 percent out of the hospital and from dying. Or, and that's authorized, that's FDA authorized. And what we've applied more recently for is to protect the immunocompromised who are the small percentage of the people who can't respond to a vaccine. This is why we need all of these. We need the vaccines, but we need these monoclonal antibodies. Okay. So now you spoke earlier about the spike protein that gets targeted. So tell me about Omicron. If somehow our current arsenal is not as effective against it, is it because Omicron, a variant of COVID-19, does not have a spike protein? Spike is a great word. It's a great word for these structures that are on the surface of the virus.

And they literally, what is the spike? It's what digs into the human cell and allows the virus to burrow into the human cell. into the human cell and allows the virus to burrow into the human cell. It's literally like a spike that the virus uses to burrow into the human cell and fertilize itself and make many copies, plant itself and make many copies. And what antibodies do is they literally cover the spike. And so the spike can't dig into the human cell. That's exactly what antibodies do. And that's exactly what the spike does. And what vaccines do is they make the body make antibodies that cover the spike. And what we did is we just picked the best of these antibodies out of mice and man to make a cocktail to cover the spike and keep it from allowing the virus to dig into

the human cells. Okay. So what's the difference between that and Omicron? Omicron. Okay. The spike of Omicron has mutated. This is what we always fear, whether it's cancer or whether it's infectious disease, that we've come up with some cure and so forth, but the cancer or the virus is so smart in terms of the principles of evolution

that it just selects for itself to mutate so that the antibody sticking to the spike, where it's stuck, mutated away so that antibodies in general, whether they're from vaccines or from monoclonal animals, might not stick as well. The big fear is we have rarely seen, certainly not in the history of COVID, but rarely seen with viruses, that you get such a seismic shift in terms of the number of mutations. Delta was one or two mutations. Beta was one or two mutations. Omicron is 32, 32 mutations in the spike protein. It completely changes the spike protein. And what that has done is it's terrified everybody that possibly the antibodies that we used to get from vaccines to stick to the spike or the antibodies that we've selected out of mice and man to give to patients will no longer stick as well to the spike. It won't cover up. And now the spike be able to dig into the human cells. 32 mutations. It's just scary.

That's insane. One, that sounds super, super dangerous. So Chuck, the viruses are even smarter than that because they invented humans and had humans invent airplanes so that the viruses can go transcontinental. Nice, nice. They're so smart that they're now getting us

to invent spaceships. Right. We can carry the viruses to other planets as well. To Mars. First they got us to invent Amazon so that we can invent the spaceships to take them to other planets. I was going to say, number one, the Omicron sounds super dangerous

and that you should maybe take action if you haven't taken action for yourself personally. Or is it that it's such a change that it won't make a difference is what I hear people saying? No, I mean, unfortunately, we don't know. People are scared now. Okay. And there's, well, you don't know yet. You don't know yet. Yeah. There's reason to be scared, but we don't know the full impact of this at this point. There's reason to have hope. And certainly just like the biopharma industry, you know, fought back, you know, against the original virus. Many of us have been anticipating this potential challenge

and that this challenge would go on and on. So many of us are trying to be prepared for the worst case scenario. So there's reason that Omicron could be a real challenge. It may diminish vaccine immunity. It may diminish the natural immunity that people get who have been nationally infected and made their own antibodies. And it might diminish many of the monoclonal antibody treatments. Many of us in the industry have been afraid that this might be the case. And you have

probably heard from the vaccine makers, such as the Pfizer's and the BioNTech's and the Moderna's, that they're already planning on coming up with potential Omicron vaccines if we need them. If we're losing so much immunity from the original vaccines that within a few months, they'll be able to have a new version of the vaccine that will hopefully protect us against Omicron. In the same way, like I said, there's a few major companies like us, like AstraZeneca and others who have made monoclonal antibodies. And we have certainly been planning for this contingency.

