Podcast: Long-COVID and Diversity

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At The Jackson Laboratory (JAX), researchers work on many projects  One of them is finding ways to study long-COVID, the challenging diversity of symptoms that people experience after recovering from COVID-19. 


Here's a conversation Nadia Rosenthal, the scientific director of JAX. It's part of my reporting for a story on long-COVID in Nature Methods. You can read the story here and find the podcast and transcript here on this page. The podcast is also on Apple podcasts, Google podcasts, Spotify and wherever you get your podcasts. 

Note: These podcasts are produced to be heard. If you can, please tune in. Transcripts are generated using speech-recognition software and there’s a human editor. But a transcript may contain errors. Please check the corresponding audio before quoting.

A conversation with Nadia Rosenthal about long COVID

Vivien: Hi, welcome to Conversations with Scientists, I’m Vivien Marx.

Nadia Rosenthal

The problem of long-COVID is utterly changing by the day.

Vivien: That’s Dr. Nadia Rosenthal, scientific director of The Jackson Laboratory. You will hear more from her and about her in this podcast.

In my reporting, I get to talk to researchers around the world and this podcast is a way to share more of what I find out.

This podcast takes you into the science and it’s about the people doing the science. You can find some of my work for example in Nature journals that are part of the Nature Portfolio. A lot of papers are published there. Those papers are written by working scientists and are about the latest aspects of their research. And a number of these journals offer science journalism. These pieces are done by science journalists like me.

This podcast episode is one of several I am producing on long-COVID, which is this puzzling diversity of symptoms that people experience after recovering from COVID-19. Scientists are working on might be causing long-COVID. I am doing a story on long-COVID for Nature Methods.

 After recovering from COVID-19, people are grateful, of course. But many people find that even months after their infection, they struggle with symptoms. They might have difficulty breathing, they might have muscle or joint pain, they might have terrible fatigue, so terrible that walking up a flight of stairs sends them to bed for a day, they might have heart palpitations, they might have sustained damage to their lungs, heart, kidneys, they might suffer from what is called brain fog. When the symptoms are severe, these people’s lives get completely derailed.

Figuring out what is causing long-COVID is difficult. One approach involves modeling the disease in animals. Yes, this does involve experimenting on animals, which I know some people are opposed to. Yes, animal experiments are uncomfortable to consider. But please give this podcast a listen. It might offer some aspects that you might not have heard yet about the value of doing ethically responsible research with animals that can potentially help people with long-COVID.

Nadia Rosenthal 2:15: The field is racing. And yet I'm not seeing that much that's really budging our understanding of what's going on in these various cases where people are really having very different responses.

And it doesn't seem to be connected to the severity of your first infection, a lot of asymptomatic people, especially younger people, which is extremely weird, are coming down with these symptoms later on after they have otherwise sort of recovered from their from their initial infection.

So you could say, well, you know, if you just have a really bad sort of response to this and your immune system isn't up to snuff and, you know, the virus gets out of control and it sticks around for a long time, and then that continues to exacerbate the situation and perhaps it incites riot in the immune system, you could say all that. But it kind of doesn't fit the data, which is that there's not that much of a causal relationship between the severity of the initial response and what's going on later.

Well, that suggests to me something that I'm particularly interested in, and that is: people are different. They start out different genetically and they then develop different because of their genetic makeup.

The immune system has its own genetics. And we know that there are certain aspects of genetic makeup that can either render you resilient and resistant to certain viral infections or really sensitive to them.

I can't imagine that it's going to be any different for long COVID. For long COVID I think there are going to be differences between people that will, in the end, if we're really, really smart, we will be able to predict from your genetic makeup just what would happen to you if you got COVID and it went on too long or maybe even predict that you are not susceptible to long COVID, wouldn't that be helpful, just at least so that we would know what the differences are and what they're really ascribe to? Is it something that is environment or is it genetics.

Vivien: At The Jackson Lab a group of people are part of what Dr. Rosenthal calls COVID Mouser group, they discuss what is needed to study COVID and long COVID. They’re committed to figuring this out.

Nadia Rosenthal: People are united in their conviction that there is something here to really help the human race, which is genetically very, very diverse. And if we can use these diverse animals to model these different disease states, we might really be able to contribute to breakthroughs and therapies that would be much more precise than they are right now.

 Vivien: Mice have been used to develop and test vaccines and are being used to study COVID-19 and long-COVID. The mice classically used in labs are not genetically diverse. But given how diverse the symptoms of COVID-19 are and long COVID, Dr. Rosenthal believes that for that research, mice need to be more diverse to study that.  

