Quirks and Quarks - New dino species in another dino's vomit, and more

Episode Date: January 9, 2026

An unassuming fossilized slab in the basement of a museum in Brazil turned out to be 110-million-year-old dinosaur vomit, and inside that vomit were the bones of two strange, seagull-sized pterosaurs.PLUS:Loss of fresh groundwater is now the leading driver of sea level riseHow doubting your self-doubt makes you doubt lessA huge black hole in a peculiar galaxy may date from the universe’s earliest moments Shining a light on where viruses hide out in our bodies, and how they make us sick

I am an actor, fresh out of theater school with big dreams and an even bigger drug habit. But things are pretty good. That is until my best friend is set up on a date with David Lee Roth. Yeah, from Van Halen. If you know, you know. From CBC's personally, this is Discount Dave and the Fix. The true-ish story about how a fake rock star led me to a real trial that held up a mirror to me. And okay, let's just say that not everyone in this story is who you think they are.

Personally, discount Dave and the Fix. Available now on CBC Listen or wherever you get your podcasts. This is a CBC podcast. Hi, I'm Bob McDonald. Welcome to Quarks and Quarks. On this week's show, a black hole from the dawn of time. This really brings the possibility that you don't form this black hole from stars. The black hole has been there way before any Star formation can happen.

And why confidence? in your goals could use some double negative doubt. You would think it'd be additive. That is doubt plus doubt equals more doubt. But in fact, what you show is the reverse. Doubt plus doubt equals less doubt. Plus, dwindling groundwater rises sea levels, discovering dynos in dino puke,

and shedding light on stealthy viruses. All this today on Quarks and Quarks. Our world is facing an increasingly dangerous water shortage. In some places like Iran, for example, the lack of available fresh water has reached crisis proportions. Iran's capital is counting down to day zero, the day the water runs out and the taps run dry. Reservoirs that supply Tehran's 15 million residents are almost empty. This is the Karaj Dam, which supplies a quarter of the city's drinking water, now just 8% full. The president has warned that people may even have to evacuate and water rationing has begun in some areas.

What's happening in Iran's capital, Tehran, is a stark example of how fragile our supply of fresh water really is. Now, it might seem like our planet has lots of water. After all, oceans cover almost three quarters of the Earth's surface. But the water we drink or use for growing crops is in short supply. In fact, we're losing fresh groundwater in some of the world's most populated regions at unprecedented rates. The situations become so extreme that now the loss of groundwater is the leading contributor to sea level rise. This is what scientists found after analyzing more than 20 years of satellite data from NASA's gravity recovery and climate experiment, or grace. Dr. James Famlietti is one of the scientists behind this research. He's a global futures professor in the School of Sustainability at Arizona State University. Dr. Famolietti, welcome to Quarks and Quarks.

Thanks very much for having me. Now, before we get into your study, just describe how our fresh groundwater has been typically replenished in the past. We rely a lot, of course, on the workings of the water cycle. So we've got precipitation, we've got evaporation, we've got runoff, just like we learn about when we're in elementary school. And the excess of that precipitation, that, that's, you know, that. that which does an evaporator doesn't run off, can infiltrate into the ground.

And that infiltration is what fuels are groundwater supply. Think about geologic time in hundreds of thousands and millions of years. You can really build up a lot of water. And so that's where our groundwater comes from. And sadly, what we're seeing around the world is that we're burning through that supply of groundwater that took hundreds of thousands and millions of years to accumulate. We're burning through it in just about a century. Wow. Well, how has this been changing in the last several decades?

So what we've been seeing regionally and globally is a very rapid disappearance of groundwater from the world's major aquifers in the places where I have lived in California and Arizona. I lived in Saskatchewan. It's happening there. It's happening across Canada. It's happening in the world's major aquifers. There's really no place. places in those mid-latitude regions where groundwater supplies are on the rise. They are uniformly decreasing. And what's the major cause of that? There's a lot of reasons for the disappearance of groundwater by and large, I think the biggest one is the human use, and especially for agriculture. Agriculture uses something like 80% of the water that we withdraw from groundwater

and from surface water reservoirs and rivers. So that's number one. But the other cause gets back to this lack of understanding, the out of sight, out of mind, the invisibility of groundwater, which has allowed it to go unprotected. So it allows for that overuse. It allows for that over-exploitation. So those two things need to be.

need to be addressed. So how quickly is our terrestrial groundwater supply drying up? You know, it really varies. But let's just say in a global level, there's so much groundwater loss. That groundwater loss actually ends up accumulating in the ocean. It's now bigger, a bigger contributor to sea level rise than either of the ice sheets, either the Greenland or the Antarctic ice sheet. The other thing I think of note that we found in the research paper,

is that the areas that are being subjected to this over-exploitation, and this we call this continental drying in the paper, in the peer-reviewed paper that we wrote, those areas that are drying are increasing at twice the area of the state of California each year. And we sort of reached a tipping point. Actually, around 2014, things really, there was a huge El Niño. It seems like the nature of the water cycle changed. we had got a lot more extremes in particular droughts.