So we already have thousands of backup antibodies, which we're testing. So we don't know yet for sure, though we're worried, whether our current cocktail is going to lose a lot of activity, but we are worried that it is. But we are prepared in that we've already even put into clinical trials new antibodies that we think will be able to still be effective even in the fit of Omicron. So unfortunately, many of us think that this is going to be a long game, a long challenge. The virus is going to have peaks and valleys and it's going to go down in its prevalence

and we're going to feel pretty good for a while. And then a new variant might come along and it might scare us. Why is it any different from the mutations of the seasonal flu? Where each year, oh, the flu changed a little bit. Let's find another vaccine for it. And you get a flu shot every year. Flu people get flu shots every year. So why wouldn't there be a COVID shot every year,

for example? It may be exactly the same thing. The only difference and the reason why the flu generally has not shut down society and COVID has shut down society and why that solution, which is, I think, maybe where we're ultimately coming to exactly what you just described, is that we're going to still have to do something to protect as many people as possible, more so than the flu, because the rate of serious disease is higher than it is for flu. So flu in general, most flus don't have a 10% hospitalization and death rate among the high-risk population. So what does that mean? Yes, we will want to have regular vaccines, okay? And in addition, we will also need, because with the flu vaccine and so forth, somebody does get the flu. We tolerate the fact that some people rarely get really sick, and we don't necessarily treat everybody who has the flu, though many of us now think that it's a worthwhile thing to do.

So we are actually developing flu monoclonal antibodies so that people get the flu, and particularly if they're older and so forth. We want to protect those people, even if their chance of hospitalization death may only be 1%. But with COVID, if it's like 10%, that's why there's so much concern. So despite vaccines, if the future state is exactly how you describe it, people will be getting sick. So we will be needing treatments, whether the treatments are combinations of monoclonal antibodies or now some of these pills that people are talking about. We will also, because of the high rate of potential hospitalization and death, we will also continue to need an alternative to the vaccine for the 5 to 10 million Americans

who will not respond to any vaccine, the immunocompromised people. So you're absolutely right. And I see it sort of the same way. This is a long haul. It's going to be a constant challenge. It's going to be, you know, back in high school, you know, I remember my English teacher, Mrs. Lasnik, she taught us about man against machine, man against man, man against nature, man against virus. This is humanity against the virus. This may be going on against this virus for a while. We're going to have to update our vaccines. We're going to have to constantly update our monoclonal antibody treatments. And we're going to probably have to constantly update oral pills as they come on.

Why? Because the virus is smart. It's going to mutate. It's going to get on spaceships. It's going to go crazy. So, okay, with that, here's what I got to ask. Neil, who did you have for English? Miss McGillicuddy.

No, I don't know. One last point before we take a break, and we're going to come back and get questions from our fan base, our supporters on Patreon, who were alerted that you'd be on the show, George. So we look forward to hearing those. Chuck has them collated over there. Just a quick point.

Okay, if Omicron does rise up, the fact that we've all been vaccinated, it won't protect us necessarily from Omicron, but it will continue to protect us from the original virus. Isn't that correct? It wasn't a waste of effort. It's not like the whole virus everywhere mutated. Is that one strain of it mutated? Now they're both out there. Isn't that a fair way to say it? That is a fair way to say it. So for example, right now, our monoclonal antibody treatment

is fully effective against every single other variant of concern that has arisen. Those will continue to circulate. And right now, Omicron is not really present at high levels. So people obviously should be continuing getting vaccinated. And if they get sick, they should be continuing to get monoclonal antibody treatments. If Omicron yields a huge surge, then unfortunately, all of those people, we don't know yet. We don't know the data. I'm not saying it will be the case. But the concern is that many of them will not be protected sufficiently from the vaccines and maybe not even from some of these monoclonal antibodies. Got it.

Let's take a quick break. When we come back, we're going to go into a Cosmic Queries mode for this episode to get questions from you guys out there for our special guest today. Old friend of mine, George Acopolis. We'll be right back. We're back. StarTalk. Third and final segment of one of our next installments on the COVID-19 virus. In particular, we're interested in the Omicron variant, which showed up just recently. And we have as our guest George Jankopouloulos. He's president of Regeneron. That's not why we have him here.

Well, it is, but that's not why I know him. I know him because we were high school classmates in the Bronx at the Bronx High School of Science. He's my valedictorian. Very proud of him. And you did good. You grew up. You all growed up.

