Speaker 1: Pushkin. Hey, it's Jacob. There's another podcast that I host
Speaker 1: called Incubation. It's a show about viruses, and recently we
Speaker 1: did an episode that I thought would be particularly interesting
Speaker 1: to you, to people who listen to What's Your Problem,
Speaker 1: it's about measles. Measles turns out to be way more
Speaker 1: interesting and way more insidious than we thought, but also
Speaker 1: measles may be a new way to fight cancer. I
Speaker 1: hope you liked the episode. I really found it interesting.
Speaker 1: One last thing, we won't be publishing episodes of What's
Speaker 1: Your Problem over the next few weeks. We'll start up
Speaker 1: again in January. I thought I knew what I needed
Speaker 1: to know about what happens when you get measles. You
Speaker 1: get a fever and a rash. Maybe you get very sick.
Speaker 1: If you're really unlucky, you die. But chances are you
Speaker 1: get measles, you get better, and that's the end of
Speaker 1: it as it happens. I was wrong. I did not
Speaker 1: know what I needed to know about measles. Because a
Speaker 1: recent discovery has blown open our whole idea of what
Speaker 1: the measles virus does to our bodies.
Speaker 2: The world thought that measles was done being discovered and
Speaker 2: then boom, all of a sudden, there's this new idea
Speaker 2: of something that really had massive, massive consequences on humans
Speaker 2: that we didn't even realize.
Speaker 1: I'm Jacob Goldstein and this is Incubation, a show about viruses.
Speaker 1: Today on the show how measles attacks your immune system
Speaker 1: and how researchers are trying to use measles to cure cancer.
Speaker 1: My guest for the first half of today show is
Speaker 1: Michael Minna. He's an epidemiologist slash immunologist, slash physician, and
Speaker 1: he's kind of a measles superfan. He did a lot
Speaker 1: of work we'll talk about today while he was a
Speaker 1: professor at Harvard. He's now chief scientific officer at a
Speaker 1: company called emed. We started by talking about a surprising
Speaker 1: thing that happened after the measles vaccine was introduced in
Speaker 1: the nineteen sixties. As more and more kids were vaccinated
Speaker 1: against measles, the rate at which kids were dying of
Speaker 1: infectious disease went down way more than anybody expected. It
Speaker 1: went down so much that it couldn't be explained by
Speaker 1: measles alone.
Speaker 2: After the vaccine was introduced, we saw market reductions in
Speaker 2: childhood mortality overall following the vaccine, which drove a lot
Speaker 2: of questions, why did that happen? Is it the vaccine
Speaker 2: actually acting directly to somehow prevent other infections, or is
Speaker 2: there something else at play?
Speaker 1: Even if zero people died of measles, even if zero
Speaker 1: children died of measles, you wouldn't get that large of
Speaker 1: a reduction immortality. Right, some weird thing is going.
Speaker 2: On, that's exactly right.
Speaker 1: Weird good thing, weird usually.
Speaker 2: That's right, A very weird good thing was going on.
Speaker 1: So now we have this interesting kind of happy mystery
Speaker 1: in a way. Why are so few children dying of
Speaker 1: infectious disease after the rollout of the measles vaccine? What
Speaker 1: do you do to try and figure out what's going on?
Speaker 2: We said, well, maybe it's because measles had detrimental effects
Speaker 2: on somebody's immune memory that might be putting them at
Speaker 2: risk for other stuff, other infections. And so what we
Speaker 2: did was we said, well, if that's the case, then
Speaker 2: if we look at a lot of data, could we
Speaker 2: map the numbers of cases of measles to the numbers
Speaker 2: of deaths from other things besides measles from year to year?
Speaker 2: And what we found was prof boundly predictive. Is if
Speaker 2: you asked what were the number of measles cases in
Speaker 2: nineteen forty nine and what were the numbers of deaths
Speaker 2: from non measles infections from nineteen forty nine, nineteen fifty
Speaker 2: and nineteen fifty one. When you accrued all three years,
Speaker 2: it became extraordinarily predictive of how many children would die
Speaker 2: over the next three years of non measles infectious related deaths.
Speaker 1: So, just to be clear, what you found is that
Speaker 1: when there's a measle's outbreak in one year, the rate
Speaker 1: at which kids died from other infectious diseases went up
Speaker 1: in the next few years.