And at that point, things really started to decline a little bit rapidly, started to more rapidly, so started to accelerate. And then I guess at that point we realized, okay, yeah, it's going to really exceed the contributions of the ice sheets to sea level rise. What about climate change in global warming? How does that factor into this? Climate change is making a difficult situation even worse. Let's take the southwestern North America region, for example.

This is a region that is getting less precipitation. It's getting less precipitation as snow, which is an important source of water in the regions that are fed by mountains. Temperatures are increasing, so evaporation is increasing. So in short, more water, you know, less is coming in, more is going out surface water, less opportunities to recharge their groundwater. And then because the surface water is disappearing, there's a greater reliance on groundwater. This is happening all over the world.

Wow. It sounds something like a bank account. You've got to watch what's going in and what's coming out. And if you're spending too much, you're going to run out. Yeah, that's really a great analogy. We use it all the time. And I like to say that groundwater is like our retirement account. And we really, you know, it took a long, long time to accumulate.

and we should be paying more attention to sustaining it and to sustaining it for future generations. So what are the implications here? If this depletion continues, what impact can we expect it to have on people's lives or even whole countries? Well, I think one of the things that has not really been fully appreciated is that groundwater is really the lifeblood of the world's drylands, the arid and semi-arid regions of the world. And these are the places where people like to live and where we grow all of our food and where there's great desire for economic expansion. So, and that's true where I live right now. Phoenix says they're tremendous, you know, it's very much a pro-growth mentality, but in the context of shrinking freshwater availability. I think that it means that we have to be very careful with the freshwater that we have available to us. It needs to be protected where it's not being protected.

because if it's not, and it continues to decline, then food prices will increase. Our economic growth will be threatened. We need water. We need water to produce energy. We need water to sustain our industries besides just agriculture. So we just need to be extremely careful because it's just not, you know, that era of abundance or the myth of abundance, I think it has been busted. So is there anything countries can do?

to rein in this freshwater loss and reverse the trend? I think understanding and awareness are the key, and that's it at all levels. It's the general population. It's the, I like to think of the practitioners and our water managers or sort of the mid-level and our elected officials in our state, provincial, and national leaders. I think they really need to understand the importance of freshwater, the importance of the particular groundwater. So that's one thing.

If they understand it, then they will understand the need for protecting those resources. And so that's the other side of the coin. Once we understand it, we need to take action in, put the policies in place across Canada, part of the Canada Water Act. There should be more groundwater protection, for example. Dr. Family Eddie, thank you so much for your time. Thanks so much for having me. Dr. James Familyetti is a professor in the School of Sustainability at Aeribaldi.

Arizona State University in Tempe, Arizona. Well, it's that time of year when many of us make resolutions to be the best version of ourselves. Maybe you want to eat better, drink less, or exercise more to become healthier overall. But sticking to long-term goals like this can be extremely challenging. Dr. Patrick Carroll at Ohio State University wanted to find out why. He began to investigate how much confidence is required to actually achieve your goals. Since having doubts can stop you from reaching them, he wondered what could stop self-doubt.

And the surprising answer is, more doubt. Dr. Carroll is a professor of psychology at Ohio State University at Lima. Hello, and welcome to Quarks and Quarks. Hi, Bob. First of all, what were you hoping to look at in your study? Well, in my previous research, as you mentioned, I had shown that doubt really kills commitment to goals. And so I began asking the question of what might kill doubt.

I came across some interesting research that was done at Ohio State University where you can have doubt at two levels. You can kind of think about it as a self-attribute. And that's just a plain thought, no different from I like ice cream. But like all thoughts, you can hold. them with either confidence or doubt. So it's ironic that doubt can apply to anything, including doubt itself. You mentioned that there's two kinds of doubt. Yes. Now, the first one I understand, okay, I'm not sure I can do this, whatever's before me, but what's the second time? It's called

metacognitive doubt. And you can think about cognition as a thought. Like, I have doubts about this goal. But we can vary in just how sure or unsure we are of those thoughts. And that has big implications for whether we use those thoughts or not. So metacognitive doubt is a subjective sense of certainty or uncertainty of the thought that you're holding. When you talk about goals in your study, what goals did you focus on? Your most important personal goal. So we left it up to them to decide what goal to think of. For the most part, I think that those are the ones that really guide us over the long term. So like, what, I want to be an astronaut one day? Exactly. And those are the types of goals that do come out is I want to become a doctor,

