Science Friday - Your Questions About COVID-19 Vaccines Answered, Placenta Science. Jan 29, 2021, Part 1

Episode Date: January 29, 2021

Everything You Want To Know About COVID-19 Vaccines The U.S. has been vaccinating people against COVID-19 for a little over a month. While there have been plenty of hiccups, over 20 million people in the country have received at least one dose of either the Pfizer-BioNTech or the Moderna shots. For the past few weeks, Science Friday has been collecting your questions about the COVID-19 vaccines on the SciFri VoxPop App—and we heard from a lot of listeners. The questions and concerns ranged from if people with antibodies should get vaccinated to if the vaccines are safe for pregnant women. Joining Ira to tackle these listener questions is Benhur Lee, professor of microbiology at the Icahn School of Medicine at Mount Sinai in New York City.   How Scientists Unravel The Mysteries Of The Placenta Here’s a fun fact for your next virtual trivia night: What’s the only organ that we can grow temporarily, and discard after it’s been used? The answer: the placenta. It may be a disposable organ, but scientists have a tricky time studying it: You can’t poke at it, sample it, or pull it out to see how it works while it’s doing its job of growing a human baby. In an effort to understand how this squishy, purplish, pancake-shaped organ performs some of its most important functions, researchers have had to turn to creative techniques. Ann-Charlotte Iverson, professor at the Norwegian University of Science and Technology, and Nicholas Heaton, assistant professor at Duke University, join Science Friday to discuss how the placenta protects a fetus from viral infection and inflammation, and what happens when something goes wrong.   A New President, A New Climate Policy When President Biden was running for office, he campaigned on re-entering the Paris climate accords his first day in the White House. He followed through shortly after being sworn in. But in the week that followed, the new President has also taken additional steps focused on reducing carbon emissions and adapting to the changing climate—like a push to move the government vehicle fleet to electric vehicles, establishing a White House Office of Domestic Climate Policy, and pausing oil and gas exploration leases on federal lands. Sophie Bushwick, technology editor at Scientific American, joins Ira to talk about Biden’s climate moves, as well as other stories from the week in science, including a study of global ice loss, a halt to Merck’s COVID-19 vaccine trials, and a question about the aquatic habits of an ancient dinosaur. Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.

This is Science Friday. I'm Ira Flato. A bit later in the hour, we'll tackle your questions about COVID vaccines. But first, President Biden campaigned on reentering the Paris Climate Agreement. His first day in the White House, he made good on that promise. And the new president has also taken additional steps, focused on reducing carbon emissions, and adapting to the changing climate. Joining me now to talk about that and other science news of the week is Sophie Bushwick, technology. editor at Scientific American. Always good to have you, Sophie. Thanks, Ira. All right, let's get into this. Let's talk about some of the climate items the Biden administration brought up this week. So, so far, President Biden has been using executive orders and memoranda telling the federal agencies what to do to get started on his goal

of eventually having zero emissions, electricity in the U.S. by 2035. So that's a pretty aggressive goal. He's almost certainly going to need to work with Congress in order to actually meet that goal. But in the meantime, he's getting started on things like eliminating fossil fuel subsidies, stopping new oil and gas leases on public lands, starting to have federal agency study how climate change is affecting global conflict and disadvantaged communities, and generally sort of changing the emissions, reductions, targets for the U.S. Are these specific hard policy actions, or is this more just signaling? Some of this is signaling.

So, for example, one of these orders is about having federal agencies when they purchase new vehicles, have those vehicles be zero emissions vehicles made in the U.S. When they set up their electricity, have them try to buy clean electricity. But he sort of told them to do that, but not given them a ton of specifics. So some of that is going to be up to the individuals. within the Biden administration. Got it. Let's move on to climate news a bit because there's news that the planet just keeps on melting

at incredible rate. Yes, a new study looked at the total loss of ice all over the earth since the 90s, and they found that we've lost 28 trillion tons of ice from the mid-90s up until about 2017. And the majority of this loss is driven by, climate change. That's right. So back when they looked at this, the number in the 90s, they say, was about 800 billion tons of ice per year being lost. And by today, that number has gone up to 1.2 trillion tons of ice per year. You know, that's a number that's almost difficult to get your head around, what the size of an ice cube would look like with that much ice. It's really, really hard