Speaker 2: That's exactly right.
Speaker 1: So you used in your answer just there this phrase
Speaker 1: that I just want to spend a moment on immune memory.
Speaker 1: What is immune memory?
Speaker 2: Immune memory is very similar to our regular memory. All
Speaker 2: of our body's memories, whether it be muscle memory, brain memory,
Speaker 2: or immune memory, is stored in cells. The way that
Speaker 2: immune memory works is when you bump up against a
Speaker 2: pathogen as let's say, a virus like measles or coronavirus,
Speaker 2: whatever it might be, your body actually sees it, it
Speaker 2: recognizes that virus. It learns from it, and it actually
Speaker 2: remembers it in B cells and T cells and plasma cells.
Speaker 2: And that's how our immune system works in terms of
Speaker 2: developing immune memory and utilizing it to combat infections that
Speaker 2: we see in the future.
Speaker 1: Is what you're finding that in some way measles is
Speaker 1: attacking the kid's immune memory. Is that the hypothesis that follows.
Speaker 2: That's exactly the hypothesis that follows. For example, if a
Speaker 2: six year old got measles, then maybe that measles infection
Speaker 2: could destroy some of the immune memory the defenses that
Speaker 2: that child gained over the last six years, and therefore
Speaker 2: when they are seven or eight years old, are actually
Speaker 2: more vulnerable than they otherwise would have been to those
Speaker 2: infections that they gained the immunity to when they were
Speaker 2: two or three.
Speaker 1: So, okay, you have this hypothesis, how do you test it?
Speaker 1: How do you investigate what's really going on?
Speaker 2: There's a long, rich history of how to predict where
Speaker 2: measles is going to go next. It's actually famous for
Speaker 2: how predictive it is because it is so infectious that
Speaker 2: you just need to know how many people are vaccinated
Speaker 2: in a community, and if there's any measles anywhere in
Speaker 2: the region, you can expect that pretty soon at below
Speaker 2: certain levels, there's going to be an.
Speaker 1: Outbreak below certain levels of vaccination.
Speaker 2: That's right, and that's why measles is considered the canary
Speaker 2: and the coal mine for vaccine rates. It's literally the
Speaker 2: thing that pops up on the radar when you say
Speaker 2: who's what communities are having trouble vaccinating their population, and boom,
Speaker 2: if you see measles, you know they're having trouble vaccinating
Speaker 2: their populations. And so what we can do is we
Speaker 2: can leverage everything we know about measles epidemiology to help
Speaker 2: identify where might outbreaks happen. And that's exactly what Rick
Speaker 2: de Swart and his team did. They are in the Netherlands.
Speaker 2: He's at Erasmus, which is in Rotterdam, and so he
Speaker 2: was able to say, hey, right in our backyard, there's
Speaker 2: a community that, for religious reasons, they chose not to
Speaker 2: vaccinate their children against measles. So they said, well, if
Speaker 2: you're not going to get a vaccine, would you be
Speaker 2: interested or willing to have us just draw a little
Speaker 2: sample of blood from your kids today and should measles
Speaker 2: catch up to them in the future. Could we come
Speaker 2: back and draw another sample of blood.
Speaker 1: You have the before measles blood samples, and you have
Speaker 1: from the same children the after measles blood samples. We
Speaker 1: have everything ready to go. What happens.