I want to become an astronaut, you know, butcher baker candlestick maker. Okay. Or in In other words, to be a better version of ourselves or a healthier version of ourselves. Exactly. Well, how did you go about studying this? Well, I did two studies. The first study was with an online sample. So all ages, all ethnicities, you know, different walks of life, the political spectrum. And we had them fill out a scale designed to measure their doubts in their most,

most personally important goal. We then asked them to think about a time when they had experienced doubt or confidence in their thinking. And then we just simply asked them to rate their commitment to their most important personal goal. And what we found was consistently the same thing. Those who had higher goal doubts and had thought about a time that they were confident, they were, less committed to their goal. But for those who had doubts and wrote about a time when they felt doubtful, they actually showed higher commitment to their goals. Wow. So it's really an ironic effect. Yeah, it is. You would think that if you're thinking about your doubts, you'd reinforce them. But you're saying that doubting your doubt actually reduces the doubt. It's like a double negative here.

Exactly. It has shown you would think it'd be additive. That is doubt plus doubt equals more doubt. But in fact, what you show is the reverse. It's non-additive. So doubt plus doubt equals less doubt. Wow. So what was the second part of your study? Second part of the study, we took a student sample because presumably they're at a point in their life where they're thinking about those, you know, personally important goals. And, And we asked them to fill out the scale measuring their gold doubts. But this time, what we did to manipulate metacognitive doubt is we drew from prior research suggesting you can do it by getting people to write their thoughts with their non-dominate hand. And it's a line of work called embodiment research. essentially people use their own bodily movements as cues to infer the validity of the thoughts they have in mind. So they take their shaky handwriting with their non-dominant hand as a cue, that their thoughts, that is the doubts they're writing out, must be invalid. And thereby they hold them with less confidence or more doubt.

And what did you find when you looked at their confidence? So we took a measure of commitment to the goals at the very end. And we showed that whereas confidence in their doubts went down, commitment to their goals went up. And so they're holding less confidence in their own doubts. And these are the people that wrote with their non-dominant hand. So their handwriting was terrible when they looked at. looked at it, and their confidence went up. Yeah.

Well, how powerful a tool do you think inducing doubts into your doubts can be in helping us achieve our goals? Well, I think it can be pretty powerful. You know, it's a simple technique. Parents, counselors, peers, friends can, you know, do this in others and get, you know, these ironic effects, greater commitment under conditions of initial doubt. Is there anything that we can do at home to apply this principle? It's kind of a hotly debated topic whether you can do it to yourself.

But, you know, write out your doubts with your non-dominate hand and, you know, kind of see how it feels. Or if you know someone who doubts whether they can achieve their goals, like a parent, knows their kid has doubts about whether they can achieve their goals. If you just tell them, just write this out with your non-dominant hand or shake your head while you're writing it out as if to say no. We use that cue as well to indicate that our thoughts aren't valid. I think you could have some pretty big effects. And it's not like it costs any money to do. So if you don't believe you can get something done, look at the reasons why you believe.

that and doubt that. Yeah. Dr. Carroll, thank you so much for your time. Well, thank you, Bob. I appreciate it. Dr. Patrick Carroll is a professor of psychology at Ohio State University at Lima. When paleontologists are working to piece together the ancient past, sometimes clues pop up in the most unexpected places. Like in a strange, ugly, lumpy fossil slab that sat largely ignored. in a museum in Brazil for decades. When scientists finally took a closer look at it, they realized this ugly, lumpy slab was actually dinosaur vomit

from 110 million years ago. And inside that vomit were the chewed-up remains of a previously unknown species of pterosaur. The discovery was made by Dr. Alini Galardi and her colleagues. She's a professor of paleontology at the Federal University of Rio Grande du Norte in Brazil. Hello and welcome to our program.

Hi, Bob. Thank you for inviting me. It's a pleasure to be with you. Well, first of all, tell me about this strange slab of fossilized vomit. Just, what's it look like? Well, it looks ugly. That's why it spends so much time in a museum drawer. Early, it was identified at very strange pieces of fishes that were unidentified for almost four decades. Well, how did you figure out that it was identified? was actually vomit. Well, that's not easy, in fact.

Basically, we combined a different line of evidences. Most of all, they were different animals all slumped together. So the pieces of pterosaur school with four fishes all aligned, that gave us the best clue that could be a vomit. Then, of course, to conclude, we compared, we uttered. We utter fossil vomit that we call in paleontology regurgitalite, and also with recent vomit or regurgitates, and we could finally put all the pieces together,

and our best hypothesis to explain this combination of strange features is that we have regurgitalite. So it really does look like something that some big animal just spewed out its stomach onto the ground. Exactly. And also it's a huge mass. of pieces of bone. So something big chewed on that.