to imagine. So, for example, I've tried comparing it. You know, I was looking up comparisons like, how many blue whales would this be? But it's a number, again, that's so high that it's still hard to picture. It's just an incredible loss. Yeah. And we're not just talking about where most of the rate of climate change is happening at the polls. This is a worldwide figure. That's right. So the researchers added up the ice loss for the ice sheets over Greenland and Antarctica. They looked at the sea ice in the Arctic and Antarctic at the polls. And they also looked at mountain glaciers all over the world. And they added up all those ice losses to reach the 28 trillion ton number. And more cheerful environmental news, if there is some, some kinds of environmental damage

might be fixable. That's always good to hear. What do you mean by that? So at the border between the U.S. and Mexico, especially the end of the Trump administration, there was a rush to build a border wall. But a lot of this was happening in areas that were impassable for humans, but that was a good habitat for wildlife. And in those cases, the wall, which also includes more than 100 feet of cleared vegetation and a road on either side, that has blocked the ability of animals to migrate. In some places, the wall has blocked the flow of rivers or of water, which has contributed to erosion. And it's just caused a lot of ecological damage. So President Biden has ordered a halt on wall construction and conservation. and conservationists are asking him to take down specific parts of the wall in the places where it is

most damaging. And they think then that the damage can be restored or reversed? Yes. For some animals, for example, oscillates, which migrate on foot and their migration has been sort of cut off by the existence of this wall. The conservationists think if they take down the wall that this population will be okay, that their ability to move will be restored. But, I mean, there's other animals that have been living in areas.

where there's been wall construction or barrier construction on and off for years, and it might be more difficult for them to recover. Yeah, so even just stopping the construction is a positive for the environment there. Yes, the construction is really disruptive. It involves, you know, digging a trench. It involves having a lot of noise and light. That's just very disruptive to the local flora and fauna. Let's move on to vaccine news this week. There's some news from several vaccine teams. Go through that with us. Sure. So first of all, Merck was developing two different vaccine candidates, and they've dropped both of them.

They released a statement that said that the ability to boost the immune response, it wasn't, they called it inferior in comparison to the amount of immune boost you get from either having survived a case of COVID-19 and having that protection or from getting a vaccine from Pfizer or from Moderna. So they're no longer going to be developing the vaccine candidates, although they are continuing to develop treatments. On the other hand, we've got news from Johnson and Johnson that their coronavirus vaccine is about 66% effective against the virus, but it's 85% effective against severe disease. So if you have that vaccine, even if you get sick, you're much less likely to get the very severe case that would require hospitalization, for example.

And that's important because that, as you say, if you don't go to the hospital, if this prevents people from going to the hospital, that takes the burden off the people in the hospital. They can work on people who are really in worse case than you are. Exactly. One other announcement that's interesting, which is coming from Novavax. So Novavax is also working on a vaccine and it works very well. Their efficacy rate was almost 90%, but it's not as good on the variant that has come out of South Africa. So in that case, it still works somewhat, but the rate is only at 50. It's actually under 50% instead of as high as you would want it to be. We'll be talking more about vaccine efficacy and answering our listener questions later in the hour. Let's move off the planet for a while. There's some space news this week. Tell us about it. So Axiom Space, which is a private space company, has announced the first entirely private mission to the space station. So in the past, space tourists have hitched a ride on, for example, the Russian Soyuz flights up to the space station. but this is the first case where you've got a private spacecraft. They're going to be flying in a SpaceX crew dragon, and you've got a private crew going up into space.

And of course, I heard that the price was astronomical to get on that Axiom flight as a space traveler. That's right. You have to pony up $55 million to join this voyage. Wow, okay. That's first class, right? I'm sure the tourists, well, there isn't going to to be a tourist class. I mean, I don't know if you can expect to be served, you know, cocktails on the flight up, but it's definitely a price tag that's kind of eye-watering. You know, I'm thinking of 2001 Space Odyssey where they have their serving drinks in flight, but that's not what this is going to be. So is this a business thing for Axiom or is it a tourist thing? What will they be doing as a private company? So Axiom is planning to have multiple

missions that are going to kind of ramp up. So this is, they're going to be the first entirely private mission to the space station. They plan to eventually attach their own modules to the ISS, and that they're hoping to use as a test bed for them eventually launching a private space station into orbit. Now, as far as I know, they don't make spacecraft, right? So whose spacecraft are they using? They are using a SpaceX spacecraft. Ah, Elon Musk is added again here in space. Well, he's showing that you can make a profit and that private industry can work in space. We're definitely seeing an increase in private space flight, in private interest in getting into space and exploring and also using resources up there.

