In the eLife podcast, a university compost heap has turned up Finland’s first documented “giant virus”. Also, why monkeys de-sand their supper, and how learning more languages actually makes brain tissue thinner. Then, the link between sugar and neonatal sepsis, and how a cancer controls its hydra host by bestowing it with extra tentacles...
In this episode
Finland's first giant virus
Gabriel Almeida, Arctic University of Norway
A university compost heap has turned up Finland’s first documented “giant virus”. Gabriel Almeida, now at the Arctic University of Norway, had been collecting samples from all kinds of environments to try to find examples of one of these agents. These entities were first recognised for what they are - massive viruses bigger than bacteria in many cases - only about 20 years ago. Previously, scientists thought they were some strange form of bacterium. But they’ve since been detected in many different environments; they often have massive genomes, the workings of which we haven’t yet unpicked but which might surrender some useful secrets including recipes for novel antibiotics, and scientists think they might be evolutionarily extremely ancient, pointing us towards how early life might have operated. Now Finland can say it’s got one too!
Gabriel - This paper shows the isolation of the first giant virus in Finland. A giant virus is a virus which is larger than conventional viruses. What makes them giant are two things. One is their size itself, and they also have larger genomes. So it means that they code for more genes than most common viruses. And they are very commonly found in marine samples, in soil, and many other places, even in clinical samples. And this one we found, for example, came from a composting soil sample. So it means that they're really widespread.
Chris - It came from a compost heap?
Gabriel - Yeah.
Chris - And so did someone actually go, or did you go looking in a compost heap to find it? Or were you looking for something else and found this?
Gabriel - I was using a collection of samples in Finland. So I was collecting everything I could from lake water, from soil, from aquaculture-related samples. And we had this composting place in the university, and I collected a small amount of that. And then I tested it, and it was positive for the virus.
Chris - How did you actually test it? In other words, when you were just given this soil sample, how did you then flush the virus out?
Gabriel - Part of what makes giant viruses special is that most of them need to be eaten. So that's why we often use amoebae to isolate them, because the amoeba actively takes in food sources from the environment. And when they eat one of these viruses, they get infected. So the process is basically to take the sample, make it into a liquid form, and then mix that with a growing amoeba culture. The amoeba is going to eat everything that's in there. And if they find a virus and get sick, they die. And you can see that under the microscope – they’re dying, and we know that the likely virus is there.
Chris - When did it become apparent to you that you'd got one of these viruses? Was that because your amoeba culture became unwell, and you reasoned, well, something's killing it, it could be a virus?
Gabriel - Yeah, exactly. So from 24 to 48 hours later, plates where this sample was added were completely clear of amoebae. Everything died. And we just took a small amount of that to infect more amoebae, and we confirmed that it was killing the new batch. Then it's not too difficult to grow enough of the virus to extract DNA, the genomes, and sequence that. And once you know the DNA sequence, you can be sure that it's a virus and also which virus it is.
Chris - And was it the genome that gave you the clue that you’d got a new one, and that it was Finland’s first?
Gabriel - Yeah, exactly. So when we got the full genome sequence, we could see that it was a virus. We also discovered it was related to other known giant viruses. Then we were able to check the genes in detail and see their peculiarities and be sure that we had a new one in Finland.
Chris - Did you image it? So have you only interrogated it genetically, or have you actually been able to see it now?
Gabriel - So I actually did a lot of imaging as well, based on electron microscopy. And a big part of this paper was actually the cryo-electron microscopy imaging. After taking images of thousands of these viral particles, we constructed the structure in very fine detail to determine how the virus is built. That’s important for knowing how it stays stable in the environment and also how the proteins interact to protect the DNA and keep it viable for a while.
Chris - What does it look like and how big is it?
Gabriel - It's around 200 nanometres. Among the giant viruses, this is a small one. I have some which are five times larger than that.
Chris - Yeah, indeed. I mean, that would be about twice the size of a flu virus, wouldn’t it? Or twice the size of a coronavirus that causes COVID-19. It’d be about twice as big as that.