Speaker 2: There was a big outbreak, and almost immediately we aren't
Speaker 2: seeing that we can measure all of these antibodies in
Speaker 2: the blood samples. And then when we actually look at
Speaker 2: the blood samples from right before the kids got measles
Speaker 2: to those same kids blood samples that they collected after,
Speaker 2: we saw marked reductions. Not just in a couple antibodies,
Speaker 2: but some kids lost eighty percent of all of the
Speaker 2: diversity of their antibodies that existed in that blood sample
Speaker 2: before they got measles. And we compared it, we said, well,
Speaker 2: maybe that's normal. So we looked at kids who had
Speaker 2: gotten vaccinated for measles. We like the kids who just
Speaker 2: had no infections, And what we saw was the average
Speaker 2: person from any two time points, there'd be like five
Speaker 2: percent difference in their overall antibody repertoire. But the measles kids,
Speaker 2: the kids who got measles lost anywhere from twenty percent
Speaker 2: to eighty percent of their whole immunological memory pool. This
Speaker 2: is the whole lifetime of immune memory that they've spent
Speaker 2: years building up and building up, just poof wiped away
Speaker 2: because of this measles infection and these kids. What that
Speaker 2: means is now, across millions and millions of kids who
Speaker 2: were before the vaccines, almost every child got measles. And
Speaker 2: so at that scale, when you have so many people
Speaker 2: getting measles and this effect happening, which we call immunological amnesia,
Speaker 2: essentially they forgot their body, forgot because of the infection
Speaker 2: the immune memories that they formed before the infection. What
Speaker 2: that means is that you have all of these kids
Speaker 2: that are more susceptible to other infectious diseases. So most
Speaker 2: most kids would survive, but it turned out that of
Speaker 2: those kids who did die from other things, about half
Speaker 2: of those deaths could be attributed to the immune amnesia
Speaker 2: associated with measles.
Speaker 1: Is there something particularly insane if that happens at a
Speaker 1: population level. If you imagine a group of people in
Speaker 1: the absence of a vaccine entirely, where it's like, not
Speaker 1: only is each kid more vulnerable, but because all the
Speaker 1: other kids are more vulnerable, everybody is more vulnerable. Is
Speaker 1: there something like that that happens.
Speaker 2: I am so happy you asked that question.
Speaker 1: You're welcome.
Speaker 2: So, yes, it is. It's a much much harder thing
Speaker 2: to measure.
Speaker 1: I mean, it's sort of like the reverse of herd
Speaker 1: immunity in some weird broad spectrum way, right.
Speaker 2: So what's so interesting that you bring that up? Because
Speaker 2: before my musle's work, I was working on influenza and
Speaker 2: its impacts on other bacterial infections. And during my PhD,
Speaker 2: I coined a term called generalized herd effects, and I
Speaker 2: explicitly didn't call it herd immunity because maybe it's not
Speaker 2: going to reduce things, but maybe you could exacerbate things.
Speaker 1: Yeah, how about herd vulnerability. I want the opposite. What's
Speaker 1: the opposite of herd.
Speaker 2: Immunity, that's herd vulnerability is a great term, and so
Speaker 2: the idea there as well. If you have a pathogen
Speaker 2: that's impacting your susceptibility to a lot of other pathogens,
Speaker 2: you could, you know, create a herd vulnerability because of
Speaker 2: infections of that initial pathogen. And on the contrary, if
Speaker 2: you figure out a vaccine against that initial pathogen, like
Speaker 2: the measles vaccine, you create massive benefits in getting rid
Speaker 2: of that herd vulnerability.
Speaker 1: So what's going on on a cellular level.
Speaker 2: As far as we know, measles is unique in its class.
Speaker 2: It's actually it's an amazing story. So if you give
Speaker 2: me forty seconds to describe it.
Speaker 1: I will, oh go, you got a minute if you
Speaker 1: need it.
Speaker 2: So, every virus has a receptor that it binds to
Speaker 2: and needs to latch onto on a cell. For measles,
Speaker 2: it's this molecule that's called CD one fifty or it's
Speaker 2: called SLAM. SLAM stands for a signaling of Lymphocyte Activation molecule,
Speaker 2: and it's when somebody gets a measles infection. The virus
Speaker 2: comes into somebody's lungs and we have these cool dendritic cells.
Speaker 2: And dendritic cells are like these cells of big arms,
Speaker 2: and they go out and reach pathogens that they that
Speaker 2: they know shouldn't be there, and they capture them and
Speaker 2: bring them in and then they shuttle them into the
Speaker 2: lymphoid system, which is where all of our immune cells are.
Speaker 2: And so normally what would happen is the dendritic cells
Speaker 2: would say, hey, immune system, you know here's a pathogen,
Speaker 2: take it and develop immune memory against it. And so
Speaker 2: it literally hands it off to B cells and T cells.