And of course, if they're going to be like a hotel in the international space station, they've got to be paying for food and board, don't they? That's right. They do. They have to, if you were staying in a hotel, you would have to pay for the space. you'd have to pay for whatever you ate, and it's the same thing here. Although I don't imagine even with the price tag for space travel, I can't imagine that they're going to be eating the finest cuisine up there.

There's limits. NASA makes a few bucks on this, then, getting reimbursed for... Yes, absolutely. Give us a timeline on this here. So they're planning, they think the earliest they could launch would be in a year in January 2020. But, you know, with all things space-related, every time you get an estimate of the deadline, you have to take it with a grain of salt because often these missions get pushed back by, you know, by weeks or months or even years. All right. Let's, let's, before we run out of time,

let's move on to a really important question about whether the dinosaur spinosaurus was more of a swimmer or a waiter. I love stories like this about scientists are passionate on both sides of this debate. They really are, they're releasing new papers. The most recent paper advances the hypothesis that the Spinosaurus, which is this like 50 foot long dinosaur, 20 feet tall, it had this big sail on its back. And they know that it lived in and around the water. But the question is, was it sort of swimming through the currents or was it more of a wader, like a wading bird?

And a lot of this involves just looking at the body and the remains that they've recovered and comparing it to existing animals. And the most recent study that has come out has now said, we think it was a waiter. A waiter, just up to its waist, maybe. Right, because they were looking at sort of the body shape and a lot of aquatic animals that spend much more time swimming have a much more streamlined body.

It's easier for them to navigate through the water. And this study is looking at various, at the bulk of the spinosaurus, at that sort of unwieldy sail, at the number of muscles in its tail. And they said, based on this information, we don't think it would have been a very fast swimmer. And we think it would have been a more effective strategy for this type of animal to stay in the wading shallows and to dip its head in. Well, I wonder what the over-under was on taking bets, whether it was the swimmer or the waiter. We'll leave that up to the Vegas bookmakers on that. Thank you, Sophie. Sophie Bushwick Technology Editor at Scientific

American. Always good to talk with her. We've got to take a break, but when we come back, we're answering your questions about the COVID-19 vaccine with an expert, so stay with us. This is Science Friday. I'm Ira Plato. The U.S. has been vaccinating people or trying to vaccinate people against COVID-19 for about a month now. And while there have been plenty of hiccups, about 20 million people in the country have received at least one dose. For the past few weeks, we've been collecting your questions about the COVID-19 vaccines

on our Science Friday Voxpop app, and boy, did we hear from a lot of you. So today we're going to tackle what you want to know about these vaccines. Joining me to answer your questions is my guest, Dr. Ben-Hur-Lee, professor in microbiology in the Icon School of Medicine

of Mount Sinai Hospital in New York. Welcome back to Science Friday. Glad to be back. Nice to have you. Boy, there are a lot of questions, so I want to get right into it. Let me start off with the basics. Here's a question we got from listener Nancy in Ohio. If you receive the COVID-19 vaccine, can you still transmit COVID-19 to others? Well, let me just say first that the initial trials will not design to test whether the vaccine can prevent transmission. It was designed to test whether the vaccine can prevent you getting infected. It's very, very, efficacious from preventing infection. That being said, it is likely that once you have a

sufficient immunity, once the full dose is given, that at the minimum, if you do get infected, the amount of viruses will be quite low. So the chances to be low. But we do not have the data one way or another yet to say whether this is fail-safe that you cannot indeed transmit the virus. So I would say let's wait for the data to come in because trials are being done to address that very point you just mentioned. Yeah, it would be safe to assume then just for safety that you can transmit it. So take those precautions. Yes, I think so. A question from Paul in New Haven, Connecticut. If someone has already gotten COVID-19 and has tested positive and recovered, are they supposed to get a COVID-19 vaccine anyway?

I think the current recommendations are to indeed get a vaccine, because right now it's just, you know, we all have to remember this is a one-year-old disease, and we're asking a lot from science to try to address it, but there's no contraindication right now. And in fact, if you work in healthcare settings, many people have gotten infected and recovered, and they will still require you to have your full dose of vaccines as part of working in this environment. So, yes. Yeah, okay. Let's go to question three. As we know, people who have been vaccinated against COVID-19 in the U.S. have received either the Pfizer-Bioentech vaccine or the Moderna one. We know that. So let's hear this question from Iowana in California.

