S3.16 Sickness and susceptibility: The ancient war between genes and disease
Kat: Hello, and welcome to Genetics Unzipped - the Genetics Society podcast with me, Dr Kat Arney. In this episode, we’re taking a look at the ancient war between our genes and the pathogens that infect us, looking back thousands of years to the Black Death and before, all the way through to our very latest foe.
Before we start, yes - one more quick plug for my new book, Rebel Cell: Cancer, Evolution and the Science of Life, exploring what we’ve learned so far about where cancer comes from, where it’s going, and how we might finally beat it. It’s coming out in the UK on the 6th of August and in the US on the 29th September - and is available now to pre-order from rebelcellbook.com - if you’re able to, please do pre-order, as it all helps to send the book up the charts in its first week, and will make my mum and dad ever so proud. Thank you.
Genetics and COVID-19
Kat: I know I promised that this would be a coronavirus-free podcast, but we’re now at the end of July 2020 and it’s not going away any time soon.
One of the most curious things about COVID-19 - the disease caused by the novel SARS-CoV-2 coronavirus that’s causing so much trouble - is the wide variation in how it affects different people, from being a very serious or even fatal illness, through a range of strange symptoms like skin rashes or diarrhea as well as the classic cough, fever and loss of smell that vary in their severity, and some lucky people who seem to catch the virus but have no symptoms at all.
So, do these differences lie in our genetics? Or are their other factors at play? One way of finding out how much of the variability in any trait in a population is ‘in the genes’, more scientifically known as ‘heritability’, is to look at nature’s own genetic experiment: twins. And how better to do that than with the TwinsUK cohort - a massive ongoing study of more than 14,000 identical and non-identical twins, set up more than 25 years ago by Professor Tim Spector at King’s College London.
By comparing identical twins, who share 100 % of their genes, with non-identical twins who are as related as regular siblings, Tim and his team are able to start teasing out the effects of genetics from the environment. For example, if identical twins tend to be more close in height than non-identical twins, then that tells you that height is highly heritable, and there’s a strong genetic component, and you can do all sorts of clever statistics to figure out how much is likely to be ‘in the genes’ somewhere.
So when the COVID-19 pandemic started, Tim and his team wanted to find a way of quickly reaching out to the twins in the study to find out how coronavirus was affecting them, and see whether there was any genetic component to the variation in responses to the disease. To do this, he brought in the health technology company ZOE, who quickly built a simple app enabling the twins to log their health and any symptoms on a daily basis. And then, he thought, why stop there?
The COVID Symptom Study app was rolled out to the public, and there are now more than 4 million people in the UK, US and Sweden using the app to log their health. Since then, the data from the app has revealed a wealth of knowledge about COVID-19 - and, by way of full disclosure, me and the team at First Create The Media have been working with ZOE since March to help with their science communications, which explains why I’ve been VERY VERY TIRED lately.
But to go back to the app’s original purpose, what does the data reveal about the variability of COVID symptoms between people, and how much might be in our genes? To find out I spoke with consultant geriatrician Dr Claire Steves, one of the similarly VERY VERY TIRED researchers at King’s College London, who’s working round the clock to analyse all the data coming out of the app.
So - first question, is there a difference between identical and non-identical twins in how likely they are to have the same symptoms from COVID-19?
Claire: We have seen that identical twins are more similar in the symptoms that they've had than non-identical twins. That hints at a genetic component to how we experience the disease.
Kat: From what I understand about COVID, there's a whole range of symptoms from that classic cough and fever, losing your sense of smell, all the way through to some gastric symptoms and some very strange things. Does the amount to which that seems to be in your genes, is that the same for all the symptoms?
Claire: Well, all of the symptoms we've found to have some heritability, but there were some that really were key, and I think are really interesting. One in particular that was the most heritable was what we call delirium.
Actually, within the app, what we asked was whether or not someone had experienced confusion, disorientation or drowsiness. This is because delirium -- which is an acute confusional state that can come with any acute illness, it's not driven by underlying neurological problems, usually. It's usually in a response to a very strong stressor.
That symptom was really highly heritable. That's one of the first times that's been identified. It's quite difficult to study delirium because it's such a transient phenomenon. But that's really interesting because it could be that this virus has what we call a neurotropism, so an ability or an affinity to get into neurological cells, as well as an ability to cause this cytokine storm and very strong fever and systemic reaction which then can lead to pressure on the brain's functioning.