Gabriel - Exactly.
Chris - And in terms of its genetic code, how big is it?
Gabriel - It has 360,000 bases. In comparison, that's about 10 times larger than a phage, for example. Much more than corona – around 10 times larger than that as well. Out of all these bases, it codes for almost 400 genes.
Chris - Well, that’s quite a lot, isn’t it? I mean, if we take, say, chickenpox or the herpes virus that gives you cold sores, that’s got a fraction – a quarter – of that number of genes. That’s a lot.
Gabriel - Exactly. And what I find interesting is that it contains genes found only on this virus. So three out of these 388 genes are unique to this isolate. And we don’t know what they do. So we could have some surprises there. And anyway, 67% of these genes are hypothetical. We know they code for something, but we don’t know their function. So there’s huge biotechnological potential here to explore.
Chris - Why do they have such massive genomes? Do we actually see all of these genes working? Are they genes that are absolutely critical to the virus lifecycle?
Gabriel - No, they have a lot of accessory genes. And as mentioned, we don’t know about most of them. But it has been shown in the literature that some can bring new traits to the host. Some might hint at metabolic pathways that they may make the host express. And we have some theories that they use these genes to compete for the organisms when infecting the amoeba.
Chris - And have you watched them replicating? Can you see where inside the amoeba they grow? Do they go into the genetic material like a herpes virus? Or do they grow in the cytoplasm, a bit like a monkeypox virus or smallpox?
Gabriel - Yeah, we were able to see that. They get taken in by the amoeba, and their replication is in the cytoplasm. They don’t enter the nucleus. They tend to form viral factories – these big electron-dense masses inside the cell where the particles are produced. And for this virus species in particular, they also tend to form vesicles containing several viruses inside the cell. That’s important because when the cell dies, these vesicles form clusters of viruses in the environment. And it makes it easier for new amoebae to find and eat them to become infected.
Chris - It’s a fascinating phenomenon, though, isn’t it? Thinking big, why do you think these things even exist? And where do we think they came from in the first place? How did they evolve? Because they don’t seem to bear much resemblance to much else.
Gabriel - They are likely very ancient. When you check the DNA sequences from the environment, you find them everywhere – including at deep sea vents, for example, where life likely originated. So at least some branches of this group of viruses might be as old as life itself.
Chris - Is there anything we could use them for? Apart from the fact they’re academically fascinating, and there may well be some unusual biology locked up in those genes that we can slowly uncover. Do they have any applications that we could exploit?
Gabriel - Yes, for sure. We have lines of work here in Norway now trying to untap these hypothetical genes and see how they can be used in biotechnology. One area of investigation is whether some of the genes are used by the virus to kill bacteria. If that’s the case, then you might have something like a viral antibiotic that could be applied in clinics.
Food-washing monkeys
Nate Dominy, Dartmouth College
Monkeys washing their food have provided scientists with an opportunity to understand how animals weigh up the cost of a clean meal against their place in the social pecking order. Taking time out to rinse sandy food ultimately limits how much food you end up eating. But forego the wash in favour of a greater energy intake to preserve your place in the social hierarchy, and you end up with sand-damaged teeth that could shorten your life. It’s a price some “top dogs” are clearly willing to pay for the reproductive opportunities that it opens up. Nathaniel Dominy, who did the work, is at Dartmouth College…
Nathaniel - Shortly after the tsunami of December 2004, researchers were moving along the coast of Thailand and Burma on boats, doing biodiversity damage assessments. They were caught by surprise when they noticed monkeys on the beach using stone tools. This was in Thailand. Primarily, they were using the tools to harvest shellfish—oysters, mussels, that sort of thing. These primates eventually became quite famous, and tourists began to visit to observe them. As tourists often do, they wanted a closer look, so they started throwing fruit onto the beach. This began happening regularly, and the monkeys got used to it. They could hear the boats coming and began to expect food from the tourists. The problem was that the food landed in the sand and became very sandy.