With several different vaccines available, is one more effective than the other? How are they different? Does it matter which one you get? All right. If IRA has two hours, I can go into the various vaccines. We don't. So let me just address the big few that people might have heard about. I just want to preface it by saying, if it has been approved by legitimate national authority, all the vaccines, if they follow with WHO recommendations, have to be at least 50% efficacious. The two big ones that you hear about that's approved in the United States are the fives, are the Pfizer and moderner vaccines, and those are more than 90% effective in preventing infection. They are both based on what you call an MRNA vaccine platform, which we'll get into later probably.

And this is a new vaccine modality, and it really does work and surprisingly well. It's not based on using any part of the infectious virus as all. It's just delivering instructions to make that particular protein, the spike protein that's outside of the virus, the corona, so to speak, when you talk about coronaviruses, and that helps your immune system to make antibodies against the spikes. So there's no significant difference between Pfizer-Modernar. They're essentially identical in terms, you know, not proprietary, I mean, not in terms of the formulation and even sequence per se, but they're both very efficacious.

The AstraZanica and probably Johnson and Johnson that's coming down, they are virally-vected vaccines. That means the instructions for making the relevant parts of the coronavirus is put into a very safe virus vector, an antivirus, a factor of some kind that does not cause disease, or it's replication incompetent. But it does sort of like irritate your immune system to think that the virus is coming in,

and so they make the right kind of antibodies as well. And then the last one is you have the killed vaccines from China, the coronavirus. And that's very traditional, like how the polio vaccines was back in the days, where you just grew up vats of viruses and you inactivated and you put it with what we call an adjuven, something to stimulate your immune system. And you get responses. The efficacy of that one is just above 50% for reasons that we are unclear because the data has not been fully released. But that's what's out there. I would say any vaccine is better than none. Let's go to Tom in Bandera, Texas, who has a good follow-up to that question.

I think I sort of understand how our current vaccines for like smallpox work, but I'm not sure I understand what is that happens with these MRNA vaccines. Can you help explain that to me? Yes, so continuing on the theme, you know, the usual vaccines, like in smallpox, is actually what we call live attenuated. vaccine that this you know back in the days you would just passage virus for a long time hundreds of passages in cell lines and eventually they lose all their virulence genes so this one is sort of like a you know a very reconversion of the virus this mRNA vaccine is a brand new technology so that no

virus is involved at all it's just the messenger the transcript for telling the cell how to make the protein. And so in biology, you know, your DNA codes, instructions, and then it's transcribed into a messenger. This intermediate nucleic acid tells the protein machinery in the cell to produce the actual virus spike. That's the antigen that your immune system sees, that elicits the antibodies that will block the actual virus from coming in. So it's very clever. Use no parts of the virus. It's very safe because there's essentially no DNA, just MRNA, the intermediate instructions. And that's why it works so well because they've optimized ways to make the instructions be efficiently recognized by yourself.

So it's actually using your own body as a bioreactors, making your muscle cells to actually produce the protein so that your immune system recognizes. Well, I hope to get my shot and be turned into a bioreactor very very much. soon. Let's come on. Great explanation. Let's go on to Julia.

Julia from Pennsylvania is up next. Is the second dose of the vaccine the same as the first in composition and amount or is the second

dose different? To save time, I'll just talk about the Pfizer and the answer is essentially yes. The second dose is essentially the same

as the first dose. And you just need a booster. So the first one is to prime your immune system, you know, start making the antibodies. And the second one is to sort of make your immune system memorize that now I've seen it twice, you know, I got my army together and then I'm ready to go. So when the active virus comes in, you know, the B cells,

which are the cells that make your antibodies, will start proliferating a lot to help protect you against the virus. Which raises the question for me, and a lot of listeners are wondering about this. Can you get your first shot from Pfizer and your second from O'Don, For example, Andrew from Equality Alabama wants to know. I understand that both the Pfizer and Moderna vaccines are based upon the same RNA sequence. That being the case, does it matter very much which booster type of shot you receive? Lots of people are asking that questions and they're looking into it. And let me just say the trials are not designed that way and nor are they appropriate.

proved that way. So instead of speculating, I withhold judgment because I don't want to confuse the audience with a lot of subtle pleas that may go wrong. I mean, in effect, the Pfizer-Moduner are sort of the same and can. We will evoke the Fouchy rule, which is what he said. If you don't know the answer, say you don't know it, right? Exactly. We'll call it the Fouchy rule from now on. Let's go to a question from listener Peter about how antibodies may interact with the vaccine. My wife and I live in Manhattan, and next week she'll be eligible to receive the COVID-19 vaccine. In July and December, she tested negative for COVID-19 on the diagnostic test, but positive for antibodies. should her positive antibody status be taken into consideration in receiving the COVID-19 vaccine?