And, well, we know the rest of the story. After that, it got vomited. Well, how is vomit preserved so well for 110 million years? Usually anything that I've spewed on the ground doesn't stay there very long. Oh, that's a very good question. In the case of the vomit, well, to protect horosophagus when the regurgitated material is coming out, our body produces a type of mucus that can hold those mass of digested, partially digested food together.

So that holds the vomit together in the environment. So what we had in the time of dinosaurs was a huge, calm, alkaline lagoon, full of calcium dissolved in the water that rapidly precipitated over the mucus involving the fossil vomit. Wow. So the mucus held it together, and then it was spewed into a lake or in water,

and then the water sealed it up. Yeah. In fact, not in the water, but in the margins of the lagoons. So you need very specific characteristics to preserve it regurgitalite. That's why they are so rare in the fossil record. Well, take me through more detail

of what you saw in this vomit when you looked at it more closely. Okay, it's important to say that, first of all, we didn't know it was a vomit. We had this strange mass of bones, and one particular was very strange. I got the opportunity a few weeks earlier to read a paper on a filtration therathing therosaur, a strange filtration therosaur from Argentina, which has a strange combination of features in its beak, which is hairy-like thief that it uses to filtrate microorganisms and water. So the structure that I saw in the regard to the light fossil were very similar.

So I took the fossil to two colleagues that are specialized in the study of pterosaurus, and they took a closer look at the material and said we had something very similar. So that strange mass of bones was a thermos. A furtrating therosaur, very closely related to Tidalstrou from Argentina. So you say it had hair-like teeth? What did they look like? They are very long and they are used pretty much as baleen in Wales to infiltrate plankton. Our terrosaur had very similar structures, not the same as the whales, of course. something in between what whales have and flamingos have

as a type of comb that holds the microorganims together. Wow. How big was this pterosaur? Not very big, Bob. So probably the size of a seagull. So if it was the size of a seagull, what kind of animal would have eaten it in the first place before it threw up? That's a very good question. We cannot know for sure, but we have a best guess. So our best clue is that in our regurgatolite, we, besides the pterosaur bones, we also have four fishes to preserve together,

which indicate that the predator ate boat, possibly the pterosaurs before the fishes, because of the way they are preserved. So, okay, we have an animal that ate fish and also pterosur. Possibly our best guess is that spinosaurian dinosaurs are involved. So we know that ecologically, from different line of evidence, that spinosaurids commonly ate fish, but we have this extraordinary evidence that was also found in the area of the basing, that they, well, at least sometimes ate also pterosaurs. Well, this terosaur that you found in the vomit that has these unusual teeth that allowed it to sort of filter,

feed the water. How does that compare to other terosaurs that were around at that time? Before this discovery, we only had evidence of future feeding terosaurs from Southern South America, from Europe, and from Eastern Asia. So it's filling a gap in the middle of the geographic distribution of this type of animal. So you can imagine this huge calm lagoon full of

well, abundant aquatic life, those large dinosaurs such as pinoceros eating fishes and terros are available, and a plenty of diversity of terrosaurus flying around, some of them with more than 10 meters in wingspan, such as, for example, Mahadactylus, and others as small as a seagull, such as Bakiribu, this new future-finding terrosaur. So are you going to start looking more close? at other ugly fossils that might be out there? Definitely.

I think that's one of the best lessons of this discovery. You could have right there in a museum drawer, an ugly fossil that you can realize it's an incredible discovery. Dr. Gilardi, thank you so much for your time. Thank you, Bob. It was a pleasure talking to you. Dr. Alini Galardi is a professor of geology at the Federal University of Rio Grande du Norte in Brazil.

I'm Bob McDonald, and you're listening to Quarks and Quarks on CBC Radio One and streaming live on the CBC News app. Just go to the local tab and press play wherever you are. Coming up later in the program, uncovering where in the body some particularly destructive viruses lurk in waiting. We refer to these regions in our DNA as these silent areas, kind of like these quiet back alleys that nobody likes to go down. I am an actor. Fresh out of theater school with big dreams and an even bigger drug habit. But things are pretty good. That is until my best friend is set up on a date with David Lee Roth.

Yeah, from Van Halen. If you know, you know. From CBC's personally, this is Discount Dave and the Fix. The true-ish story about how a fake rock star led me to a real trial that held up a mirror to me. And okay, let's just say that not everyone in this story is who you think they are. Personally, discount Dave and the Fix. Available now on CBC Listen or wherever you get your podcasts. There's a cosmic monster lurking near the edge of our early universe.