Speaker 2: In this case, when the dendritic cell does exactly that
Speaker 2: same process, it hands off Measles virus to B cells
Speaker 2: and T cells. And this is a big mistake because
Speaker 2: now you have a virus that, instead of being handed
Speaker 2: off to a B and T cell and having that
Speaker 2: B and T cell you know ingest it and learn
Speaker 2: from it. The Measles flips on it receptor utilization and
Speaker 2: grabs city one point fifty or slam these molecules on
Speaker 2: the outside of the B cells and the T cells
Speaker 2: and it actually invades them like a trojan horse.
Speaker 1: Aha. So it's like a like a trick, right, Like
Speaker 1: Measles is there acting like a normal virus until it
Speaker 1: gets to the B cells in the T cells in
Speaker 1: the immune system. And normally the B cells in the
Speaker 1: T cells would destroy Measles, would destroy the virus. But
Speaker 1: in that case this doesn't happen, right, So what does happen?
Speaker 2: Now It's in the cushy lymphoid system and it's just
Speaker 2: full of food and it just replicates like crazy inside
Speaker 2: the immune system all the while cell by cell destroying
Speaker 2: the valuable immune memory is stored inside each of those
Speaker 2: cells that it's destroying.
Speaker 1: That is very compelling. That it's like a viralogical horror
Speaker 1: movie inside your body.
Speaker 2: It absolutely is. And what we see when we see
Speaker 2: the prototypic measles rash, which is like dots all over
Speaker 2: a child's body, red dots, it is truly the tip
Speaker 2: of the iceberg in terms of where the damage is
Speaker 2: being done. The real damage inside a child is much
Speaker 2: much deeper and much much more profound in terms of
Speaker 2: destroying a huge, huge population of very important cells inside
Speaker 2: of our body.
Speaker 1: So if you sort of step back and think about
Speaker 1: this idea that measles not only gives you measles but
Speaker 1: makes you vulnerable to lots of other infectious diseases, does
Speaker 1: it make you think differently about viruses, about the immune system,
Speaker 1: Like where do you land?
Speaker 2: Measles brings together for me mathematics, biology, ecology and evolution
Speaker 2: and vaccinology, And I love bringing those pieces together. It
Speaker 2: gives you a very deep appreciation for the delicate balance
Speaker 2: we have between infectious diseases, immunity, cancer, and autoimmune disease,
Speaker 2: and how those all interplay with each other. You know,
Speaker 2: the world thought that measles was done being discovered and
Speaker 2: then boom, all of a sudden, there's this new idea
Speaker 2: of something that really had massive, massive consequences on humans
Speaker 2: that we didn't even realize, and so it drives this
Speaker 2: renewed excitement around measles vaccination and the importance of it.
Speaker 2: It's not just a cool finding. It hopefully helps us
Speaker 2: move further and further towards eradication of the virus altogether.
Speaker 1: It was great to talk with you. Thank you so
Speaker 1: much for your time.
Speaker 2: Well, thank you so much. It was a lot of fun.
Speaker 1: Michael Minna is Chief science Officer at EMED Digital Healthcare.
Speaker 1: He was previously a professor at the Harvard School of
Speaker 1: Public Health. When we come back using measles to fight cancer,
Speaker 1: going back all the way to the eighteen hundreds, which
Speaker 1: was before anybody even knew what a virus really was,
Speaker 1: there have been occasional reports of cancer patients who get
Speaker 1: some kind of viral infection and then go into remission
Speaker 1: from cancer. And at a certain level, this makes sense.
Speaker 1: Viruses are highly evolved to enter and destroy cells. Normally
Speaker 1: we think of this as a bad thing, but if
Speaker 1: a virus is entering and destroying cancer cells, this ter
Speaker 1: a cell and destroy it property might be a very
Speaker 1: good thing. By the nineteen fifties, researchers were actively trying
Speaker 1: to figure out how to use viruses to treat cancer.
Speaker 1: But then new kinds of cancer drugs were discovered, basically chemotherapy,
Speaker 1: and researchers got less interested in that virus cancer link.
Speaker 1: My guest for this half of the show is Stephen Russell.
Speaker 1: Stephen has spent his career trying to use viruses to
Speaker 1: cure cancer, and as you'll hear, he and other researchers
Speaker 1: in the field have made real progress. When Stephen was
Speaker 1: starting his career in the nineteen eighties, he was interested
Speaker 1: in using retroviruses as possible cancer treatments. Then he told
Speaker 1: me he turned his attention to measles.
