Dr. Lawrence Purpura explains monoclonal antibodies and the different types of treatments that could help us fight the coronavirus. Plus: learn why the universe seems to hate odd numbers.
Dr. Lawrence Purpura explains monoclonal antibodies and the different types of treatments that could help us fight the coronavirus. Plus: learn about the Oddo-Harkins rule and why the universe seems to hate odd numbers.
Why the Universe Seems to Hate Odd Numbers by Cameron Duke
Additional resources from Dr. Lawrence Purpura:
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Find episode transcript here: https://curiosity-daily-4e53644e.simplecast.com/episodes/what-are-monoclonal-antibodies-w-dr-lawrence-purpura
[MUSIC PLAYING] CODY GOUGH: Hi you're about to get smarter in just a few minutes with Curiosity Daily from curiosity.com. I'm Cody Gough.
ASHLEY HAMER: And I'm Ashley Hamer. Today Dr. Lawrence Purpura will talk about the different types of treatments that could help us fight the coronavirus with a focus on monoclonal antibodies. But first, you'll learn why the universe seems to hate odd numbers.
CODY GOUGH: Let's satisfy some curiosity. The universe is full of patterns. For example, when scientists were taking inventory of all the known elements, they noticed that the ones with even numbers of protons were a lot more common than the ones with odd numbers of protons. So what does the universe have against odd numbers? Well, it all comes down to how elements form.
And the pattern is pretty striking. If you took all 92 naturally occurring elements off of the periodic table and you put them on a graph to show how plentiful they were in the universe, you would notice two things right away. First, you would see that elements generally become more rare as their proton numbers increase.
So for example, the elements with one proton, hydrogen, is super common while the element with 92 protons, uranium, is the rarest of them all. Second, that line would zigzag like an alligator's teeth. That's because the elements with even numbers of protons are way more common than elements with odd numbers of protons.
Carbon with six protons is way more common than nitrogen and boron-- it's odd proton neighbors. Aside from hydrogen and a couple of other outliers, this pattern holds for all the elements. Weird, right? This phenomenon is called the Oddo-Harkins rule and it's named after the two physicists who discovered the pattern in the early part of the 20th century-- Giuseppe Oddo and William Draper Harkins.
And this all begs the question of why there's this strange pattern. Does the universe hate odd numbers? Probably not. The pattern has more to do with the way elements are assembled than with any cosmological superstition. Elements are assembled in stars. Stars are mostly made of hydrogen, which has one proton. And a star's core, hydrogen atoms, are smashed together by gravity to make helium, which has two protons.
As the density of helium goes up, the star begins smashing those helium atoms together into carbon, which has six protons. Carbon is smashed into even larger even numbered atoms as the star becomes denser. And that continues up until the star begins making iron with 26 protons. Then it explodes in a supernova. Ashley, that's what a supernova sounds like.
ASHLEY HAMER: I don't think there's sound in space, though.
CODY GOUGH: No, I tracked it down. It's real.
ASHLEY HAMER: OK. Got it.
CODY GOUGH: Anyway, that's supernova. Is where the star produces odd-numbered elements and elements heavier than iron. And that happens when an even-numbered element grabs a rogue neutron or smashes into leftover hydrogen. Those rogue neutrons often degrade into protons and that creates an atom with an odd number of protons.
Tons of the heavier elements like gold were made that way. The supernova also scatters the star's atoms in all directions. Ultimately, some of those atoms became part of planet Earth. And a tiny bit of that became us. To paraphrase, Carl Sagan, "We are all made of star stuff." Most of it, within even number of protons.
ASHLEY HAMER: We're about nine months into the coronavirus pandemic. And the science has been moving fast. As a result, it's been kind of hard to keep up with all the new treatments being developed in order to bring this pandemic to an end. You've got antivirals, monoclonal antibodies, mRNA vaccines. It's hard to keep them all straight. So to clear it all up, we decided to talk to an expert.
Dr. Lawrence Purpura is a physician and researcher at Columbia University's division of infectious diseases where he looks into diseases ranging from HIV to Ebola to SARS-CoV-2-- the virus that causes COVID-19. He has a very long resume that includes working as a field epidemiologist for the CDC in West Africa during the 2014-2016 Ebola outbreak. And he's currently a co-investigator on a number of studies in clinical trials on SARS-CoV-2 infection and treatment.
So Dr. Purpura knows his stuff. Natalia and I began by asking him what exactly is a monoclonal antibody.
LAWRENCE JAMES PURPURA: So a monoclonal antibody, as the name implies, involves one specific type of antibody. When you have an infection which just SARS-CoV-2 is an example. You're going to create many, many, many different antibodies that are targeted towards this virus. Some of them will be neutralizing antibodies, which will actually help sequester it and decrease activity. And some will be just binding antibodies that can bind to the surface of the virus and maybe flag it for variance by other cells.
Now, a monoclonal antibody is a single antibody and we use it therapeutically. So we try to find the best lock and key fit, the antibody that results in the best clearance of an invader. And what we can do is we can actually mass produce it. And the history of this type of therapy is-- it's quite interesting and it's really changed the way we treat many diseases. Not just infections, but also autoimmune diseases and even it's used widely for transplant patients.
ASHLEY HAMER: Could you just lay out what the difference is between a vaccine and a monoclonal antibody treatment? Specifically in the context of COVID.