It's an unexpectedly strange galaxy with a monstrous black hole that formed 13 billion years ago. Now, most black holes form when a star collapses at the end of its life, leaving an invisible hole where gravity is so extreme that light or just about anything else cannot escape from it. But not every black hole is necessarily the result of a collapsing star. Back in the 1960s, theorists suggested that black holes could also have been created in the very early universe, shortly after the Big Bang. These ancient objects are called primordial black holes. The problem is, there's never been any proof that primordial black holes exist. But now tantalizing observations of this distant galaxy made with the James Webb Space Telescope,

along with some computer simulations, suggest that these ancient black holes may really be out there in the universe. Dr. Boyan Liu is a postdoctoral researcher at the Center for Astronomy at Heidelberg University in Germany and is one of the authors of this study. Dr. Liu, welcome to Quirks and Quarks. Hello, everyone. I'm really happy to be here and to share my research. Well, first of all, tell me about this 13 billion-year-old galaxy

and what you saw with the James Webb Space Telescope. Yeah, this galaxy is really special because we see a very massive, very large black hole, and the mass is around 50 million solar masses, and it's similar to the size of the black hole we have in the center of the meteor way. Wow. Yeah, yeah. But with such a massive black hole, we basically have no evidence for the existence of stars in this system. And also, we don't see any heavy elements or a protein.

docks that are, you know, the results of any stars. That's why this object is really special. What made you suspect it might be a primordial black hole? Because if you form a black hole from stars, you can't form a two massive black hole because the stars, they have their own limits, right? You can't grow a two massive star, which means that the initial mass of a black hole will be much smaller than what we see in this galaxy. So this black hole, if it forms from a star, it has to grow to be what we see.

But then it is very likely that when you grow this black hole, you will form some stars around this black hole. And the stars will evolve and produce some elements from inside the stars. And we should see these stars and also the elements produced. But for this object, we didn't see any. And then this really brings the possibility that you don't form this black hole from. stars, the black hole has been there way before any star formation can happen. Well, take me through that scenario then. How do these primordial black holes actually form? The basic theory is that we have some density fluctuations in the early universe from quantum

fluctuations at the very beginning. And then when you have some dense regions, when they can interact with gravity, these regions will collapse. And if the over density is high enough, you can form black holes. Okay, so you're talking about the very, very early universe right at the Big Bang when it's super dense and super hot. Yeah, yeah. And there are some areas, it's not sort of smooth everywhere. There are some spots that are a little denser than others, and that's what gives you these black holes. Yes, exactly.

So did it start out massive like it is now, 50 million, or did it grow? There are different scenarios. It can be that you form these black holes already very massive as what we see and later on they don't grow much. But you can also start with something smaller and they grow by just engulfing matter around them. Or you form a small cluster of multiple premodial black holes and they can merge to form a larger black hole later on. And our study doesn't really distinguish these different scenarios. just assume you have some massive premodal black hole early on. Oh, I see. So it could have been born big or it could have grown with a bunch of smaller black holes getting together.

Yes, yes. How does this particular black hole, this giant, fit into what we know about other black holes that existed back at that time, 13 billion years ago? Yeah, that's a good question. So speaking of the mass of this black hole, it does not stand out a lot. We do see similar mass, the black holes with similar masses at this age of the universe. And they are really hosted inside galaxies. So we do see stars as well in those systems. And they are like more normal or like not so interesting.

What really makes this object different is that we almost don't see stars. And we don't also we don't see elements produced by stars. So these elements are, we call them, There are elements heavier than helium. And if you compare the chemical composition of this object with the Milky Way or with the sun, the amount of heavy elements in this system is less than 1% of that of the sun. And if you look at other galaxies with similar black holes, we usually see much more heavy elements than what we see from this object.

Well, do you think there are a lot of primordial black holes out there? there? From theory, indeed, you can form a lot of primordial black holes. And from this one observation, it's hard to tell because it's only one object. It's very difficult to estimate the, say, the number density of such things. What fraction of galaxies will be in this particular phase, because it's a really small number, only one object. But from theory, it is possible to have a broad range of abundance of these primordial black holes. It really depends on what kind of density fluctuations you have in the early universe. That's from the theoretical perspective.

And then another interesting thing is you can maybe see the effects of these primitive black holes if they exist from other observations, not like just one galaxy because these black holes, they can produce radiation and they can heat up the gas overall in the universe, and those effects will have some other observable signatures as well. So if there were a lot of these primordial black holes back then in the early universe, would that help to explain the mystery of dark matter? I mean, could they have contributed to that factor in the evolution of the universe?