Speaker 3: Yeah, well, measles became the next love.
Speaker 1: You fell in love with measles? Yeah, of course, why
Speaker 1: do you fall in love with measles? Well?
Speaker 3: All viruses are quite beautiful, I have to say, and
Speaker 3: the life cycles are extraordinarily elegant. But measles I could
Speaker 3: do things with. I knew that there was a very
Speaker 3: remarkable case of a boy with a retro orbital Burkitt lymphoma,
Speaker 3: a very aggressive lymphoma that was sort of bulging his
Speaker 3: eye out, and he went to a clinic and was told, well,
Speaker 3: come back in a couple of weeks and we'll start
Speaker 3: the therapy. And he came back in a couple of
Speaker 3: weeks and the tumor had just resolved. But in the
Speaker 3: meantime he'd had a severe measles infection. Huh, And so
Speaker 3: it looked like it was pretty certain that the measles
Speaker 3: infection had driven this response that he had.
Speaker 1: Burko lymphoma also caused by a virus, right, the first
Speaker 1: tumor we knew was caused by a virus.
Speaker 3: Epstein By Yeah, so go on, I apologize. So anyway,
Speaker 3: I looking at measles, it seemed to tick a lot
Speaker 3: of boxes. But there was this whole history of the
Speaker 3: development of a vaccine strain of measles, and measles had
Speaker 3: been the vaccine had been created by taking a virus
Speaker 3: from the throat of a patient with measles. He was
Speaker 3: an eleven year old boy at the time, David Edmonstone
Speaker 3: in nineteen fifty four, and then growing that virus on
Speaker 3: cancer cells in tissue culture, and the virus had required
Speaker 3: the ability to propagate efficiently in cancer cells, but it
Speaker 3: lost the ability to cause measles.
Speaker 1: And wait, I just just to be clear, this was
Speaker 1: just they weren't trying when they were doing this to
Speaker 1: fight cancer. They were just trying to develop a measles vaccine.
Speaker 1: They were just saying, we're going to grow this measles
Speaker 1: in culture over time and make it be attenuator, make
Speaker 1: it be weaker. And it adapted in such a way
Speaker 1: that it preferred to infect tumor cells and not to
Speaker 1: infect non tumor.
Speaker 3: Cells because of the way they adapted it. Because remember
Speaker 3: that the cells that they were growing in the lab
Speaker 3: that they could put the measles virus on were basically
Speaker 3: cancer cells.
Speaker 1: And is that just because those are easy cells to
Speaker 1: grow because they liked to propagate.
Speaker 4: Yeah.
Speaker 3: Yeah, It's very, very difficult to grow non cancerous sects.
Speaker 1: Yeah, it's like the problem with cancer, right, it just
Speaker 1: loves to divide.
Speaker 3: Yeah. Yeah. So they put this virus on on the
Speaker 3: cells in culture, and the virus had actually adapted and
Speaker 3: it had learned to use a receptor that is more
Speaker 3: abundant on cancer cells than on normal cells, and it
Speaker 3: was losing all sorts of things that it needed in
Speaker 3: order to cause disease because it didn't need them to
Speaker 3: be able to propagate the cancer cells. So it spontaneously
Speaker 3: attenuated through a lot of mutations that arose in the
Speaker 3: viral genome. And so there it was and had been
Speaker 3: given to billions of people, and it looked like it
Speaker 3: was fairly well adapted to test in human studies against cancer.
Speaker 1: The measles virus used in the vaccine didn't make people sick,
Speaker 1: and it tended to attack cancer cells. So Stephen started
Speaker 1: using that form of the virus in studies to see
Speaker 1: if measles could treat cancer. Eventually he landed on a
Speaker 1: kind of cancer called multiple myeloma that can take hold
Speaker 1: in the bone marrow and suppress the immune system. And
Speaker 1: there was one multiple myeloma patient in particular who had
Speaker 1: a huge effect on how Stephen thought about using measles
Speaker 1: to fight cancer. The patient's name was Stacy.
