Are We Prepared To Fight ‘The New Polio’?

[AUDIO LOGO] FLORA LICHTMAN: I’m Flora Lichtman, and you’re listening to Science Friday.

A mysterious disease has been showing up in emergency rooms. Doctors have been seeing it for about a decade, and there have been fewer than 800 confirmed cases. But it’s what they’ve been seeing that’s raised concerns, otherwise healthy children showing up unable to move their arms and legs and in some cases eventually becoming completely paralyzed.

The disease is called acute flaccid myelitis or AFM, and if the symptoms sound a lot like polio, that’s because the virus that causes AFM is a cousin of the polio virus. Journalist and physician Eli Cahan has been following the path of this disease for us and is here to tell us what doctors are seeing, what researchers are doing to find a vaccine, and what this new polio might tell us about our preparedness for future disease outbreaks and pandemics. Eli, welcome back to Science Friday.

ELI CAHAN: Thanks for having me, Flora.

FLORA LICHTMAN: Eli, you spend a lot of your time in emergency rooms. What can you tell us about the disease? What do physicians know about it?

ELI CAHAN: Yeah, this is a disease that if we rewind the clock back to 2014, it really stumped doctors and researchers alike. Here you had a swath of children coming in, and their manifestation of disease looked a lot like polio, which is something that certainly one generation, at least multiple generations of doctors possibly thanks to vaccines, had not seen. And so here you had a number of kids coming in. They were limp. They couldn’t move their arms or legs. They couldn’t lift their heads off the tables.

And all the tests that doctors were running were coming back negative, meaning we were sending off all these swabs and blood tests and urine samples and samples of CSF, cerebrospinal fluid, which bathes the brain. And we weren’t getting any answers, which if there’s one thing that doctors hate, Flora, it’s not having answers. And the question was, what is causing this.

Thanks to a tremendous amount of work from a variety of groups across the country and internationally, they eventually discover that this syndrome, which doctors started calling the new polio because of how similar it looked to polio had a association with a certain type of enterovirus. It’s called enterovirus D68. It’s just a way of classifying this virus. And they saw that over and over. Patients who had this syndrome were presenting with this enterovirus, which led them to ask themselves where is this virus coming from and if it’s been around us all this time, why is it suddenly causing this syndrome that is awfully terrifying.

FLORA LICHTMAN: And is it always kids who contract it?

ELI CAHAN: It is certainly not exclusively kids, but we did see these clusters of outbreaks in children in 2014, again in 2016, and again in 2018, which I think much like polio, the OG polio, led doctors and researchers to wonder, well, is this a disease only kids can get or is it a condition that everybody can get but kids are more likely to get the severe manifestations, which is what we see in OG polio and what we were seeing in enterovirus D68 as well.

FLORA LICHTMAN: Are there treatments for this disease?

ELI CAHAN: So it’s a good question. There are some potential treatments in the pipeline which we can get to, but certainly in 2014, the treatments that we think about are maybe a phrase that people got tired of hearing during COVID, which was supportive care. When medicine is resorting to supportive care, what we’re talking about is putting people on supplemental oxygen, sometimes putting– needing to put patients on ventilators because they are that incapable of even initiating their own breaths.

But suffice it to say, when you’re toolkit is limited to supportive care, you’re in a bit of a jam, and you certainly are not treating the underlying cause of these syndrome, which, again, in this case, researchers and doctors alike and the CDC thought was most likely to be this virus enterovirus D68.

FLORA LICHTMAN: What percentage of people recover once they’ve contracted it?

ELI CAHAN: Yeah. It’s a good question. It’s a complicated question because I think when we talk about recovery, recovery looks very different. So there’s survival, which I think the sweeping majority of patients who contracted enterovirus D68 survived and eventually made it through. The same is true for polio.

And so the question is when you survive, which the vast majority of patients did, what happens next? And that is really uncharted territory. Years and decades after patients have gotten polio, they still have dysfunction in their muscles and in their nervous system that leads them to struggle to lift their legs up. If they’re sitting on an airplane for a while, getting up from the airplane seat because your hip muscles which allow you to stand are really weak or trying to reach to the top shelf in your cupboard to grab that jar of peanut butter because you finally run out, those sorts of things can be really challenging for folks with original polio, and we’re seeing much the similar patterns in patients recovering from enterovirus D68.

Of course, the other open question here is we don’t what the long-term trajectory of these patients looks like. If we really started diagnosing cases in any significant quantity in 2014, we’re now 11 years out, which is a very long window for a child who was two years old and now they’re 13, and is a very short window when we think about medical science and monitoring these patients for decades of life to see, well, hey, if you don’t have your muscle function in your elementary school years, teenage years, early years of productivity as an adult, mid years of having kids or whatever you do, those are all open questions in terms of how the folks who recovered from this, how they’ll look decades down the road.