Yes, we almost know for sure that for these massive remote black holes, It is very difficult for them to explain all dark matter, because if you make all dark matter, these massive primordial black holes, they're going to mess up a lot of observations. So too many black holes, they do too many things, and they are not consistent with observations. But it's likely that when you form these premodular black holes,

they have a mass distribution. They are not always the same mass. You have bigger ones and smaller ones, and in some series you can have many smaller ones, with like close to the mass of the sun, and they explain all dark matter, and then you have a tail of the distribution. You also have some massive ones that are not too many, but maybe enough to explain what we see in this object.

Boy. Dr. Liu, thank you so much for your time. Thank you. Thank you. Dr. Boyan Liu is a postdoctoral researcher at the Center for Astronomy at Heidelberg University. Viruses can be sneaky little invaders. They can't reproduce. on their own, so their survival depends on infecting hosts by hijacking their cells to make copies of themselves. And once they get in, they can be hard to get out. At any given time, there are around

300 to 400 trillion viruses throughout the average human body. Most are benign, and some are even beneficial. But other particularly crafty and menacing viruses play hide and seek with our immune systems. Some hide out in our bodies and wreak havoc, like the SARS-CoV-2 virus has been found to do in many cases of long COVID. Others lay dormant for years, just waiting for the right moment and circumstance to spring back into action and make us sick. Like the recent discovery that a virus that's present in almost every adult could be behind the autoimmune disease, Lupus. Here's Dr. Bill Robinson, the scientist behind that study. is at the heart and center of the mechanism that causes lupus in our opinion. And we think that this

is just a foundational fundamental discovery. We'll hear more from him in a moment. But first, HIV. Its capacity to hide in the body is one of the reasons it is notoriously difficult to treat. Because it doesn't just hide out in the body. It hides in the DNA of infected cells. Well, now, scientists have a much better idea of how HIV does that and where it goes in the DNA when it's hiding. Dr. Stephen Barr is a virologist from Western University in London, Ontario, who oversaw the study. Hello and welcome back to Quirks and Quarks. Hi, thanks for having me. Now, before your study, what did we know about how HIV hides in the body? Well, one of the things that we did know is that the virus itself can insert itself into our own DNA.

And when it does this, it usually has two major options. The first option is really entering into these regions of our DNA that we refer to as very active. You can think of them as busy neighborhoods, lots of energy, lots going on. They're producing lots of proteins that help our cells really survive and replicate. And so when virus likes HIV enters into these regions, they love this environment. so they can produce lots of copies of itself, infect other parts of the body, and eventually spread person to person. So that's the first option. The second option is that it wants to hide out because it wants to hide from our immune system.

And we refer to these regions in our DNA as these silent areas, kind of like these quiet back alleys that nobody likes to go down. And when HIV gets into these areas, they basically. basically go to sleep. And so they can hide out. They don't have to produce a virus. So the immune system can't find them. And what happens is they stay asleep for decades until something reawakens them later on. And that's when they restart their infection and cause disease. Well, what does that mean in terms of how to treat the virus? Well, it makes it very difficult. If I go back maybe in time a little bit to the early 80s when HIV AIDS started spreading in populations around. the world. It was really a, you know, a time of fear and stigma for many people. And for about 10

years or so, researchers were trying to really understand the virus and how to stop it. They had some success with the development of early forms of antiretroviral drugs, but they soon learned that the virus was really adapting in the body and becoming resistant to these drugs. And so when the virus is actively replicating, that's when they're most prone to these drugs. And the ones, the viruses that are asleep in the cells, they aren't affected by the drugs because they're not reproducing. They're not replicating. And so they can escape the effects of these drugs and our immune system, which is designed to seek out and destroy cells that are producing virus. So the virus that stays asleep can do that indefinitely because there's nobody looking for them. And I understand that's one of

the reasons why HIV can spread so widely worldwide is because people can be infected and not know it. Exactly. Exactly. Yeah. What kind of cells does HIV typically infect? So they typically infect the immune cells that are designed to really kill itself. So it infect cells such as T cells, which are really designed to seek out and destroy cells that are infected with HIV. So by infecting these cells, they can deplete them so that they're not around, and the virus can just go on happy as can be without any threat. So how did you go about tracking down these dark alleys where the HIV is hiding in our DNA? Around, I guess, the early 1990s, a group of people were living with HIV in Alberta.

decided to do what they could do to help researchers understand the virus and the disease. And what they did was they decided to donate punch biopsies from multiple different organs in the body, such as the colon, intestines, stomach, esophagus. Some also donated their brains to research after they had passed. And this happened for multiple years, and they would take these punch biopsies all at the same time. So you can imagine how uncomfortable that would be for these. individuals. And for me, that's, you know, a very brave and, you know, an act that's had huge foresight that would really help researchers such as ourselves, you know, some 35 years later.