Nadia Rosenthal  5:20: I think what we can offer is a an avenue of investigation that will take us down into the genome. And the reason that's interesting is because every cell has to manifest the genome.

And for the most part, you're manifesting an invariant genome. Now, that's not true. And immunology is the one place where you actually rearrange things in the genome, but nevertheless, you're arranging, rearranging parts and those are the parts you were born with. So you can you can sort of simplify it by saying that you're dealing with a genomic makeup and that everybody's is different unless you're an identical twin. So the question is, what can those differences in different people's genetic makeup tell us about this disease?

Vivien: One of the difficult aspects about this project is that mice don’t get COVID-19. Some of the new variants of SARS-CoV-2, the virus that causes COVID-19 do appear to infect mice. But when the pandemic first hit in early 2020, lab mice couldn’t be used to understand what was going on in people because the mice didn’t get sick.

What labs needed were mice that were a bit more like people. Researchers do this by engineering the animals to express some human genes. The problem then is: these mice died quickly when they were infected, just like many people have. So these mice don’t get long-COVID.

Nadia Rosenthal 7.05: So I'll just disclaimer is that long COVID is a long study and therefore we are only at the beginning of it because people haven't been followed for long enough to know what's going to happen. And it's true for the experimental animals as well.

Most of the studies on animal models of COVID look at time points that are acute, like three days, six days, nine days, maybe 21 days maybe, and although mice have a compressed lifespan, the virus is basically running the same show.

And so you really need to take these mice out for months to understand whether we have the right models for long COVID and the study of long COVID.

Vivien: But the genetically diverse mice are ones that labs might be able to be used model long-COVID. That’s the goal the Jackson Lab is now pursuing.

Nadia Rosenthal 8.00: When the pandemic became evident, let's say a year ago in and we should have been going, it should have been evident in January, but we were all being 'heads in the sand' about it. The first thing that we at The Jackson Laboratory thought about was, geez, we need a mouse model for this. And we knew from the from the literature that this model, this particular variant of coronavirus SARS CoV-2 did not infect mice.

And the reason for that, it's pretty simple or maybe deceptively so. There is a receptor called the ACE-2 receptor. It sits on the surface of many cells in your body. It has its own function that has nothing to do with viruses. But the virus has very cleverly, you know, essentially exploited the shape of that receptor to model its own docking protein called the spike protein

It’s on the edge of those spikes that you know. And so the virus sort of bashes up against the cell and gets that lock and key situation set up. And then it knows it can get inside the cell because that cell can actually take up the virus and the receptor into the inside of the cell. And then all sorts of strange things happen.

The virus has all sorts of other tricks. It interacts with other gene products to start its viral cycle because it's got to take all of the machinery that the cell normally uses to replicate RNA. Because these are RNA viruses, they have to make more of the RNA and then they have to package them in proteins that are encoded by the RNA that it just you know, it's a it's a spectacular piece of, I don't know what chicanery, machinery.

Well, it's beautiful in its terrifying way because of the extraordinary intelligence of this evolutionarily adjusted, semi-living thing that gets in anyway. I used to be a virologist, so I'm always excited about them.

Vivien: This viral chicanery is also the reason why we don’t get a lot of infections that afflict animals. There are some important differences between people, bats and mice.

Nadia Rosenthal 10:25: So if you look at the sequence of the protein that comprises the ACE-2 receptor and you line it up with the human and let's say the bat, which we know is infected by this virus and other other animals. And we line them all up and then we put the mouse sequence in there. Here you can see where there's a change and the mouse has the wrong amino acid at the right place to completely discombobulate this virus, and so the virus goes, oh, well, that doesn't fit.That lock doesn't fit. I got to go to the next house.

And so it gets into the mouse lung, but then it can't get into a cell. So what can it do? It can't replicate. It needs the cell to replicate so it doesn't get into the cell, that's it. That's the end of it in the mouse. The immune system probably takes a look at it and says you're not supposed to be here. Macrophage, take it away. So that's what happens in mice.

And, you know, we are lucky because we have a similar non-parallel situation with many of the viruses in the Animal Kingdom and we don't get sick from those for the same reason because we're just not we're not aligned at the molecular level.