FLORA LICHTMAN: Is the polio vaccine useful as a template here? Are people at work on a vaccine?

ELI CAHAN: People are at work on a vaccine, Flora, and there are some really promising candidates in terms of things that still have lots of years of research to go but show promise in mice. And, in fact, if you look back to the timeline of science after this 2014 outbreak, what researchers were able to pull off characterizing this disease and developing it into a potential vaccine in a short amount of time, to say that that was a monumental achievement and testing those to ensure they don’t cause all the bad things that everybody is afraid of with vaccines, you want to make sure you’ve gotten that totally right. And so there remains years of research around these vaccine candidates, and there’s promise.

FLORA LICHTMAN: Do we know where this came from. You mentioned at the top. It’s an open question. Did it evolve? Has it been with us all along? But is this the kind of virus that has an animal reservoir? What do we about it?

ELI CAHAN: I don’t think that this is a similar pathway as COVID in terms of having an animal reservoir. The hypothesis is that this thing is circulating all the time, and the corroboration of that is what we observed during the pandemic years, which is that there was a drop of acute flaccid myelitis cases, the new polio syndrome, following the pandemic. And so the thought is, well, some of the pandemic measures may have helped to stamp down the circulation of enterovirus D68 as well.

The thing that researchers are working really hard to try to understand is what is it about this exact breed of antivirus. There are mules, and there are horses. And the horses are the rhinoviruses, and the mules are the enteroviruses. But there’s black mules and brown mules and white mules and all the mules under the sun.

And, listen, I’m a kid from New York City. What do I about mules? But I know they come in different colors, and in the same way could have an enterovirus D68 that causes very severe respiratory disease. You could have an enterovirus D68 that causes this acute flaccid myelitis syndrome. And the question is where have those ones gone, and is there a risk that they could come back?

FLORA LICHTMAN: You’ve been tracking this story. Why is it interesting or important to you?

ELI CAHAN: I think that when we try to understand the ecosystem around learning about new threats, when we have a medical mystery that we suspect is infectious, there are so many things that go into discovering what is causing that infectious threat and what we can do about it. And all of that machinery is the exact same machinery that we need when we think about pandemic preparedness and pandemic prevention and pandemic response.

So all the machinery that in a technical way, all that expertise that we use to identify a virus like D68 is the exact same that we use whenever we hear about a new virus overseas whether that’s bird flu, whether that’s a new SARS-COV-2 variant circulating, all that machinery is so important. And so in that way, this AFM story for me, Flora, was really a microcosm of much bigger questions around our ability to detect and respond effectively to pandemic threats.

FLORA LICHTMAN: Well, what do we need to detect and respond effectively in a nutshell?

ELI CAHAN: Yeah, yeah. If it was only so easy. In a nutshell, we need aware doctors of what this syndrome can look like who then are equipped with tests that work quickly, that are effective, that are widely available. Then you have to ideally have measures you can take in the short term both to protect that patient, things like monoclonal antibodies, which are medicines that are currently in development for AFM and we saw them utilized for COVID. This is remdesivir is a monoclonal antibody.

And then hopefully you have vaccines so that not only you can prevent that same kiddo from getting the future AFM case, but also you can protect everybody who came in touch with that individual following contact tracing. You can do prevention for those folks in the event that there is a single case identified.

FLORA LICHTMAN: Eli, thank you so much for taking the time to walk us through this.

ELI CAHAN: Thanks for having me, Flora.

FLORA LICHTMAN: Eli Cahan, journalist and physician. You can read more of Eli’s reporting on this story at sciencefriday.com/newpolio.

[MUSIC PLAYING]

After the break. Ira’s got a story about why cancer researchers are starting to pay attention to non-cancerous cells.

SYLVIA PLEVRITIS: Some of the hardest to treat tumors are actually non-cancer cells.

FLORA LICHTMAN: Don’t go away.

Hey, Flora here. We’re wrapping up Science Friday’s fiscal year on June 30th, and we could use your support. I know don’t need to tell you, it is a tenuous time for science and for public media, and we are relying on donations from our listeners more than ever. We’re aiming to raise $40,000 to close out our budget, and with your help, I know we can do it.

So if Science Friday is valuable to you, if you rely on our reporting to make sense of the world or just to give you a little joy, please consider going to sciencefriday.com/donate to make a donation. It’s fast, easy, secure, and any amount you can swing will help sustain us in this critical moment. Thank you. We have said it before, and we really mean it. Science Friday can only continue with your support. That’s sciencefriday.com/donate. Thank you.