And you did good. You grew up. You all growed up. So, George, you're Greek. You're culturally Greek. I mean, your parents are Greek. I remember meeting them. The Omicron is a Greek letter of the Greek alphabet.

And if I remember my Greek alphabet, I got alpha, beta, gamma, delta, epsilon, zeta, eta, theta, eta, capital, lambda, mu, cry, Omicron. It's like 15 letters deep into the alphabet. So does that mean there were 14 other strains of COVID-19 before we got to this one, which is of special note? Yeah, they have. I don't know whether I should be offended or not. They decided that it was wrong to name these by country of origin. But it seems like nobody was concerned about giving them Greek letters as names. Blame the Greeks.

I'm just glad, you know, the next letter after Omicron is pi. And we got pi in math. Don't be naming your viruses after pi. Just letting you know, okay? We're going to have to talk. They've skipped a few letters because I guess other people have played playing to them.

And so I don't know. I mean, I'd have to go back and think about it. But there have been quite a few viruses or variants of concern, as they call them. They call, you know, the first one was obviously what they call alpha, which was the original, you know, virus. Then there was one of concern called beta, then a gamma,

and then a delta. And we sort of skipped a few and we're at Omicron now. Yeah. Well, Omicron is O, so maybe it's because this one is O, you know what? Yes. A lot of people are worried about that. Like, yeah, this is the OS virus. So Chuck, you know what? Yes. There's a lot of people worried about that. Yeah, this is the OS virus. Oh, Chuck, you got questions. It's okay. Yep, let's get to it. You got questions from our people.

These are Patreon supporters who are now only, they're exclusive access to our Cosmic Queries format. So here you go. So let's jump right to it. This is Thomas Cockran who says greetings dr tyson greetings dr young coppola and hello dr chuckles i am a pediatric hematology oncology fellow physician in kansas city where i am thrilled dr young coppola was able to join this installment of star talk your work sir on cytokine traps is fascinating and seems like it

could help reduce the cytokine storms that are leading to the overwhelming inflammation and formation of blood clots that we're seeing in our pediatric population. Will we be able to use this biological technology specifically for treating patients infected with COVID? If so, will we see it in the hospital formulary? That is a great question. And so what this question is about, obviously, this is a very educated consumer. I assume a lot of your audience is. What he's referring to is the fact that when some people get infected, they get very sick. And one of the reasons they get very sick is that their body's immune system overreacts,

not in terms of the antibodies, which are a good thing to make, but in terms of they make these things called cytokines. And it results in a cytokine storm that many of us have heard about. And too much of these are defense mechanisms that are literally like bullets that the body sends out to kill invaders. And when you have too much of them, the bullets actually turn on the host itself and they can literally like kill your lungs. Friendly fire. Yeah, it's friendly fire.

So friendly fire. And one of the most important cytokines that has been shown in this disease is known as interleukin-6. It's a cytokine. And as this educated consumer indicated, we actually have a number of approaches, but we have an approved antibody that blocks interleukin-6. It goes by the brand name of Kizara. We've actually done

clinical trials, as does Roche. They have their own anti-interioleucine 6 antibody called tocilizumab. In any case, both of these have now been recommended by the World Health Organization that if people are sick and if you think they're suffering from cytokine storm, you should give them things like steroids because steroids calm down cytokine storms too. But they also recommend that for certain of these patients, they should also get these cytokine blockers, these IL-6 blockers. So these are being used in many settings for hospitalized patients when the physician thinks they're suffering from cytokine storms. And we are looking at the potential of further advancing this approach. So antibodies are specific targeted bullets to fight back against the virus. Cytokines are the body's sort of non-specific way to protect itself, but it can kill itself by friendly fire. And we do have a drug that is being used in the space already to protect ourselves against the cytokine storm, you know, death by friendly fire. So, George, you make the stuff in the lab and you have your consuming base,

which is the medical professionals out there in hospitals with actual patients. And so do you have some medical newsletter or something that shows up or does the FDA report it or the governor? Like, how do you get that information out there? Medical education, it's a serious concern and how to do it and how to optimize it, particularly in a setting of a pandemic. Imagine, and we were working hand in hand with them, imagine the thousands of frontline workers. They're dealing literally, they're in a war zone, at least as you guys remember, because you were like us in the epicenter of it back in March of 2020. OK, they were just trying to keep people alive as best as they could.