The monkeys quickly figured out that they could take the food to the ocean, dunk it, and remove the sand. That was exciting, because it recalled a very famous moment in primatology where something similar happened in Japan. Those food-washing behaviours inspired us to conduct an experiment where we gave the monkeys food designed to trigger washing, to see what would happen.
Chris - What might be the reason why an animal wants to wash food? I know why I would—sand tastes awful, and the sensation on your teeth is horrible. Do you think the monkeys are thinking along the same lines?
Nathaniel - It stands to reason, right? It’s a relatable problem. Anyone who’s had a picnic at the beach knows that sand in your mouth is objectionable. Back in 1952, when monkeys were first observed washing sweet potatoes that researchers had given them, the assumption was that they didn’t like the feeling of sand in their mouths. That was thought to be the motivation behind washing their food. That idea has persisted ever since, but no one had actually tested it.
Chris - So how did you test it?
Nathaniel - We had three trays and gave the monkeys cucumber slices, which have a sticky surface that’s good at picking up sand. We offered three options: very sandy cucumber, non-sandy cucumber, and something in between. If the monkeys cared about sand, we expected them to spend more time cleaning the sandier pieces. And that’s exactly what we found. When the cucumber slice had a lot of sand, they spent significantly more time trying to remove it.
Chris - Thing is, whenever there’s an action, there’s a consequence. And in this case, there’s a delay before they get their reward. Depending on how sandy the food is and how far away the water is, there’s an energy cost too. So what are the impacts of that? Is there a trade-off? Do they weigh up how far they’ll have to go and how much sand they’ll tolerate? Or did they always wash the food regardless?
Nathaniel - You raise a great point. What we found is that some animals were making shrewd calculations. For some, it just wasn’t worth the time and energy to walk to the ocean. Because the cucumbers are in their hands, they have to rise onto their hind legs and walk bipedally—like a human. But their muscles and bones aren’t well-suited to walking upright, so it’s very energy-intensive. There’s also an opportunity cost: if their hands are full and they’re walking to wash the cucumber, they’re missing out on eating other slices. So some animals chose to tolerate a bit of sand so they could eat more quickly. Others were more averse to the sand and were willing to pay the price of washing properly.
Interestingly, these decisions varied depending on the monkeys’ social rank. Dominant animals, for instance, have higher energy needs. They need to fight off rivals, stay alert, and expend a lot of energy asserting dominance. They have to eat a lot and eat quickly to meet those energy demands. We found that it was these dominant animals who couldn’t be bothered to wash the food properly. Walking to the water just took too long. Instead, they would brush the cucumber a few times with their hands and eat it—sand and all. And we calculated that a lot of sand was going into their mouths. That was probably ruining their teeth.
Sand is highly abrasive. It can chip teeth and cause serious wear. So we think they were paying a long-term price by shortening their lives—just to eat faster in the short term.
Chris - How does this fit with our theories about how hierarchy affects behaviour? It sounds like this supports the idea that animals—and perhaps people—make trade-offs: choosing short-term gains, even if they come with long-term health costs, because they improve reproductive chances.
Nathaniel - That’s exactly right. There’s an idea in evolutionary biology called the "disposable soma hypothesis." It suggests that some tissues in the body are expendable—and teeth might be one of them. A famous study from the UK looked at red deer and found that male teeth wear out quickly. Their strategy seems to be: get energy now, find mates as quickly as possible, and don’t worry about long-term survival. The benefits of reproducing early outweigh the benefits of a longer life. We think these monkeys were doing the same—making a strategic decision. They knew the sand was bad for their teeth, but they were willing to pay that price for more mating opportunities in the short term. It’s a “live fast, die young” kind of strategy.