[AUDIO LOGO]

IRA FLATOW: When you think about how cancer spreads in the body, you’re probably thinking about the cancer cells, right? They divide uncontrollably, form into tumors, hide from the immune system, so it makes sense that studying the behavior of these cells is critical to understanding cancer.

But now researchers are beginning to look more closely at the non-cancerous cells that coexist within tumors and the surrounding tissues. It’s called the collocato. Taking this from a holistic approach may help explain why some treatments don’t work for all patients, and eventually may lead to more effective therapies.

Joining me now to talk about her research in this field is my guest, Dr. Silvia Plevritis, professor of biomedical data science and radiology and chair of the department of biomedical data science at Stanford University in Stanford, California. Welcome to Science Friday.

SYLVIA PLEVRITIS: Thank you for having me.

IRA FLATOW: You’re quite welcome. I’m really interested in this topic because it’s something that people really don’t talk about very much, the non-cancerous cells. What made you study the non-cancerous cells, and why are they important, too?

SYLVIA PLEVRITIS: No, that’s a great question. So a tumor is not just made of cancer cells as you just explained. It’s made of cancer cells and non-cancer cells. And, in fact, some of the hardest to treat tumors are actually non-cancer cells. And so we now have technologies to better understand the role of these non-cancer cells in maintaining the tumor and enabling it to progress and metastasize.

And so the focus on the non-cancer cells is a new area, and it is underlying the theme of the colocateome like what are the cells that are co-located in the neighborhood of the cancer cells and how do they influence the cancer cells to do what they do.

IRA FLATOW: I’m looking at a ball of cancer cells, a tumor. Are they mixed in homogeneously with the cancer cells or the normal cells are all surrounding it or– what does it look like?

SYLVIA PLEVRITIS: So, yeah, imagine that ball. The non-cancer cells are mixed in with the cancer cells. And what we’re recognizing is that they have a very specific architecture, and we’re trying to understand that architecture. What is really the spatial organization of the cancer cells and the non-cancer cells because we really believe that understanding the organization is going to help us understand tumor biology much better than we do now.

And so examples are non-cancer cells are just blood vessels that race through the cancer. So they have a very clear structure. But then there are other cells, immune cells, that are mixed in, and then there are other cell types called stromal cells.

IRA FLATOW: What are stromal cells?

SYLVIA PLEVRITIS: So stromal cells are really the most understudied cells in the tumor. And a type of stromal cell is called a fibroblast. And they are often the cells that are most known for creating something called the extracellular matrix, which is the scaffolding that the cells sit in. And so they have a very active role in the tumor and in tissue in general, so they are one of the main components of the tumor. And, in fact, some of the hardest to treat tumors like pancreatic cancer is primarily stromal cells.

IRA FLATOW: Is it hard to treat because you have the stromal cells there?

SYLVIA PLEVRITIS: Yes. So the stromal cells are often thought of creating a protective barrier to the actual cancer cells. But we have come to realize that they have more varied roles in the tumor microenvironment than we first appreciated, so it’s not just a function of them creating a barrier. From our research, they do actually influence the behavior of the cancer cells and actually help protect them from different treatments by actually causing the cancer cells to switch their cell state. So that’s a whole other concept, and we do see that some stromal cells really enable the cancer cells to transition to a state where they’re more resistant to treatment.

IRA FLATOW: So the cells surrounding the cancers are really not helping you when you’re trying to treat cancer.

SYLVIA PLEVRITIS: No. Those cells are helping the tumor. So many of those non-cancer cells, which are really normal healthy cells have been conned by the cancer cells to really support the tumor and its growth and progression. And so we need to understand exactly why they’re doing that and how to get them to stop so that we can more effectively eradicate the tumor.

IRA FLATOW: So do they help the cancer spread, metastasize?

SYLVIA PLEVRITIS: Yes. And, in fact, the stromal cells in particular really provide avenues for the cancer cells to actually migrate out of the tumor and migrate toward, for example, vasculature and to get into the blood circulation and actually just spread even locally within its original region.

IRA FLATOW: Is this a newly discovered thing about how they act?

SYLVIA PLEVRITIS: Well, I wouldn’t say it’s a newly discovered property of tumor biology, but I would say it is a property that we have the technology to better understand now. And because we can study it and quantify it, we can start understanding what it is that we need to control.

IRA FLATOW: So how do you study cancer cells along with the non-cancerous cells that surround them? You said you now have better techniques if I understood you.

SYLVIA PLEVRITIS: That’s right. So there have been so many advances in biotech and AI that are working hand in hand to enable us to do that. So we are at a point now where we can study all the individual cells in a tumor, and so we can see it. It’s in native environment.

And so we can now look at a tissue, which is maybe a region of hundreds of thousands or millions of cells, and for each cell, we can, again, measure hundreds to thousands of molecular markers. So we have this data now where we can have a molecular map at single cell resolution of tumors. So we could really understand really the cancer cells and they’re– the neighborhoods that are surrounding them that are supporting their growth and the promotion of the tumor.