Speaker 3: Erholtz, so Stacy. She had multiple myeloma. She had been
Speaker 3: on treatment for ten years, on and off, but probably
Speaker 3: more on than off treatment for the first ten years
Speaker 3: of her diagnosis, because every time she stopped the treatment,
Speaker 3: or even if she continued on it, the disease would
Speaker 3: come back and then she needs switch to something else.
Speaker 3: She had a large tumor on her forehead that was
Speaker 3: destroying the underlying bone and compressing her brain. She had
Speaker 3: four other solid tumors, and then her bone marrow was
Speaker 3: diffusely infiltrated with myeloma and it was moving fast, and
Speaker 3: she was out of treatment and options at the time.
Speaker 3: I mean, there was nothing.
Speaker 1: She was going to die soon.
Speaker 3: She was going to die, yeah, and she had three
Speaker 3: children still at school and everything to play for. She
Speaker 3: was fifty years old at the time. We'd moved up
Speaker 3: through every dose level that FDA had negotiated with us.
Speaker 3: Based on a starting dose level of a million, we'd
Speaker 3: gone up to just tenfold short of a billion.
Speaker 1: Like, how much did she get compared to how much
Speaker 1: somebody gets when they get the measles vaxing.
Speaker 3: It's about ten million doses of vaccine, okay.
Speaker 1: For this one person, So she's getting quite a lot.
Speaker 1: And what happens.
Speaker 3: Well as with other patients, she had a reaction to
Speaker 3: the infusion of virus. So she got the virus infused.
Speaker 3: She felt fine for a couple of hours, and then
Speaker 3: she started shivering and shaking, and her temperature rose and
Speaker 3: she felt pretty unwell overnight, but by the following morning
Speaker 3: it had settled down.
Speaker 1: And is that essentially like a response to a massive infection.
Speaker 1: She's essentially has this massive infection.
Speaker 3: Yes, it's similar to that, although it wasn't causing measles
Speaker 3: in her so it was it was more the body
Speaker 3: reacting to the foreign stuff in the blood and a
Speaker 3: very kind of rapid reaction. That settled down, and then
Speaker 3: she left hospital, went home and after a few days
Speaker 3: she started noticing that the tumor on her forehead she
Speaker 3: and her family had named it Evan, and this tumor Evan,
Speaker 3: started to shrink and actually melted away. And you know,
Speaker 3: we conducted thorough evaluations on her intervals thereafter, and we
Speaker 3: were staggered to see that she went into a complete
Speaker 3: disease remission. She felt fantastic. You know. We thought at
Speaker 3: the time, Okay, we've got it. This is the way
Speaker 3: to cure multiple myeloma, and so we gave it to
Speaker 3: a lot of other multiple myeloma patients and it didn't
Speaker 3: work nearly so well. There was some partial responses, but
Speaker 3: there was really nothing as dramatic as Stacy. So we
Speaker 3: studied Stacy pretty intensively. To try and understand what was
Speaker 3: special about her, because that would be the key to
Speaker 3: the success of virotherapy. I mean, what we knew from
Speaker 3: Stacy as wow, this can actually happen. You can give
Speaker 3: a virus systemically nothing else, and you can get a
Speaker 3: dramatic resolution of tumor at all sites. So the studies
Speaker 3: that we did on Stacy showed that number one, she
Speaker 3: had no anti measles antibody detectable. She had, however, been
Speaker 3: vaccinated as a child, and then she had lost her
Speaker 3: immune and she'd been revaccinated after her first stem cell transplant,
Speaker 3: the immunity had come back, and she'd lost it again
Speaker 3: after the second stem cell transplant. Huh, So she had
Speaker 3: no antibodies to block the virus from getting to the target.
Speaker 1: So basically, her immune system was the same as the
Speaker 1: immune system of a person who has never had measles
Speaker 1: and not been vaccinated for measles.
Speaker 3: Not quite, because we looked at her T cells, the
Speaker 3: cells that come into the tumor and attack the virus
Speaker 3: infected cells, and she had a very high level of
Speaker 3: anti measles T cells.
Speaker 1: As it turned out, this was a perfect combination. Stacy
Speaker 1: didn't have any antibodies, so the measles virus was free
Speaker 1: to go into her body and infect her tumor cells.