I think that's going to be a very interesting area of research, because many doctors are concerned about the potential mental health effects of this virus as well, in the short and the long term.
Kat: With the twins study, you are basically comparing identical twins and non-identical twins and getting an idea of how much any of the symptoms or effects of the virus are likely to be in the genes, compared to not in the genes. Do we know anything about the actual genes?
Because obviously the immune system is incredibly complicated and there must be many, many thousands of genes involved in it. Do we know any of the prime suspects that are involved in the response to coronavirus or the development of COVID-19 as a disease?
Claire: Well, that's a very good question and it's a question that we are in a really good place to answer now, having gone through the last twenty years of the human genome project. Very large studies around the world have got genetic information on cohorts of individuals.
There's a big consortium initiative coming together across the world, and specifically across the UK, trying to look at symptoms from coronavirus and testing from Coronavirus against genetic architecture. Those studies haven't yet come to fruition.
It's really important in genetic studies that they are carefully conducted, to make sure that the population are balanced and also that you replicate signals across different communities and populations. So, that process is ongoing. It won't be very long until we have an understanding of what the genes are that are driving this heritability that we see.
Of course, there may be a difference in terms of heritability or genes that lead to somebody having the infection to the genes that lead to somebody having the infection in a certain way, so with certain symptoms. I think that's going to be key as well. Not just to look at the genes which define whether or not you have had exposure, that it has got into your body, but genes that define how your body then reacts to it, which is all around symptoms.
Kat: So, the way that you've been gathering data from the twins is through the COVID Symptom Study App, which is also gathering data from the much wider population. I think it's very interesting, some of the findings that have suggested that certain populations such as black and ethnic minority populations, different parts of the country, different ages, different sexes may be at different levels of risk.
What is the next stage for really trying to get to grips with all that data? What picture is emerging about coronavirus across the UK and the other countries where the app is working?
Claire: The main picture that is emerging is actually that one of the biggest risk factors which is there is around age and frailty levels. That's something that isn't genetically defined, although of course one's aging response, there are certain characteristics of biological aging which could be related to genetics. That risk is not really clearly genetic. I think it's that demographic architecture that is defining the disease as it is presenting, most of all.
The secondary thing is of course the effect, the really important effect of social distancing and the things that we are all doing to keep each other separate from each other. Because those affect the environmental transition of the disease.
I guess that's where the complexity comes again, in looking at genetics because in order to do so, you really have to keep those things stable. So for example, when we've been looking at our twins, where we've been looking in detail at twins that are involved in the app and also twins that we are involving in serology studies that we're doing, we've made careful pains to make sure that we have adjusted for their environmental distance.
In some cases, we are just using twins who live within a certain radius of each other because then they will be experiencing the same environmental context. Because of course, when you look at genetics and heritability, you are always balancing that influence in the environment against the influence of genetics. And where certain things like living in the city in the middle of a pandemic, that can be very overwhelming and overwhelm the signal.
I think that's kind of what we've seen across the demographics of the UK, that it's really been in urban centres. I think that's a real lesson that we all know, isn't it? That tracking, tracing, understanding where the virus is, is really important for spread.
Kat: Claire Steves, from King’s College London.
Back in Black (Death)
While Claire and her colleagues are looking at how genetics affect our susceptibility to a very modern pandemic, Christiana Scheib, head of the ancient DNA research facility at the University of Tartu, Estonia, is looking at much older plagues - including the grandaddy of them all, the Black Death.
Christiana: Well, I'm very interested in all of the factors that relate to susceptibility to infectious disease. For example, we know from looking at modern people that a lot of things affect whether or not you are going to be susceptible; your age, your diet, maybe your oral microbiome, your immune state, stress, whether you've got some other infection.
What we're trying to do is disentangle these in ancient populations. So, we want to say, for example, look at a plague pandemic, let's say the Black Death. We've got a site in Cambridge and we want to know okay, we've got 20 victims in this site but we've got 40 people who don't seem to be victims of the Black Death, but they are in the same time period. We want to know why did those people die of the Black Death, but others didn't?
Kat: And presumably also, what did those other people die of?
Christiana: Exactly, yes, we want to be able to diagnose them as well. There are some things that fall through the cracks when you are doing normal techniques, normal metagenomic screening, so what we are trying to do is layer multiple techniques so that we can get as much information out as possible, and come to some sort of diagnosis for those seemingly healthy dead people.