Well, that's astounding that these people did that because punch biopsies, that's where you actually take a sample. Like you take pieces of tissue out, right? It's like an extraction. Absolutely. And they did this for multiple years. So there's such a valuable group of samples because they froze the virus in time. So at an early point in time, before the virus has learned to survive in our bodies and really understanding the virus and how it changes over time

is, in our opinion, a very important way to identify new targets and learn how the virus adapts and changes to our treatments in our body. So what did you find when you looked at the DNA of these samples from the 80s? What we found was that, that indeed, each tissue has a very unique entry point into our genomes that the virus likes to use.

In most tissues in the body, like the blood or the gut, HIV usually tucks itself into those active parts of our DNA, those happy neighborhoods. And in the brain, the virus predominantly wants to target those quiet back alleys. So they would get into the brain and be very silent so that they don't attract a tank. and from the immune system, and they could survive there for many, many years. And so that was a really interesting finding that we found is that it differed so much from the rest of the body. And when we took a closer look at the mechanism of how the virus actually chooses those specific sites in our genome, we found a very interesting feature of the DNA called non-B DNA.

What's that? So if you think of DNA as this two-stranded double-dial. helix that everyone envisions when they look at DNA, it's far more complex than that. The DNA can breathe. So those two strands can open and close in order to be able to express the genes and all the proteins that our cells need. And when the DNA breathes and opens up, it forms these unique structures called non-B DNA structures. When it opens up, it can form, it twists and loops. folds into these unusual shapes that we sort of think about as little bumps or knots on the DNA. So if you think of Braille as being bumps that change how your fingertips read the line of text,

non-BDNA can be bumps on the DNA that things like HIV can read and find those specific bumps that they like to bind to, grab hold of, and insert into our DNA. So we found that these non-B structures differ in the different tissues, and that's what gives it the unique ability to target these sites. Well, now that you've finished the game of hide-and-seek with HIV, it found its hiding place. What does that mean for future treatments? Well, what we are looking at specifically is really to better understand the mechanism of how it does that.

So if we compare our data from this earlier form of HIV, to the HIV that's present now, we can really identify parts of the virus that have changed over time. And if we can identify those parts, we can then tailor some drugs that will target those regions and hopefully prevent the virus from finding these particular bumps on the DNA. So if we can really get to the bottom of that mechanism, we really hope that we can develop drugs that will supplement, you know, other therapies, that exist today to really push in the community towards a cure. And so we are hopeful that our research will advance later on to that stage.

You want to flush it out of hiding so you can target it. Exactly. Exactly. So once it's out of that hiding place, the immune system is ready to jump all over it. So it's just trying to trick it into awakening up when we wanted to. Dr. Barr, thank you so much for your time. Thanks for having me. Dr. Stephen Barr is an associate professor of virology at Western University.

Now, another virus that can get into ourselves and lay dormant for decades is the Epstein-Barr virus. EBV, as it's known, is one of the most common viruses in the world. 95% of all adults carry it. Most people catch it when they're younger. It's spread in saliva, and while it causes mild or no symptoms in some people, In others, it can cause mononucleosis, more famously known as the kissing disease. That can lead to profound fatigue, sometimes for months. Once infected, Epstein-Barr mostly just lurks in our body, hanging out, not doing much of anything.

It was only in the last little while that scientists started linking it to diseases that develop later on, like rheumatoid arthritis, some cancers, Crohn's disease, and multiple sclerosis. otherwise known as MS. It was this link to MS that led a team of researchers at Stanford University to investigate whether EBV is connected to the emergence of another autoimmune disease, lupus. And they found that up to 100% of lupus cases could be caused by this virus. Dr. Bill Robinson is the professor of immunology and rheumatology at Stanford University who ran the study. Hello and welcome to our program. Hello.

First of all, explain the Epstein-Barr virus. How is it so common? Epstein-Barr virus, or EBV, is a virus that infects approximately 95% of us over the course of our lives. It hides out in B cells and epithelial cells, and it's transmitted via saliva. So if you're a child and you share a spoon or a bowl or a cup with your brother or sister, it's transmitted that way. And obviously, as you highlighted, it's also the kissing virus, meaning teenagers who haven't yet been infected, frequently get infected by kissing. Now, you say it hides in B cells. What are they? B cells are the immune cells that produce antibodies. Antibodies normally protect you against viruses like influenza or COVID or bacteria.