Vivien: There was an outbreak of a viral respiratory disease caused by an airborne coronavirus. The outbreak started in China and spread to a few other countries. This might sound familiar.  The virus is SARS CoV-1, and the disease: Severe acute respiratory syndrome. That scary outbreak and some deaths--estimates vary but probably around 800 deaths worldwide--that scary outbreak lasted from 2002 to 2004. Mice weren’t susceptible to SARS-CoV-1. So for work on that coronavirus strain, labs had developed a mouse model.

Nadia Rosenthal 12.20: What can you do to make mice more susceptible? Well, the obvious thing is put in a human ACE-2 gene. We can do that in our sleep up here at The Jackson Laboratory. So it turned out we didn't have to, at least for the short term, because another group had been working on another virus in the coronavirus family called SARS. And this group was run by Stan Perlman, who is in Iowa, and his very talented postdoc, Paul McCrae, who now has his own lab.

And in 2007, they developed a virus that had a human ACE-2 receptor in it because other viruses also use that receptor and they were studying the interaction. So it became clear that we really needed to find a mouse fast. We didn't have time to monkey around with it. We had to get the mouse. If it existed, we had to expand it because that's what we do here, we expand the numbers of mice that we need to send out to the world.

Vivien: Next the scientists needed to figure out if this mouse model that worked for SARS-Cov-1 would work now.

Nadia Rosenthal 13:30: The big question was, would this work for the SARS CoV-2? And there had been some in vitro work in cells that suggested that it would and guess what: it did. One little problem and by the way, though, those mice are now all over the world, but one little problem was that the mice died too quickly

They got sick too quickly, they would die by, let's say, day six after you had infected them, and that's not really the way humans respond to this virus.

It's a fantastic platform for doing things like antibody, antiviral and vaccine because you just give it to them.And if the mouse doesn't die, you know that you've done it and you've got them, you know, because it's such a severe phenotype. So if you give the mouse a vaccine and then you give it the virus and the mouse walks away from it, you've validated your vaccine.

Vivien: Let’s go back to that bit about mice not getting COVID-19. It seems kind of difficult to model a human disease in mice if the mice don’t get that disease. Nadia Rosenthal explains what was tried.

Nadia Rosenthal 14.35: In this case for this mouse that I'm talking about. It was made, you know, quite a while ago, over 10 years ago. And at that time, they knew that this virus would infect epithelium, which is the stuff on the outside of your vessels and lung and all the rest of it.

And so they found a gene that was expressed in the epithelium and they stole its regulatory regions and they hooked that up to the ACE-2 gene so that now the ACE-2 gene would be expressed in the epithelium and at very high levels because they didn't have enough information about how to give that human ACE-2 gene a mouse ACE-2 regulatory region.

So they so they kind of the jury-rigged it. And it's very, very effective, except that the that promoter is actually not expressed in the same places as the ACE-2 gene. So it's like ectopic expression. It's too high and too and mis-located.

That's our theory about why this mouse is not the perfect model. But be that as it may, it's been extraordinarily useful for many, many studies.

Vivien: That mouse had been engineered to have the human ACE-2 gene and to have its cells express the protein ACE-2, which is a kind of doorknob into cells the virus uses to infect them.

Using this model and a few others, vaccine studies have been pursued and as we now  know vaccines resulted in record time that could then be tested in people. But this was not quite the mouse model that will be useful for studying the diversity of COVID-19 and long-COVID. 

Nadia Rosenthal 16.25: But I took a look at it and I thought, you know what, I bet if we took that mouse and crossed it with another breed of mouse, another strain of mouse, and we have 11,000 to choose from at JAX, I wonder if that would shift the phenotype.

You know, the response to the virus, because I knew that different people respond to the virus differently. Some people get sick, some people don't. And that smells like genetics to me. So I said, let's play around with what we call the host genetics, which is the genetics of the host animal that's being infected and see if we can't just budge that rather severe response a little bit to the north or south. And that would tell us something about the genetics as well.

Vivien: In order to do that work you need a lab where you can work with SARS-Cov-2, you need a lab outfitted for work with deadly viruses. Nadia Rosenthal contacted colleagues she knew at Rocky Mountain Labs which is run by the NIH National Institute of Allergy and Infectious Diseases.

Nadia Rosenthal 17.40: I called up this woman, Sonja Best, and who I had met through a friend of a friend. And I said, look, I've got this crazy idea. I want to put that particular transgenic construct onto many different backgrounds

And it's easy to do because I'll just cross the mice and then I want you to test to see if it will have any effect. Well, I had given a talk out there two years ago telling them all about how genetic diversity in humans had to be modeled by using the genetically diverse animal models. You can't use one inbred mouse to represent the entire human race. So why were we doing it that way? It was crazy.