16:42 - What learning more languages does to the brain
What learning more languages does to the brain
Olga Kepinska, University of Vienna
People with more grey matter in the auditory areas of the brain should be better linguists, right? Wrong! It turns out, based on findings from a new study, that the more languages a person speaks, the thinner the cortical tissue in the auditory brain becomes. Specifically, it’s one region - the transverse temporal gyrus - where greater lifetime language exposure, and a greater divergence of those languages - in other words, the more different they are, the greater the effect - where this is seen. Study author Olga Kepinska, from the University of Vienna, thinks it’s because a thinner cortex is a more efficient structure, honed by language experience. But, were the subjects born that way, or did their lifetime linguistic experience mould their brains?
Olga - Bilingualism shaped the brain, but in our research, we're going beyond bilingualism and looking at people who speak anywhere between one and seven languages. The subjects were healthy individuals who underwent MRI scanning a couple of years ago at University College London in a large-scale study investigating relationships between language processing and language experience. We looked in particular at the structural scans—scans where we can distinguish differences in how the brain is shaped.
Chris - So because you know which parts of the brain have previously been linked to language, you're saying: let's look in this group of people at this region of the brain in detail and see if there are any structural changes that map onto their linguistic abilities?
Olga - Exactly. And not only linguistic abilities, but experience linked to the sounds of different languages. We know that the brain processes sound in structures termed the auditory cortex, and we know that this structure is very diverse across individuals. My auditory cortex will look very different from yours or others’, and we wanted to zoom in on this structure to see if this variability has any neuroanatomical links to lifelong language experience.
Chris - What did you see when you did this? Was there a relationship between people speaking more languages and more variation in this sound-decoding part of the brain?
Olga - Yes, this was very exciting. In this group of approximately 200 people, we saw a lot of variability in how the auditory cortex is shaped. Some people have one bit of cortex devoted to sound processing; others have two or three. And when we looked in detail at these areas, we isolated the second transverse temporal gyrus as being specifically related to someone's language experience.
Chris - So if you were to draw a graph between how many languages someone speaks and the size or shape of that bit of the brain, what's the relationship? What's the pattern?
Olga - The more languages you speak—and the more diverse those languages are—the thinner this brain structure is. In the context of this study, it means that people with more varied language experience need less tissue in the auditory cortex to do its job.
Chris - That seems a bit paradoxical, doesn’t it? We often talk about grey matter being the processing power of the brain, and now you’re saying the more languages I speak, the less of it I’ve got. But you're arguing that it's because the brain is working more efficiently. It's presumably been honed by language experience, which means the processing is as good as it's going to get, and so less is required?
Olga - That's what we think. When I think about these results, I often picture marathon runners, who are extremely efficient and very lean. They have a lot of muscle, but that muscle is shaped to allow them to run for long periods.
Chris - Do you think people with a thinner part of the brain are naturally better at language, or did it become thinner through learning? I’m thinking of studies on the hippocampi of taxi drivers, where it was shown that learning the streets of London changed the hippocampus, and that this occurred through experience. So, is the change you're seeing a result of learning, or was it already there in accomplished linguists?
Olga - That's an excellent question. It’s difficult to draw that conclusion from our study because we only looked at one time point. But we have reasons to believe that language experience actually shapes this region. We ran two analyses. First, we associated language experience with the thickness of this region and found an association. Then we added information on the overlap between languages—phonological inventories—telling our model what the participants' language experience looked like. We controlled for the variability of sounds across languages, and it turned out that both the number of languages and their diversity were better linked to the thickness of the auditory cortex. So, the more languages someone speaks and the more divergent they are, the thinner the cortex. This is why we think it’s the experience shaping the auditory cortex—especially since many of our bilingual and multilingual participants were raised with different languages and didn’t choose which ones to learn. That suggests it's the diverse experience itself that shapes the cortex.