And you're expecting them to like learn a whole new field while they're on the front lines of a war. It's very, very challenging, very, very difficult. And this is why we count. We count in many cases on our government leaders, people like Dr. Tony Fauci and others. While they're educating the public, they also have doctors out there who can listen with a little bit more sophistication and knowledge. And so it's very important to try to communicate these complex issues because even to doctors, especially those who might have been trained before, monoclonal antibodies are a relatively recent treatment.

Okay, mRNA vaccines are also brand new. So communicating how doctors should use them, it's not easy. And unfortunately, you know, you can't criticize anybody really because it was a war really. Yeah, it was a fog of war. The fog of war when nobody knows what's going on. We could have done better. The communicators could have done better. You going on. We could have done better. The communicators could have done better.

You know, the government could have done better. Like I said, I mean, it's great that we treated over 2 million people with our monoclonal antibody treatments and saved probably hundreds of thousands of people. OK, but we could have probably saved more. And hopefully we will do better going forward because as we've talked about, you know, unfortunately this virus may be with us for a while, especially now with Omicron. And so hopefully we will continue to learn how to better communicate, how to get doctors the information they need, even when they're, you know, in the fog of war. You know, Chuck, I keep thinking of the video game here. You know, a new vaccine is produced, but their distribution channels are shut down. Oh, go back three spaces or whatever. I don't know.

There is, you know. All the factors. because everything was shut down. And they're showing me there are internet games. There are viral games that have gone viral now about beating it. And the tools at your disposal are vaccines, monoclonal antibodies, masks. Okay, so there is something going on. Okay. That's kind of cool, actually. There are viral games.

My kids will play. All right. Mm-hmm. All right, here's Matthew Dean. All right, we have time for a couple more questions. Here we go. Matthew Dean says this. Viruses mutate. Hey, here's Matthew Dean. All right, we have time for a couple more questions. Here we go. Matthew Dean says this. Viruses mutate.

Hey, come on, that's what they do. Should we be treating every newfound mutation with its significance by blasting it all over the media? Will the hype over mutation cause the public to ignore future warnings of mutation? Of course, there's the old adage, what doesn't kill you mutates and tries again. And then Kay Travosky, which is a very funny saying, Kay Travosky actually adds on to this. What needs to happen for the sociopolitical and public health standpoint before we can calm people down with respect to these new variants?

So one, does it make people ignore what they have to do? And two, how do we calm it down? Chicken Little, calm down. You know, I'm one for transparency and trying to get as much information out there. I think that there is real reason to be concerned and we should all try to prepare as much as possible. I hope that somehow we can prevent panic from setting in. But of course, we also don't want people to become complacent because, oh yeah, it's just another mutation. I do think, I hope, that the people who need to take this seriously in terms of figuring out how we're all going to

fight back, people like all the people at Regeneron who are already working on the next monoclonal antibody if we are going to need it, or the people at the vaccine companies who are already working on the next monoclonal antibody if we are going to need it, or the people at the vaccine companies who are working night and day right now to come up with the next version of vaccine in case we need it against Omicron. I think that it is important. So all of us who are in the front lines, whether we're the ones who are dealing with the patients or the ones who are coming up with the bioweapons to fight back. We need this information. We need to share it.

We need to communicate it. And I hope, I hope people, there are people like you guys. I mean, it's such an important function to correctly get the information out there and prepare the people so that they can do what's right and they can understand what's right and they can be prepared. So it's a viral literacy. It's a virus. Think of mathematical illiteracy. There's a viral

illiteracy that needs to be combated, as well as the virus itself. I think it's so critical. You don't want people going off and talking about crazy things. We need education here. I'm one who believes that an educated public, an educated consumer, like some of the folks who are asking your questions, I mean, they can be an asset to all of our efforts to fight back. It can prevent panic. And we can all do better. Because like I said, we all have to do better. Cool.