Kat: Well, I mean they're dead, so they're not that healthy.
Christiana: Yes, but some people don't die of disease. Plenty of people die from trauma, which you can sometimes see on the skeletons very easily. You can see somebody has had a knife wound to the head that hasn't healed, or they've been crushed by some sort of horse cart or something like that. Or some people do just get old and die and it's not necessarily from an infection. Those are the things that you're not going to be able to tell from finding a bacterial agent in their blood.
Kat: So, tell me a bit about the project and the people that you are studying?
Christiana: I'm working on a project called the ‘After the Plague Project’, which may be a bit of a misnomer because we are looking at both before, during and after the plague. The point of it is to understand the medieval health in Cambridge.
To do that what we are doing is taking a time transect of skeletons from the Cambridge area. We are keeping it local so we can avoid the variables that come into play when you look at multiple geographic locations.
We're going from the Neolithic up until post-medieval, early modern people. We are looking at those skeletons to find traces of how the Black Death affected their health.
Kat: Tell me a bit more about the life and times of your patients.
Christiana: First we are looking at Neolithic, which is actually only two samples which we published recently in Annals of Human Biology. That's between 6,000 to 4,000 years before today. Then we have quite a few individuals from the early Roman period. We have early Anglo Saxons, late Anglo Saxons, Medieval period and post-Medieval, early modern. So basically, from the year 0 and just before until just before modern day.
Kat: And where are these people in Cambridge? Where are you finding them?
Christiana: We wanted to look at urban versus rural. So, some of them are from archaeological sites in Cherry Hinton, Duxford, Gamlingay, Barrington, Edix Hill. The core medieval population comes from within Cambridge itself. The Saint John's Divinity School site, All Saints by the Castle, Saint Bennet's Street, The Augustinian Friary on the New Museum site. I think those are the main ones.
Kat: So, you're finding all of these different people from all these different times in these locations. How are you looking at them?
Christiana: We have quite a large team from various backgrounds. They are looking at the bones, they are looking at how much usage the people got out of their bones, they're looking at what they ate and how did this affect their chemical signature in the bones. People are looking at lesions from diseases that they may have had. Then of course, we are looking at the DNA and the proteins that are stuck inside the teeth and the bones after they died.
Kat: So, what kind of things can you actually pull out? Because I know that you can look at basic genetics, understand the genome of these people, but what can you understand about disease?
Christiana: Well, first of all you can find an actual infection that the person had, if it's present in the bloodstream in high amounts, once you die, your bones act like a sponge and just absorb whatever is happening.
So we are able to say in the case of the plague, we can find plague DNA in the teeth, we are able to find hepatitis B virus in people's teeth, we can find leprosy, tuberculosis, any of these bacterial or viral diseases that have affected people for a long time. We are able to find those.
Kat: Can you tell whether that actually killed someone? How do you understand what the impact of the infection was and was it the infection that actually sent them off?
Christiana: That's a bit more difficult but some diseases, you can be fairly certain. Plague causes death because it is septicaemic when it gets into your blood stream in high amounts. So, if we find it in somebody's tooth, it's very likely that they actually died from that. Now, tuberculosis for example, you can live with for a long time. If we find that in your bone, you could have died from being stabbed in the heart, but you also had tuberculosis, so it's not really diagnostic in that way.
Kat: You mentioned that you are looking at genetics but also proteomics. What do you mean by that, and what can studying proteins tell us, that studying DNA can't?
Cristiana: DNA is like a blueprint. If you want to understand the actual execution of the plan, they you need to look at the protein. The DNA tells us what proteins are being expressed. If we want to understand whether someone was exposed to a disease, then we have to not only find the DNA of the disease in their bloodstream, but it would also be really good to see if they have any immune proteins that match a particular disease.
Or, if we want to find out about their diet, sometimes it's easier to find proteins. Like milk proteins we often find in their teeth, which are often easier to find than say, milk DNA or something like that.
Kat: You also mentioned looking at microbes. Obviously, there are microbes that cause disease and are very nasty, but we are also full of microbes that are the good bacteria; the microbiome that live in our guts, in our mouths and all over our body. Can you study those and find out what that might say about health?
Christiana: Absolutely. Before modern dentistry, people didn't brush their teeth as much and so they have what we would call dental tartar or plaque, or we would call it dental calculus, which is actually the preserved, calcified biofilm that builds up on your teeth when you don't brush them.