Yeah, this is similar to one of your earlier questions. So there's no contraindication once again that just because you have recovered from an infection, so the fact that she has antibodies means she was at one time infected. And so, like I said, if you work in a healthcare facility and depending on what category, a risk you're under, you are encouraged to actually receive the vaccine. So if you're scheduled for it, I would receive it and there's no contraindication against it. Listener Darrell from Louisville, Kentucky has this question. I'm going to be getting my shot. I'm over 70 soon. I wonder how long it's going to last. Am I going to have to have a shot a year from now?

invoking the faulty rule, like you mentioned earlier, I just want to remind people that this is a one-year-old disease. So people are asking a lot of questions that scientists are trying to address. But historically, what we can say is that coronavirus, once you've been infected with it and you're generating antibodies, they usually hang around for a few years. It's not going to be a one-year deal, because from what we know about the four coronaviruses that are, already endemic into the human populations. In this is may not know, but 25% of seasonal colds are caused by coronavirus. It's just that we didn't care before about making vaccines against sniffles.

But based on those data, these antibodies, you know, they hang around. They're good for a few years, give or take, until, you know, the virus changes into a new genotype, for example. And then you get reinfected and then you make a new set of antibodies. So I would say, let's wait and see and see how fast this virus evolve and whether we need updates or not. Listener, Keenan from Salt Lake City is up next. Is the coronavirus going to mutate every year like the common flu? That's a great question.

And one is hearing a lot of things on the internet and social media. All viruses mutate. That's what they do. That's their way of living. They're small little things. They replicate in billions of copies. So there's nothing wrong about mutation, and most mutations are not fit. And by that, I mean, most mutations are actually bad for the virus.

And so they don't necessarily work. The question is, you know, do you get the fit mutations that will allow the virus to escape the immunity? And there's some indications now that we might be worried about some of these new variants that we heard about. But I want to say that it's not like an on-off switch, you know. Most of these vaccines generate very high. tighter of antibodies. So when you hear things out there that this is, you know, you need five or more antibodies, that's fine because, you know, these vaccines elicits, you know, much higher, tighter of antibodies than we do need. So they'll still provide some protection. And as we speak,

a moderner is discussing about, you know, how do they update their vaccines easily. But for right now, every year, I don't know. Let's wait and see. Luckily not. I'm Ira Flato. This is Science Friday from WNYC Studios. In case you just joined us, we're talking with Dr. Ben Hurley, professor in microbiology in the Icon School of Medicine of Mount Sinai Hospital in New York, answering your questions about the vaccines. A lot of people are asking about kids and children and pregnancy. Let me go to Kim and Honolulu, who has a question about pregnancy. What do you advise? young mothers or upcoming mothers to do if they are either pregnant or plan to have children soon?

Should they take the vaccine? And can you explain more about how the MRNA components will not affect reproductive systems? That's a great question. Let me just say that trials are designed in general not to include pregnant women because they have a special category. But having said that, We do administer vaccines all the time to pregnant women, influenza, pertussis. So it's not as if they can receive vaccines. The mRNA vaccines is very safe, like I said, that it's just the intermediate instructions on making the protein. So there's no chance zero that that will affect your genes, your genetic composition.

It's not a retrovirus, so it's temporary, basically, and eventually degrade. So the only plus side is that when you make the antibodies, the mother can actually transfer some of the antibodies to the child, the fetus. And so in the first six months of an infant's life, a lot of the protection is actually from the maternal antibodies that's transferred to the placenta. So those are the good things that can happen to your child if the mother received the vaccine. So while the trials are not specifically included a pregnancy, the major health organization, American Association, OBGYN, have not said that it was contraindicated pregnant with it either. I want to sneak in one last question of my own because I was thinking about this.

Let's say you test positive for the virus and you're in the early stages of it. Would it help to get the vaccine anyhow to fight off the infection by trying to flood the body with the vaccine instead of having the virus multiply? Oh boy, that's a good question. So you mean like if you're symptomatic or you know you've been just exposed? Like, you know. Yeah. If you're early symptomatic or you're asymptomatic and you know you've been exposed,

you've tested positive, would it help to get that vaccine and get the MRI moving and flooding the body with the good stuff is sort of in competition with the virus? That may be true. so invoking the how she rule again, I can only speculate. I think it's difficult to generalize about such questions because if you're truly asymptomatic and healthy and stuff, one must remember that most, not to be little of this at all, but the vast majority of infections results in mild or asymptomatic disease. So your immune system is fine to take care of it.