But in autoimmune diseases, B cells can make auto antibodies, antibodies that bind and cause destruction to your own self-tissues. Now, before your research, where did we think lupus came from? I think people didn't really understand or know. Lupus is a multi-system disease, meaning it affects many different tissues and organs, everything from the skin to the lining of the lungs and the gut to the brain, to the blood cells, to the coagulation system. and it's been an enigma or a puzzle for many decades.

Well, how did you investigate the link between Lupus and Epstein Barbeyers? So for a long time, people have speculated that EBV might be a cause of lupus, but the data were not fully compelling, meaning there were little glimmers of data, but there wasn't a really strong mechanistic basis for how EBV could cause lupus. And so one of the major challenges has been inability to identify the EBV positive B cells that are present only at about 1 in 10,000 B cells. So my lab developed a sequencing method to pinpoint those cells to study them, and we thereby discovered that they are driving the autoimmune response in lupus. Well, take me through that.

The EBV virus is hiding in the B cells, which are part of the immune system. happens when they get active? So we show that the EBV virus, when it infects the B cells and lupus, it activates inflammatory signaling in those B cells and activates them as what we call antigen-presenting cells that activate helper T cells and systemic immune responses that mediate lupus. So it turns the immune system on the body itself? Yes, exactly. instead of attacking invaders like other viruses that would come in. Yes. And one of the key discoveries that we made is that in lupus,

the EBV directly infects the auto-reactive B-cell, the B-cell that's making the antibody against the body in lupus and reprogram them into commander B-cells that then orchestrate the broad autoimmune response against the body's tissues to mediate lupus. Whereas in like, for example, in healthy individuals or in multiple sclerosis or in other diseases, the EBV infects other B cells that don't attack the lupus targets in the body.

So if 95% of us have EBV in our bodies, what makes it flare up as lupus in some people but not in others? Does it depend on what type of B cell that this virus infects? Yes, that's what our discovery implies. It's all about which B cell, but EBVs happen to infect. So in your body, B cells contain like 10 to the 12th, so like a billion different specificities against every conceivable virus or bacteria that you could encounter. So it depends which B cells happen to be infected by EBV when you're infected. And it appears that in lupus, the EBV happens to infect out of these 10 to the 12 B cells, the B cells that specifically attack the nuclear antigens that are the target of the autoimmune response in lupus.

Oh, I see. So that's what makes lupus somewhat rare. Why, everybody doesn't get it. You have to have that infection in the right type of cell to get it. Exactly. Exactly. So what does this change in terms of treating lupus? Well, there's a new generation of therapies that's currently in early clinical trials. They're called car T-cells or T-cell engagers. And these therapies result in ultra-deep depletion. of every B cell in the body. And what's been discovered is that these therapies, when given to a lupus patient, appear to result in long-term disease-free remission, which is an essence cure. But do you really want to eliminate all the B cells?

I mean, wouldn't it be better to target just those that cause lupus and not wipe out the entire immune system? Yes, by far the best way would be to surgically take out with a rifle shot, just the EBVB cells in my lab and also a startup. company we're working on, are working to develop that type of therapeutic strategy. So just generally, what can findings like yours tell us about these viruses that can hide in our bodies for such a long period of time, but then become activated to cause something more serious? Yeah, I mean, I think herpes viruses, which lie latent in the body, so herpes virus include

the chickenpox virus, varicella zoster. They include CMV, which is cytomegalovirus. They include HSV-1 and two, which are oral and general herpes, and they include EBV. And in each case, these viruses lay dormant in the body once were infected for the course of our lifetimes. And for example, varicellazoster virus, it was just recently reported by investigators at Stanford that the varicellazoster virus vaccine, the chickenpox vaccine, appears to dramatically protect people against the risk of developing Alzheimer's disease. and our studies are implicating EBV as playing a really critical role in lupus and potentially other autoimmune disease immunity. Dr. Robinson, thank you so much for your time. Thank you so much.

Dr. Bill Robinson is a professor of immunology and rheumatology at Stanford University in California. And that's it for Quarks and Quarks this week. If you'd like to get in touch with us, our email is Quirx at cbc.ca. You can find our webpage at cbc.ca.ca.com. where you can read my latest blog or listen to our audio archives. You can also follow our podcast, get us on SiriusXM, or download the CBC Listen app. It's free from the App Store or Google Play. Quarks and Quarks is produced by Rosie Fernandez, Amanda Buckowitz, and Dan Falk.

Our intern is Dion Sudiol. Our acting senior producer is Sonia Biting. I'm Bob McDonald. Thanks for listening. For more CBC podcasts, go to cBC.ca slash podcasts.