Very cool. Chuck, maybe time for two more. We'll do them quick. Go. Do them quick. Here we go. Amy A. says this. And Kevin DeSamelier has the same question. So, guys, I'm

mentioning both of you. We have a Semi-A in there? We have a Semi-A. That's Kevin DeSamelier. I wonder what he drinks, too. I hope it's my favorite, Chateau Neuf-de-Pape. If this variant is less deadly, but more transmissible, will it take

over and out-compete the other variants? If this is the case, then maybe COVID will drop down to the status of something like the flu. Oh, interesting. Yeah. Do we know the lethality of Omicron yet? That is a hope. This is why we're all working so hard to better understand Omicron. It may be exactly like that listener just suggested, that it may be more transmissible. It may actually spread faster, but if it's much less lethal, and there's some reason to hope or believe that this in general happens to viruses, they don't select to be more lethal. They select to spread faster.

And so by selection, by the evolution that selects for spreading faster, they may actually lose some of that early lethality. Let us hope that that's the case. You know, we will learn. This is why it's so important for all of us now to have our antennae up, all of us who track all this information. We're going to learn about this in the coming weeks. And we may get some bad news that, oh, maybe this virus is much more infectious and much more transmissible. Maybe we'll get some bad news

that maybe the vaccines don't protect as well against it. Then maybe some of the monoclonal antibodies don't deal with it as well. But maybe we'll get some good news like this listener suggests that maybe it'll be a much milder disease. So this is why there's, you know, we shouldn't be panicking.

We should be trying to understand as much as we can right now to understand what we have to do to fight back. And George, there's this interesting fact that, correct me if I'm wrong, the more lethal a virus is, the less of a chance it has to spread. Because if it kills you before you cross the street, you couldn't spread it against into the people who you were going to meet in the park because you died on your way there so the highly lethal diseases have working against them their inability to spread for that reason is that they're killing your supporters it's that's exactly it's it's it's all you have to do is think about evolution and how it would work okay okay? It's a combination of, it's not only how lethal it is, but if it hits you and you become symptomatic right away, that's why Ebola, thank God, does not spread that much

because people get sick very quickly. And when you see, I mean, I hate to put it this way, but blood coming out of everything from people, people avoid them, okay? They avoid, like the plague, okay? So it's a combination of how fast you get sick, the worst kind of situation. And this is one of the reasons why COVID,

you know, has probably spread so fast is there's a lot of people who are asymptomatic. And so they're like typhoid nares. They're spreading the disease. And there are a lot of people who do really well and you don't even know itres. They're spreading the disease. And there are a lot of people who do really well, and you don't even know it. And they're spreading the disease. So that's one of the reasons it has spread, because there's a lot of people for whom the disease is uneventful.

And in the early days, they might have had a little sniffle or something. They're still going to work, and they're spreading it. And the disease loves that. The disease loves that. Right. Right. There's nuances on it, spreading it. And the disease loves that. The disease loves that. Right, right. There's nuances on it, but it's pretty much like you say. I mean, the sicker somebody gets, the faster they get sick,

the more we know as humans throughout time, avoid those people. To avoid them. And the spread is slow down. George, we got to call it quits there. This has been a highly illuminating and fascinating conversation. And I'm just glad to be, I need to remind her every now and then

that you're out there because you're, I feel kinship with you for having shared teachers and classroom schedules and handball in the yard. And it's just great to see what's happened in your life and in your career. And you're doing right by civilization. So thank you for existing. Thank you for being my valedictorian, my graduating year. And it was just great to have you here. Well, thanks for having me. And thank you for being everyone's,

including my kids, favorite scientist. Okay. And Chuck is their favorite comedian, for sure. Is that right? Yeah, we are. Absolutely. Dr. Chuck. Go ahead. Listen, I'll take the charity, guys. I'll take it. All right, everybody. This has been StarTalk.

Yet another COVID installment. This time, trying to get a handle on the Omicron variant. I'm Neil deGrasse Tyson, your personal astrophysicist. As always, keep looking up.