Vivien: It was March 2020 and it was sadly becoming clear what COVID-19 was doing to people around the world. Hospitals were overwhelmed with sick people, many could not be treated effectively and died. Beyond the immediate need to stop this tragedy, researchers knew they needed to understand the mechanism behind COVID-19.

As people recovered, many of them talked about their lingering symptoms. Long-COVID was beginning to make its ugly appearance. A mouse model was going to be needed to study that as well to help researchers develop potential treatments and understand what was happening in people with Long-COVID. To Nadia Rosenthal, diversity was going to be the way forward.

Nadia Rosenthal 18.50: But I convinced Sonja and her colleague, Shelly Robertson, and the two of them, decided to try my crazy experiment. It it just so happened that I had also been down to the NIAID, the National Institute of Allergy Infectious Diseases, where Steve Holland, who is the intramural chief, was very interested in my ideas about genetic diversity and infectious diseases.
This was long before COVID-19 hit, a year before I'd been down and gave a seminar.
And after he says, we got to do this, we've got to find a mouse model that's really good for TB, a mouse model that's really good for Zika, a mouse model… I said, you're singing my song, let's do it. And then we got busy and then COVID hit. And I called him up and I said, Steve, it's showtime. And he goes, you bet. And he said Godspeed  It was incredible that happened it happened in weeks.

Vivien: The team began breeding mice and getting them to Rocky Mountain Laboratories to test. The mice weren’t at all like the lab mice the staff at the lab were used to.

Nadia Rosenthal: They were quite horrified, by the way, in which their expectations of the way mice behave were dashed as new, different strains popped up.

There was one little guy who's literally half the weight of any normal mouse. So a normal mouse weighs between twenty five and thirty five grams. And this little fellow, his name is Castanius and he weighs about 10 to 12 grams. Really just adorable, except it's half the height and twice the bite, these guys are vicious and they are nasty and they're like wild mice. You know, a wild mouse doesn't allow you to just pick it up by its tail. It'll turn around and bite your fingernail off.

Vivien: The scientists wanted the diversity of these mice and the scientists devised a way to work with them.

Nadia Rosenthal 20.50: The way we did the experiment. we had to kind of engineer a bit and fudge it because we needed this human gene in there. And in all the other experiments with viruses, nobody had to add a human gene because the virus would infect the mice directly. So there were all sorts of technical reasons why I could imagine this not working at all. That is to say that all the mice died at day six, just like the C57/black 6 six original mouse, which is the sort of workhorse of our field anyway.

 We had eight different strains at the beginning, so we could get enough numbers if you varied the genetic background, not by going to a different species but by going to a different subset of mice, you could change the response to the virus.

What we were hoping for was a spectrum of responses each one of which would have some relationship to a human response. We know some humans get really bad lung infections, some humans lose their taste and small, other humans get thrombosis. we have no idea why. so the question was could you actually predict from the genetics of an animal, what type of disease the animal was going to get.

And the answer was: we could We could tell if the animal was going to develop high titer of the virus in the brain. We could tell if that animal would then only develop lesions in the brain, which is, by the way, where your taste and smell sensors go. That's the information processing for your smell and taste. And it's the place right next to the olfactory bulb in the brain. So it may be that the virus was just kind of taking a hitch over into the hindbrain and making hay while the sun shine in there. I don't know. I mean, that's we're still doing all the histology on these animals.

Vivien: The scientists have started looking at the responses of the mice to being infected with SARS-CoV-2 also paying attention to gender differences.

Nadia Rosenthal 23.00: Well, girls and female mice have a lot in common. And the fact is that we found some of those eight strains that only responded to the virus in the male, the males. So only the males got sick. And then another one where only the females got sick every time, every mouse the same. Well, and then we had one where the guy just walked away, gained weight.

One of the first things that happens is a mouse loses weight. It's probably because it's not feeling well and it's also probably lost its taste and smell and isn't eating. And so you see the weight going down. And that's the first indication that the animal is sick because it doesn't go. ‘Mommy, mommy, I don't feel so good.’ So you have to look at things like weight loss.

That’s a way you can tell an animal is sick. Some animals just drop weight precipitously, but then bounce back again and other species dropped a little weight and then just died and then other species went right up and just gained weight as if othing had happened, just like a lot of our asymptomatic patient, you know, people who know they test positive, but they go, ‘I didn't even know I had it.’