But if you are in certain high-risk groups in something, that we do have treatments now that have done early. So I will focus on those treatments that are effective. The monoclonals that have been shown to work, a lot of treatments are effective when you start it early. So many questions, so little time, as always, Dr. Lee. Thank you very much for waiting into this with us. Thank you, Ira.

I appreciate all your listeners questions. Dr. Ben Hurley, professor in microbiology in the Icon School of Medicine that's at Mount Sinai Hospital in New York. And if you have any lingering questions about COVID-19 vaccines that did not get answered today, please let us know we're planning to do more segments like this one. So send us your questions. And you can do that with the Science Friday Vox Pop app wherever you get your apps. We have to take a break, and when we come back, we're going to dive into a topic even scientists know very little about the ins and outs of placenta science.

Actually, one of my favorite topics to talk about after this. This is Science Friday. I'm Ira Flato. Here's a fun fact for your next trivia contest. What's the only organ that we can grow temporarily and discarded after it's been used? The answer? The placenta. Cool now? The placenta may be a disposable organ, but scientists can have a tricky time studying this odd-looking afterbirth. Sci-Fri's Katie Feather has more. Maybe you're already grossed out by the word placenta, the way some people will shudder at the word moist. If so, think about this. Everyone on earth was once familiar with the placenta. It shows up at every single person's birth. On the other hand, maybe you're really comfortable with the idea of the placenta as a symbol of mystical feminine power. Perhaps you've eaten one for its purported health benefits or buried one as part of a sacred ritual.

So there's a lot that comes up when people mention this squishy, purplish, pancake-shaped organ that makes growing a human possible. A lot of stories, a lot of symbolism, but not a lot of science. Because when it comes to studying the placenta, scientists are at a disadvantage. Since you can't poke at it, sample it, or pull it out to see how it works while it's doing the job of, you know, growing a human baby. But my next two guests found creative ways around that, in their effort to understand, how the placenta does one of its most important jobs, protect a fetus, and some ways that can go wrong. Here to explain what they did and to talk about the mysteries of the placenta are my guests. Dr. Anne Charlotte Iverson is a professor at the Norwegian University of Science and Technology

in the Center for Molecular Inflammation Research in Trondheim, Norway. And Dr. Nicholas Heaton is an assistant professor in the Department of Molecular Genetics and Microbiology at Duke University. Welcome both of you to Science Friday. Thank you. It's great to be here. Thank you. So Dr. Iverson, I want to start with you. Can you take us back to high school biology and remind us what the placenta actually does? So the placenta has many functions to provide the fetus with sufficient nutrition and oxygen

and also remove the waste products from the fetus. In addition, the placenta must protect the fetus from infections. And also the placenta is the setting where it is established a coexistence between these two different individuals. And that's a big immological challenge. You mentioned that the placenta actually has two sides, one side that connects to the mother with these certain types of cells and a different group of cells that are on the fetal side. That's so cool. I didn't know about that. Yeah, that's true. So when the placenta starts forming, the blastocysts attached to the

urine wall, and then these specialized fetal cells called the trophoblasts invade the urine wall of the mother, and they start forming the placenta. And these trophoblasts, they are the cells that meet the mother directly in the uterine wall, where these specialized fetal cells sit and interacts with maternal cells, and they are also close to the urine blood vessels that supply the placenta with blood. So one reason it's so hard to study the placenta is because ethically you can't access it while it's in use, right? Yeah, that's right. We have to wait until delivery. So how do you get around that obstacle when you're studying the placenta?

Tell me, how do you get your placenta? So we get our placentas from cesarean sections because then we can avoid the stress of labor and delivery on the placenta. So the placenta is delivered and we take samples from the placenta itself. And then to get to that maternal side of the placenta, we do a vacuum suction method where the placenta was sitting in the urine wall to get access to that tissue that represents the maternal side of the placenta. And we sample these tissues as soon as possible so that it's as much like as it was in vivo or in the mother as possible.

I'm imagining it like when someone is donating an organ, there's a very rapid process of getting that liver or whatever to where it needs to go. So like how quick is as soon as possible for a placenta? So we ask the mother before the cesarean section. So that is in place and she will give her consent for us to take out the samples. But ideally from when the placenta is taken out, we would like to have the samples stored either frozen or fixated within half an hour. and that's a challenge. So we have to have everything set ready for the sampling for each delivery. So one of the things that the placenta is doing is helping to protect the fetus from viral infection.