Speaker 1: But she did have anti measles T cells, so once
Speaker 1: the measles infected the tumor cells, those T cells could
Speaker 1: attack hack her tumor cells. So now she had both
Speaker 1: the measles virus and her own T cells attacking and
Speaker 1: destroying the tumor. Stephen told me he learned a lot
Speaker 1: from Stacy's case and it helped him figure out how
Speaker 1: to move forward with his research.
Speaker 3: Yeah, so there are two pathways that we took. One
Speaker 3: was to switch to a different virus that people do
Speaker 3: not have prior exposure to, and so we started working
Speaker 3: with the sicular stomatitis virus VSV, which causes naturally a
Speaker 3: blistering illness in cattle.
Speaker 1: Uh huh. So that's that's one way to get around
Speaker 1: the immunity to measles problem. Right, You're you're using a
Speaker 1: virus that most people don't get and are therefore not
Speaker 1: immune to. How is that going?
Speaker 3: It's going. It's going well. Where you know, it's not
Speaker 3: in every cancer that we see anything, but the results
Speaker 3: that we have at the moment are looking very promising
Speaker 3: in certain indications. The other approach we took was to
Speaker 3: stealth measles virus so that it would still be measles virus.
Speaker 3: It would still be that vaccine strain, but it would
Speaker 3: have a new coat, huh, that was no longer recognizable
Speaker 3: by circulating antibodies, And so we would in that situation,
Speaker 3: we would have a virus we could give systemically that
Speaker 3: would penetrate the tumor, and that would then be subject
Speaker 3: to attack by these t cells that exist in people
Speaker 3: who've been measles immunized.
Speaker 1: Well, does it work in mice? Okay, it's a start.
Speaker 3: We haven't taken that one into human clinical tests yet.
Speaker 1: Let's talk for a minute about using viruses to treat
Speaker 1: cancer more broadly. Right, people have been trying other viruses
Speaker 1: to treat other cancers. What's the state of the field
Speaker 1: more generally?
Speaker 3: There has been incremental progress, and there are viruses that
Speaker 3: are looking very promising in brain cancer injected into the
Speaker 3: brain tumor, in bladder cancer instilled into the bladder, and
Speaker 3: I think many ongoing programs which show great promise. So
Speaker 3: I'm still a complete believer in the capability of viruses
Speaker 3: to really bring a transformation in the approach to cancer therapy.
Speaker 3: I feel like it's coming soon, but not everybody agrees
Speaker 3: with me.
Speaker 1: I appreciate your time so much. It was great to
Speaker 1: talk with you.
Speaker 3: Great talking with you too. Thank you very much.
Speaker 1: Stephen Russell founded the Department of Molecular Medicine at the
Speaker 1: Mayo Clinic. He is currently the CEO of Viria, a
Speaker 1: company that is trying to use viruses to treat cancer.
Speaker 1: One last thing, Stephen told me that he's still in
Speaker 1: touch with Stacy Airholtz, the patient who had multiple myeloma
Speaker 1: and went into complete remission after being treated with measles.
Speaker 3: Stacy Holtz is, you know, a guiding light for me.
Speaker 3: I'm friends with her, I'm in contact with her on
Speaker 3: a regular basis, and she's got grandkids. She's having a
Speaker 3: happy life. She's a very positive woman.
Speaker 1: Thanks to both of our guests today, Michael Minna and
Speaker 1: Stephen Russell. Next week on the show, I talked to
Speaker 1: a scientist who discovered an entirely new kind of virus,
Speaker 1: and it turns out this virus is everywhere.
Speaker 4: Boiling Springs Lake, deep Sea Sediment's Korean air sample, monkey feces,
Speaker 4: dragonfly guts, soil just outside the lab at Portland State University.
Speaker 4: Basically anywhere that we have looked, we found these cruci viruses.
Speaker 1: Incubation is a co production of Pushkin Industries and Ruby
Speaker 1: Studio at iHeartMedia. It's produced by Kate Furby and Brittany Cronin.
Speaker 1: The show is edited by Lacey Roberts. It's mastered by
Speaker 1: Sarah Bruguer, fact checking by Joseph Friedman. Our executive producers
Speaker 1: are Lacey Roberts and Matt Romano. I'm Jacob Goldstein. Thanks
Speaker 1: for listening.