So just out of eight mice, we were able to really pass out a lot of the responses. And once we knew that those responses were genetically determined, we could now make the argument that with these mice, with further work, we could actually drill down into the nuts and bolts of those genetic differences, because we know everything about these eight mice.

Vivien: Other mice in the works are being engineered slightly differently with the human ACE-2 gene and the human gene regulatory region for the ACE-2 gene. 

Nadia Rosenthal 25.00: So we will see whether that's a little more. You know, we get more natural variation using that.

Vivien: Right now they teams are still testing how these mice are responding, all of this takes time. Of course this is all urgent. But the teams don’t want to draw the wrong conclusions or have the data reflect only what happens in a few mice. That will not adequately represent what happens in people

Nadia Rosenthal: Once me and my colleagues out of Rocky Mountain are are feeling secure about the numbers because obviously you want the statistics to bear out. That means more animals and more tests once we've had a chance to really look in in some depth at the histology. We're also doing a huge amount of transcript comics, but I don't have time to wait for that. That'll be really exciting because then you can use the expression QTLs if you know what that means

It's basically using expression patterns to get it at genetic networks. So we're going to be able to do that in different tissue types also.

Vivien: The scientists are looking at lung and brain tissue and they also plan to look at heart tissue. And for studying long-COVID they need to observe and assess the mice for longer periods

Nadia Rosenthal: The first thing I want to do is the minute that we have the time and the breadth to do it is to get these mice onto an aging program so that we can look at long covid the biggest thing because we have to infect them.

Vivien: The virus doesn’t sleep or rest, it keeps changing so labs need models that reflect the changes to the virus. One aspect The Jackson Lab team is exploring is to work with viruses that are slightly different they are called ‘mouse-adapted viruses’.

Ralph Baric at the University of North Carolina and his team have found a way to passage the virus through the mouse . It’s a way to nudge the virus to undergo artificial evolutionary shifts. The mouse’s physiology forces the virus to mutate, to change.

And: New viral variants are popping up around the world and some of those seem to naturally infect mice without any engineering needed.

Nadia Rosenthal 26.50: So it may very well be that we can use our genetically diverse panels with the variants directly and then we don't have to do all that breeding, which really speed things up, a lot.

Vivien: The challenge of long-COVID is difficult because of its dizzying array of symptoms. Brain fog, heart problems, fatigue. The mice, says Dr. Rosenthal, will likely present a variety of symptoms, too.

Nadia Rosenthal 27.15: I suspect it will be. But on the other hand, you know, inasmuch as the brain fog and the heart problems are popping up in very sort of unpredictable ways. And we have, for instance, one animal that is showing up micro-thrombi in in the heart, which is one of the problems we're worried about. The clotting cascade is a very likely target for this virus. That means that we have something to go on then, because if we know that we get the same symptom over and over and over again in a particular background, that tells us that the genetics is there to unravel. And that we could figure out what it is that actually makes that mouse susceptible to brain fog or to the heart.

So it really isn't that we're going to necessarily model every single aspect of human responses, but I think we're going to get damn close with some of these with some of these animals. And we've just begun. We've looked at eight animals.

Vivien: To be able to make credible statistically sound conclusions, the scientists need to breed many more mice and to give labs around the world the opportunity to explore targeted research questions with them, But even with only eight genetically different mice. Dr. Rosenthal believes she and her team can find out important aspects of COVID and long-COVID.

Nadia Rosenthal 28.50: Right now, what I want to do is to try to figure out if there's a way that we can predict from the information that we get out of the mice that we've already used, is there a way that we could predict some configuration, some level of expression of a gene in the lung that could predict for us that that mouse is tracking with a particular response to the virus, because then you're onto a network of some sort and then you can start using various clever tricks to get to the other members of that network. And from there, you can infer without having to do a blind screen.

Vivien: The scientists want genetic variation but not an infinite amount of genetic variation.

Nadia Rosenthal 28.40: You have to narrow the number of different gene variations that we call the alleles that you that you have in the collection simply because otherwise it gets a little bit hard to follow track which part of the phenotype or the response is coming from which component of a mouse genome. And I say component, meaning hundreds or thousands of genes on a chunk of DNA that seems to be tracking with that particular response. And so you say, well, it's got to be in there somewhere, but you don't know exactly where.