LAWRENCE JAMES PURPURA: Yeah. So I think the best way to approach all of these treatment options for COVID is to look at where along the life cycle and also the development of infection in the host. So the first phase is the [INAUDIBLE] phase. So meaning when you're exposed to a virus like SARS-CoV-2, you have high replicating levels of virus in the sites of your body that the virus prefers and for SARS-CoV-2, it's the upper airway and lower airway.
And you want to target that. So at that point, you can give antiviral treatments. So a drug like remdesivir is an example of a drug that is actually targeting the virus itself. And you can think of a monoclonal antibody as being somewhat similar. Meaning that you're infusing these laboratory-produced antibodies to try to actually eradicate the viral infection.
Now, that's just kind of one flavor of how we can approach treating coronavirus. Now, the next would be how do you prevent infections from even happening? And the way to do that would be to have the host system create their own antibodies to prevent the virus from ever even being able to replicate and to cause infection to begin with.
So they both involve antibodies. The vaccine is stimulating your own immune system to make your own antibodies and a monoclonal antibody would be the infusion of externally made or laboratory made antibodies that are only temporarily circulating in the human body.
ASHLEY HAMER: And so the vaccine would be given before you get the virus and the monoclonal antibodies would be given after?
LAWRENCE JAMES PURPURA: Yeah. For the most part. So this brings up a good point on when do we think monoclonal antibodies are most effective? So for Ebola virus, the approved antibody cocktail that's being used now that was found to be most effective early on. So meaning, when someone becomes symptomatic, every day that goes by, there's an increase in mortality if they didn't receive the medication early.
And we're seeing something similar with SARS-CoV-2. So there are several monoclonal antibody treatments that are being evaluated right now. And the early data is showing that in severe disease, they're not as effective and that one of the clinical trials was stopped early in this severe category group.
But what it's showing is actually that it's beneficial when given early in SARS-CoV-2. So our efforts now are trying to get patients who have not even been admitted to the hospital, who are maybe having mild symptoms at home and the outcomes that are being studied are, does the monoclonal antibody actually prevent them from ever being admitted to the hospital or requiring a level of care that can only be provided in the hospital setting? And the early data is actually showing that it is promising.
So yes, you can give it early on in the disease and there's also thoughts that can you actually use monoclonal antibodies to prevent infection? And this is also something that we know from other prior infectious disease research, specifically for HIV. So there are monoclonal antibody treatments that are being studied right now for HIV and a lot of them are in the realm of treatment or prevention-- treatment and prevention.
So you can actually use monoclonal antibodies to also prevent the acquisition of an infection similar to a vaccine. But still, the difference is that you're using this externally made antibody to provide protection, whereas the vaccine, you're creating your own antibodies.
ASHLEY HAMER: That was Dr. Lawrence Purpura. A physician and researcher at Columbia University's Division of Infectious Diseases. You can find links to Dr. Purpura's publications and more in the show notes. Dr. Purpura will be back tomorrow to bust some myths about herd immunity.
CODY GOUGH: That was fun. Let's recap today's takeaways, Ashley.
ASHLEY HAMER: Well, we learned that it turns out odd numbers are the odd number out in the universe. That's because the stars that create most of the elements have helium at their core. And helium has two protons and those two keep multiplying to get even numbers. That is, until the star explodes and becomes a supernova. That's when a rogue neutron gets added to the mix, which degrades into a proton, which leaves you with those odd elements.
CODY GOUGH: Odd both numerically and in regularity.
ASHLEY HAMER: And their personalities, I'll just-- trust me.
[LAUGHTER]
CODY GOUGH: We'll do. Do you know how hard it was for me to find audio of a supernova explosion? You're not going to tip your hat to that.
ASHLEY HAMER: I do. I believe how hard it was because I don't believe it exists. I think you had to make it whole cloth with your mouth. Also I watched you, I watched you do it.
CODY GOUGH: Oh. Well, fine.
ASHLEY HAMER: It was very skillful. I applaud that.
CODY GOUGH: Thank you. We also learned that scientists can mass produce monoclonal antibodies to treat someone with an infection like COVID-19. Now, monoclonal antibody is a single antibody and scientists can find the best one to target a virus. It is different from a vaccine because a vaccine stimulates your own body to produce antibodies to ward off an infection before it starts. Although monoclonal antibodies may be able to be used to do that too. There's more than one way to skin a coronavirus.
ASHLEY HAMER: That's right. There's more than one way to unspike a coronavirus.
CODY GOUGH: Is that what they're doing? Unspiking it?
ASHLEY HAMER: Well, there the spike proteins are very important to the coronavirus and to our fighting of it. So I would think that maybe that's what they're trying to do. Just give it a little shave.
CODY GOUGH: You know what it sounds like when you despike a coronavirus?
ASHLEY HAMER: All right. I believe that.
CODY GOUGH: Good. It was really hard to track down that audio. So-- Today's first story was written by Cameron Duke and edited by Ashley Hamer who's the managing editor for Curiosity Daily.
ASHLEY HAMER: Scriptwriting was by Natalia Reagan and Cody Gough. Today's episode was produced and edited by Cody Gough.
CODY GOUGH: Join us again tomorrow, and we'll blow your mind. And you'll learn something new in just a few minutes.
ASHLEY HAMER: And until then, stay curious.
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