23:30 - The sweet side of sepsis
The sweet side of sepsis
Ole Bæk and Ninh Nguyen, University of Copenhagen
Sepsis is an overwhelming infection that triggers a dramatic inflammatory response that becomes over-exuberant and self-destructive. One sector of medicine where this is, regrettably, all too common is in neonatology. Premature infants are particularly at risk. But what Ole Bæk and Ninh Nguyen have discovered at the University of Copenhagen, using pigs to model the problem, is that blood glucose levels, driven by the sugar load in intravenous nutrition, seem to play a big role in sepsis risk. It’s a fine balancing act though: there needs to be enough calories coming in to support growth and a healthy immune response. But, push the sugar too high, and it can spark sepsis…
Ole - We are very interested in the immune systems of newborns, particularly premature ones, because theirs are not fully developed. These babies have a very high rate of infections just after birth, which can develop into sepsis—a condition where the immune system overreacts and causes serious, potentially lethal complications. At the same time, these very preterm babies need nutrition. They often receive what’s called parenteral nutrition—nutrients delivered directly into the bloodstream. But this often contains a lot of sugar, which increases blood glucose levels.
We study how blood sugar and immune response interact. Immune cells need energy to fight infections, so they use sugar from parenteral nutrition. That’s good—if it’s regulated well. But if glucose levels get too high, immune cells can overreact, leading to sepsis. So we wanted to find out if lowering glucose levels in parenteral nutrition could prevent sepsis.
Chris - Sounds like a necessary evil, Ninh. You need sugar to support growth and the immune response, but too much is bad. How are you studying this?
Ninh - We’ve developed a newborn preterm pig model. We deliver pigs prematurely, and they have an immature immune system similar to human preterm infants. We provide parenteral nutrition as they would receive in neonatal care. In our proof-of-concept study, we compared different regimens with high and lower glucose levels. We saw improved survival in infected preterm pigs who received the lower-glucose nutrition compared to those given the standard, higher glucose.
Chris - But how low can you go without causing harm from too little sugar? Hypoglycaemia isn’t good either.
Ninh - In this study, we halved the standard glucose dose given to preterm infants. We still kept blood glucose within the normal range, so there was no hypoglycaemia. Yet these animals still mounted a good immune response and survived infection.
Chris - Ole, why were we using the higher glucose levels in the first place? Was it just the way it had always been done?
Ole - Parenteral nutrition regimens were designed to support infant growth, but they don’t take into account what happens during infection. The physiology shifts from growth to immune defence, and that changes the nutritional needs. We believe these regimens should be adapted based on whether the infant is fighting an infection.
Chris - What kind of lead time do you have, Ninh? Can you lower sugar after infection starts, or is it already too late?
Ninh - That’s a tricky issue. In our study, when we lowered glucose after symptoms began, it didn’t reduce mortality. That suggests clinicians need to recognise early signs of infection—only then will lowering glucose be effective.
Chris - So, Ole, does that mean the answer is vigilance—monitor closely for early signs of infection and lower the sugar then?
Ole - Yes, and also monitor glucose levels constantly. Clinicians are rightly cautious about hypoglycaemia, which has immediate consequences. Hyperglycaemia, though, is often treated as less urgent—but perhaps it shouldn’t be. Think of sugar as fuel for the immune system. You want to keep it in the normal range.
Chris - Have you got enough evidence now to turn this into clinical policy?
Ole - It’s already known that hyperglycaemia should be avoided during infection. What we provide is a mechanistic explanation of why high blood sugar leads to poorer infection outcomes. So that strengthens the case. But despite the policy, hyperglycaemia remains a common issue in neonatal clinics worldwide.
31:11 - Can cancers control their hosts?
Can cancers control their hosts?