Vivien: One of the hunches about long-COVID is that it might be due to an autoimmune response, the immune system is over -responding. Some groups, for example Rockefeller University researcher Michel Nussenzweig and his team and colleagues at other institutions, have found viral reservoirs in the gut of people who have survived COVID-19, they still have virus in their gut. And these viral remnants are immunoreactive.

Nadia Rosenthal 30.45: It just means that you've got antibodies to it. But that that doesn't necessarily mean that what they're picking up in the gut is making you sick. But it could.

And the other thing is that the other thing that Iwasaki said, I think it was literally today in The New York Times, I was very impressed with the clarity of her thinking that there may be a post viral response that is actually resembling an auto-immune disease. Now, I'm particularly interested in that because we've published recently that any injury to the heart has the capacity to launch an auto immune response to the heart tissue itself.

And the virologists know all about that because there are certain viruses that aren't very prevalent in the United States but are very prevalent in South America, India, China called Coxsackie I don't know if you ever heard of that virus. But in any case, people who get Coxsackie viral infections, it tends to get in their heart and it tends to give them something called auto-immune myocarditis. And that's basically the auto-immune system attacking your heart just like it attacks your myelin sheath in an MS patient.

So the possibility is that some of these viral infections are producing an over active auto immune response.

Vivien: The fact that a viral infection stays with people who recover from these infections: the symptoms indicate their immune system had stayed in overdrive. This all connects long-COVID because people with long-COVID are saying that they feel better when they have been vaccinated.

Nadia Rosenthal 32.35: Yeah, Coxsackie tends to be,  because I work on the heart, I know a little bit about that one, but there are other viruses that produce auto-immune diseases as well. And so her theory is that the vaccine in long COVID patients may stimulate a kind of counter-response of another part of the immune system, the innate immune system that dampens down these kinds of auto-immune responses, which is why you suddenly feel so much better, because your body isn't attacking itself

So, you know, things like your joints and your sore this and you're feeling like you're just falling apart. You know, all of a sudden what you're doing is you're stimulating another arm of the immune system that comes in and says, ‘knock it off, buster.’ And the trouble is that that is usually a transient response because autoimmunity is a pernicious thing. And indeed, we know that vaccines tend to give transient relief.

So I kind of believe Iwasaki. I think she's brilliant and I don't know anywhere near as much as she does about any of this. So I am fascinated by her thoughts on this, and I'm just passing them on.


For Nadia Rosenthal modeling long-COVID and COVID-19 with more genetically diverse mice is not just about genetics, it’s about the role of the environment too.

Nadia Rosenthal 33.50: Of course, it's not just genetics. The environment is very important, the diet is very important. You know, all sorts of other aspects, you know, stress that screws up your immune system. It goes on and on.

But with mice, we can control many of those things. And that means that we can actually distinguish the basic genetics from some of the, let's say, immune experiences that these mice have had, because it is really an experimental thing

The immune system, it sees the rest of the world. It's your feelers, your molecular feelers for what's out there. I think there's a really enormous amount that we can learn by just having a little more control over each one of those variables so that we can see a little better what's really going on underneath.

Vivien: At The Jackson Lab as in many labs around the world scientists are motivated to make a difference in many aspects of COVID-19 that are still a big puzzle and causing so much suffering. For her and her team, mouse genetics is a way to study COVID and long-COVID.

Nadia Rosenthal 34.55: We're in the middle of a mystery, a really complicated mystery. And many of us don't really know that much about viruses, and many of us don't know that much about immunology. But what we all know about is mouse genetics. And so that's what's holding the whole thing together, is that people are united in their conviction that there is something here to really help the human race, which is genetically very, very diverse. And if we can use these diverse animals to model these different disease states, we might really be able to contribute to breakthroughs and therapies that would be much more precise than they are right now.

Long COVID. But I mean, I can't wait to get those mice aged out and see what happens to them. I mean, I just, I just I wish I could put the clock forward nine months and just see what happens.

Vivien: That was Conversations with Scientists. Today’s episode was with Dr. Nadia Rosenthal, the scientific director of The Jackson Laboratory. And I’d like to give a shout-out thank you to Sarah Laskowski, also at the Jackson Laboratory who set up this conversation.

Just wanted to say, because there’s confusion about these things sometimes, The Jackson Laboratory did not pay to be in this podcast. This is independent journalism, produced by me in my living-room. I’m Vivien Marx. Thanks for listening.

Vivien Marx

Journalist , Nature Portfolio

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