Dr. Heaton, how does the placenta do that? Yeah, I mean, this is a great question. And there's multiple kind of layers that go into this. I mean, the primary function, the way the placenta keeps pathogens out is just by serving as a barrier. Right. If there are pathogens that are circulating in the maternal blood, these specialized cells that were, referred to earlier, these prophyblasts actually form barriers that stops pathogens from getting across. And that works in the vast majority of cases. But in addition to the actual

pathogen itself, crossing the placenta, there's also this issue of inflammation that needs to be dealt with. And really, those are the two ways, at least when we think of it from an infectious disease side, those are the two kind of functions the placenta has to play. Yeah, tell me more about inflammation. That's the body's response to a virus. It's an immune response. So obviously the mother needs that inflammation response to help combat the virus, but it can be bad for the fetus. So what's the placenta's role there? Yeah. The immunological system here is really complex because the immune system is basically designed to identify what is self and what is non-self.

And the fetus has genetic material from the father. And so it already starts out as genetically different than the mother. So there's already some complex kind of immunological processes at play here. But it gets more complicated during a maternal infection. Now you have a system like you just alluded to where the mother needs to fight off this infection, while at the same time not fight off the developing fetus, right? And so inflammation is kind of a generic term, but what the body has to do is identify that there's a pathogen and then start secreting these inflammatory mediators, which are called cytokines and chemokines,

which basically tell the body that there's a pathogen that has initiated infection and start the process of fighting it off. And then, you know, the mechanisms for how that's controlled, how the antiviral response in the case of a virus infection, can do that and preserve maternal health while at the same time avoiding those same processes in the placentin developing fetuses is, you know, an area of, active investigation. So you conducted a study where you found that the placenta was good at protecting the fetus against influenza, but not against Zika virus, which is a mosquito-borne virus that causes fetal abnormalities and babies whose mothers contract it. So what did you discover is happening in the placenta with these two viruses? Yeah. So one of the really interesting questions that our group has been focused on is why is the placenta able to deal with inflammation in some cases and not

in others? And so in a study that we just completed, we really looked at pathways that can protect the developing fetus from maternal infection caused by influenza virus compared to inflammation after Zika virus infection. Both of these infections induce similar types of inflammation, but there are key differences in where the virus is replicating. And so, you know, the key finding from our study was that there's a key inflammatory pathway to suppress virus replication. And both influenza and Zika virus induced this pathway. But we found a protein that's able to suppress the activities of the inflammatory type 1 interferon.

We used an influenza virus infection system where it works. And so we know the answer for flu, the question is why isn't that enough for Zika? And, you know, we don't know the answer to that yet, but we suspect that it has to do with the local concentration of these inflammatory mediators that ultimately are responsible for a lot of the birth defects that we see. You didn't investigate this with SARS-CoV-2, but would you guess the immune response to coronavirus would be more like Zika or more like flu in pregnant women? Yeah, so the coronavirus, it's certainly much closer to flu than it is to Zika, and we know that

SARS-CoV-2 is not associated, at least with severe birth defects like we see after Zika. And so we think it definitely falls much more into the flu side of things and this J-B-1-mediated suppression pathway. It's probably at work protecting the fetus when pregnant women are infected by SARS-Co-2. That's great. Getting back to that question of how do we even study the placenta because it's such a complicated organ doing a very important job and we can't get to it. So how do you access placentas for your research? Yeah. So we used a combination of human tissue samples that were collected just like Dr.

Iverson described. But we really took advantage heavily of some animal models of virus infection because our goal here was to manipulate the inflammatory signaling pathways and see what the effects on the developing fetus would be. Obviously, this is something that you could never do in people. What's the best animal model for placenta research? Yes, that's a complicated and difficult question. We use mice in this study because they're a good model for the pathogens that we were using, influenza virus and Zika virus. mice have a different structure to the placenta than humans do. So, you know, it's never a perfect comparison, but we think we can learn enough from these

systems and then validate key findings in human tissues to draw these conclusions with high confidence. Dr. Iverson, one of the biggest concerns for mothers and their medical providers is the development of proclampsia during pregnancy. So can you tell us what that is? So preclamcia occurs in 45% of pregnancies and may lead to severe sickness and even death in both the mother and fetus. So this might pose a serious threat in pregnancy. It's diagnosed in the late stages by onset hypertension and most often proteinuria in the mother.