Justine Boutry, University of Montpellier
Can cancers control their hosts? The reason for posing the question is that, in many respects, tumours behave like parasites, which have a long track record of host manipulation. So, in theory, cancers may well do the same. In fact, in a previous episode of the eLife Podcast, we heard how some tumours establish connections with the nervous system, leading to potential changes in host behaviour, perhaps accounting for higher rates of depression reported by cancer victims. Now another intriguing model has presented itself: a heritable tumour in hydra; these are small carnivorous, jellyfish-like animals, which catch their prey using an array of tentacles. At the University of Montpellier, scientists have been studying a laboratory line of these jellyfish that, when they reproduce, which they do by “budding off” a clone of themselves, the offspring also inherit some tumour cells from their parent. These newborns show the unusual trait of growing double the normal number of tentacles, but not from the tumour cells: clearly the tumour is somehow making the offspring do this. It’s tantalising to speculate that the effect is to enhance the growth and reproductive potential of the host, which keeps the cancer alive. Animals without the extra tentacles don’t fare well. The observations have intriguing insights into how tumours can manipulate remote host tissues, like blood vessels, to enhance their own growth. Justine Boutry…
Justine - We observed some jellyfish named hydra that had different reactions when they had cancer. Some had cancer but a regular number of tentacles—seven, eight tentacles. Some had transmissible tumours that they inherited from a previous hydra, from their mother, and they had many more tentacles, sometimes up to twice as many, even up to 20 tentacles. We wanted to understand if it's the cancer itself triggering these new tentacles to appear, and what the benefit might be—either for the cancer or for the host, if it's a reaction.
Chris - How do you know, though, that it's not a third option—that whatever caused the cancer is also causing the extra tentacles to form?
Justine - Indeed, there are also bacteria that can be present in some of the cancers. But in the transmissible cancer, we had two different lines, and one didn’t have any bacteria inside their tentacles. So we grafted several types of tumours—some that trigger more tentacles in their original host and had bacteria, some that didn’t have any bacterial changes, and also some tumours that were completely spontaneous (not inherited) and didn’t trigger this trait. We grafted these various types of tumours into new recipients to see how they would react, whether they would develop more tentacles, and which ones would.
Chris - So you physically took tumour cells from a—let’s call them a donor animal—and put those into a recipient to see whether just moving those cells across, with or without any freeloading bacteria, would trigger the formation of extra tentacles?
Justine - Yes, exactly. We took tiny pieces from the donor, put them into new recipients, and observed that only the tumours that had been inherited in the past—those already present in the mothers and with no correlation to bacteria—were able to trigger new tentacles in the recipients. The spontaneous tumours did not cause the appearance of new tentacles in the recipients.
Chris - And to be clear, the tentacles are growing from the recipient's own tissue. It's not that the cancer or tumour cells turn into tentacles—it's that they're sending some sort of signal that makes extra tentacles grow.
Justine - Yes, indeed. They're sending a signal. We still don’t know what that signal is, but ultimately, it's the recipient that grows the new tentacles. It’s similar to what we see during metastatic processes—sometimes tumours trigger the formation of new blood vessels. It's still the person’s own blood vessels growing, but the tumour cells are signalling them to grow inside the tumour to bring in more nutrients.
Chris - Is the tumour making the recipient grow more tentacles so it can catch more food and support a bigger tumour? Or is it the recipient that’s growing more tentacles to get more food and withstand having this freeloading tumour attached to it?
Justine - With more tentacles, they get more food and produce more offspring. Because there’s a correlation between producing offspring and transmitting tumours to that offspring, it was difficult at first to determine who benefits more. But what we’ve seen is that there are definitely benefits for both. However, because it’s the tumour that triggers this mechanism, it seems more crucial for the tumour than for the host itself.
Chris - There are some big animal transmissible tumours—only two: dogs that transmit venereal cancer through mating, and Tasmanian devils that transmit a facial tumour through fighting. Might they be useful models to see if those tumours affect the behaviours of their hosts?
Justine - Indeed, we have these two models. Especially in Tasmanian devils, there's huge interest in understanding how transmissible tumours affect them, because this cancer is currently pushing the population close to extinction. So it’s very timely to understand how the tumours might manipulate Tasmanian devils—perhaps making them more aggressive towards each other to increase transmission. And there are also other kinds of transmissible tumours that you didn’t mention, which occur in mussels and cockles. These are leukaemia-like tumours, and they’re also very interesting. They can help us to understand transmissible cancer more broadly.
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