IRA FLATOW: So just that I understand what you’re saying because this sounds really amazing, are you saying you can keep the tumor alive outside of the patient’s body when you study it like that?

SYLVIA PLEVRITIS: So the answer is actually yes. So that’s happening as well. What I just explained is that when we take let’s say a research specimen of a human tumor and we study it in the lab, we can analyze that tissue specimen at a single cell level with deep molecular profiling of the individual cells across the entire tissue. Now to get to your question about actually studying it more experimentally, we can do that. We can take that tissue, and we can create what we call organoids or assemblies and keep that tumor alive so that we can see how it behaves to treatment and understand how not only the cancer cells are responding to the treatment but how the non-cancer cells are responding to the treatment and how they’re modulating the response of the cancer cells to the treatment.

IRA FLATOW: Is AI helping you out in your research here?

SYLVIA PLEVRITIS: Yeah. For me, AI is everything.

IRA FLATOW: AI is everything.

SYLVIA PLEVRITIS: So absolutely. This is so much data that we couldn’t analyze it without AI. And so we are putting together information across hundreds of thousands of cells for just one tumor specimen, but, of course, we’re trying to look at hundreds, if not thousands of tumor specimens. And so the scale of the data is enormous, so we absolutely need AI.

IRA FLATOW: You recently looked at how lung cancer cells interacted with the cells around them. Tell us what you found.

SYLVIA PLEVRITIS: Yeah, it was really interesting. So we created one of these assembloid models where we took human lung cancer cells, and then we put them together in a culture with human stromal cells, the fibroblasts. And then we watched what would happen.

And then when we treated that model of those two cell types together, we found that because of the stromal cells, the cancer cells were now resistant to the treatment. If the cancer cells were alone, they would be sensitive to the treatment. And what we found is that the cells rearranged when we treated them as if there was a different type of arrangement to protect the cancer cells under the stress of the treatment.

And that was fascinating to us because it really shows us that there is a very significant role of the microenvironment that we need to understand why is this new rearrangement important. So it’s giving us clues as to what spatial organizations and specifically neighborhoods of cells we really need to focus on when treating cancer, and specifically how do we alter the behavior of those non-cancer cells so we could really effectively eradicate the cancer cells?

IRA FLATOW: What is your biggest barrier to doing your work, and what kind of knowledge or equipment or whatever would you love to have that you don’t have or a question you’d like to answer that you don’t have the answer for now?

SYLVIA PLEVRITIS: Well, I have to tell you, I’ve been working as a PI for several decades now, specifically in cancer. And the question that has been driving me is how does cancer progress in an individual. Because once we see cancer in a patient, we use everything at our disposal to eradicate it because we don’t ethically do not want to track this disease over time. But we can reverse engineer what is the trajectory of cancer because we can look across large populations.

And so the resources that we need is to really amass data from many people because we detect cancer at many different stages across different patients, and through analyzing data across hundreds of thousands if not millions of patients, I truly believe that we’re going to be able to understand the dynamic nature of cancer because cancer is not a static disease and until we can really understand that progression and evolution, the dynamic nature of the disease, I don’t that we’re going to have full control of it. But I’m optimistic that we will get there very soon because we have all the tools now. And with that understanding, I really believe we’re going to have much more success at controlling this disease.

IRA FLATOW: Well, we wish you much success in your work.

SYLVIA PLEVRITIS: Thank you.

IRA FLATOW: Thank you for taking time to be with us today. Dr. Sylvia Plevritis, professor of biomedical data science and radiology and chair of the Department of Biomedical Data Science at Stanford University.

[MUSIC PLAYING]

FLORA LICHTMAN: Thanks for listening. Don’t forget to rate and review us wherever you listen but only if you like the show. It really does help us get the word out and get the show in front of new listeners.

Today’s episode was produced by Dee Peterschmidt and Shoshannah Buxbaum, but a lot of folks helped make this show happen every single week including–

PRAISE AGOCHI: Praise Agochi.

SANTIAGO FLÓREZ: Santiago Flórez.

JORDAN SMOCZYK: Jordan Smoczyk.

EMMA GOMETZ: Emma Gometz.

FLORA LICHTMAN: I’m Flora Lichtman. Thanks for listening.

Copyright © 2025 Science Friday Initiative. All rights reserved. Science Friday transcripts are produced on a tight deadline by 3Play Media. Fidelity to the original aired/published audio or video file might vary, and text might be updated or amended in the future. For the authoritative record of Science Friday’s programming, please visit the original aired/published recording. For terms of use and more information, visit our policies pages at http://www.sciencefriday.com/about/policies/