So preclampsia starts most often by improper placenta formation and this leads to a dysfunctional and stressed placenta that is characterized by harmful inflammation and oxidative stress. And as the fetus grows, this dysfunctional placenta sends more and more stress signals to the maternal blood. And this eventually becomes too much of a burden for the mother, and she develops the clinical science, hypertension and proteinuria. So most often, preeclampsia consists of the two components, placental dysfunction, and the maternal response. Also, to add to this, we have no effective treatment of preclampsia

other than delivery of the baby and the placenta. And therefore, preeclampsia is often associated with preterm delivery. This is Science Friday. I'm Katie Feather. Talking with Dr. Anne Charlotte Iverson, professor at the Norwegian University of Science and Technology, and Dr. Nicholas Heaton, assistant professor at Duke University, about the mysteries of the placenta. I have to say when I was going through this, most recently, the coronavirus was definitely a concern of mine, but I was terrified of proclampsia because everything I read and everything I'd heard suggested that we don't know why women get it. It just happens.

And then you combine that with some very severe outcomes, like you said, increased maternal and infant mortality rates, preterm delivery. So it just seemed very terrifying and unknown. So how much do we know about how and why this placental dysfunction occurs? So we know something about how this develops. It will start as early as during placenta formation when these trophoblasts invade the uterine wall. Then they participate in remodeling of the uterine spiral arteries. They are being remodeled to wide vessels that will ensure sufficient blood flow to the placenta.

And in the early stages of preclampsia, the invasion of trophoblast and the remodeling of these vessels doesn't occur the way it should. And the result is the placenta that gets abnormal blood supply and develops to be a stressed organ. So we know something about the initial phase, but then we have this whole development of this stressed organ and how it affects the mother and what parts and what inflammatory and oxidative. stress mechanisms that are at play. And there's a whole lot more to figure out to be able to both treat this disease and also to predict it. You mentioned inflammation, and I'm seeing a connection between this condition and mediating viral infection, which is what Dr. Heaton was talking about. Given that inflammation seems so disruptive, couldn't we just treat the inflammation? To be able to handle the harmful inflammatory levels that we see in diseases such as preeclampsia,

we need to understand where is the line between harmful and normal and what types of inflammatory activation is mostly causing the harmful inflammation we see in disease. So in our study, we relate to the similarities between cardiovascular disease and preeclampsia. We know that in arthroscarosis, cholesterol crystals induce a very potent inflammation and promote development of atherosclerotic lesions in the blood vessels. And what we did reveal indeed is that there are cholesterol crystals present at the maternal side of the placenta. And we know that preclincy and cardiovascular disease have so many similarities. So it makes sense that the same consequence of too much cholesterol accumulations, in the tissue leads to production of these cholesterol crystals,

which are potent harmful, induces of inflammation. And Dr. Heaton, I know the placenta isn't the focus of your research all the time, but you've waded into these waters now. So do you have any future plans to continue studying the placenta? Yeah, absolutely. I mean, like I said, I think, you know, like a lot of scientific questions, the more we learn, the more we realize we don't know. one of the things that we're most excited about following up now is, you know, in our previous studies,

we've identified some pathways that are important and we know that they're important because we broke them and we made things worse for pregnancy. And, you know, really what we want to do now is look at the flip side. Now that we know these pathways are important, instead of breaking them, can we make them work better? Can we make them stronger to potentially protect fetal health under conditions where, you know, things aren't? aren't working correctly. And then, you know, we're seeing things like birth defects. I want to thank you both for taking on the task of describing this research for our listeners today because it seems very complicated.

So you guys both did an amazing job. Why is it so hard to talk about this type of science? No, that's a good question. It's very motivating to be working in this field, but it's very complex. And there's a lot of processes that occur at the same time. And we have to approach it from our different platforms and try to work together to figure out this complex setting. I mean, the placenta wasn't even particularly well named. I mean, it was referred to as after birth, right?

It's just something that happens after the birth. So when you want to talk about this, that you have to start with like a, here's what the placenta is, here's why it's cool, here's the problem, and then here's what we found. Well, thanks so much again for joining us. Yeah, thank you. It's great chat. Thank you for having you. Dr. Anne Charlotte Iverson is a professor at the Norwegian University of Science and Technology at the Center for Molecular Inflammation Research in Trondheim, Norway.

And Dr. Nicholas Heaton is an assistant professor in the Department of Molecular Genetics and Microbiology at Duke University. For Science Friday, I'm Katie Feather. And that's about all the time we have this hour. Charles Berkwurst is our director. Our producers are Alexa Lim, Christy Taylor, Katie Feather, and Kathleen Davis. B.J. Lederman composed our theme music. I'm Ira Flato.