When we extract DNA and proteins from that, we can actually find all of the species of bacteria and viruses that were in their mouths. It's layered as well, so it's throughout their lifetime, or at least the lifetime of that calculus building up. That can tell us a lot about what was going on with their periodontal disease and potentially as well about other states they would have had.
Kat: So, bringing all of this information together about the people, the bones, their proteins, their genetics, all sorts of things, where they ate, where they lived, what picture is starting to emerge about the life and times of the people of Cambridge?
Christiana: Well, not so different from modern day, I would say. Except today we have --
Kat: Less Wi-Fi!
Christiana: Yes, exactly. The thing you learn the most about when you look at the past is that people are just people. People have always been people. A lot of the fears and hardships that people have faced in the past, we still face today. Although I would say that things are much, much better now than they were in the 14th Century - the 14th Century was a dire place. But of course, they wouldn't have realised that because they didn't know any different.
We do find plenty of people living to ripe old ages. Lots of little old ladies living in hospitals and in rural communities. We find lots of children suffering from diseases, malnutrition, which is much less prevalent today.
In general, a lot may be quite different about the past, in that there's a lot more disease than we have today, however genetically the people in Cambridge are actually very similar to the people that live here today who are locals. So as everything changes, a lot also stays the same.
Kat: The project is called After the Plague. Tell me a little bit more about the plague, the Black Death. We have this idea of this horrific pestilence that swept certainly through Europe. Do any of your findings shed light on these epidemics and what they can tell us about humans and the Plague and the epidemics of the past?
Christiana: Absolutely. The one thing we are learning more and more from ancient DNA specifically of the Plague is it's not just the Black Death and it's not just The Plague, which we tend to think of as a singular event.
We should actually be calling our project After the Plagues, because actually it has been affecting humans for thousands of years, since the Neolithic period. In fact, there's the Neolithic Plague, the Bronze Age Plague, there's the Justinian plague or the Anglo-Saxon period Plague.
Then you've got the Black Death, finally. It comes back into England over and over again, recurring for hundreds of years until finally we get antibiotics and we are able to wipe it out.
Kat: Thank goodness there is no more plague in the UK, but there is plague in the rest of the world. Is there anything you can take from your findings that might shed more light on the plague that is still around?
Christiana: Yes. Our goal is to try and identify regions of the genome that have been selected for by past plague pandemics so that we can understand the evolution of the plague, the co-evolution with the human genome. This might help us develop new therapies or understand just why some people are more susceptible to plague than others.
Kat: Because humans have evolved with our pathogens as long as we've been around and as long as pathogens have been around.
Christiana: Exactly, yes. And we have to understand that deep history in order to predict where we're going in the future and to help us to combat these pathogens in the future. Because they're not going to go away. We haven’t been able to eradicate most of them, so we need to have this information to help us in the future.
Kat: Christiana Scheib, from the University of Tartu, Estonia
Battling with our bugs
Kat: As Christiana mentioned, we humans are locked in an ongoing struggle that’s been waged over thousands of years against the pathogens that infect us, of which SARS-CoV-2 and the Black Death are just two in a seemingly endless army. And now that we’re able to look at DNA from ancient human remains, researchers like Lucy Van Dorp from University College London are able to act as genetic archaeologists, searching for the remnants of past battles within our genomes. So what are our oldest foes on the disease battlefield?
Lucy: Trying to understand how old some of our pathogens are, some of the really common human associated pathogens today, is quite difficult. It's a question which many geneticists and evolutionary biologists have been asking for a long period of time. What we're finding is that the age of many of our pathogens keeps changing as we get more data and more evidence; we keep changing our minds.
Currently I would say that one of the pathogens that we think is the oldest, that might have plagued us for the longest period of time is the Plasmodium species. These are the agents of malaria.
I say this because in human genomes today, we see quite a lot of evidence for selection for traits that help reduce your susceptibility to malaria, particularly in African populations. For these traits to rise to the kind of frequency that we observe, we really think these pathogens must have been exerting a selective pressure for a long period of time.
Other interesting and very old bugs are for example, a pathogen called Helicobacter pylori, which is found in our stomachs. This seems to be as old as maybe 100,000 years or so. So really consistent with the origins and spread of Homo sapiens as a species.
Then we have other diseases, plague and tuberculosis which are a little bit more recent in time. These are much more consistent with the timings of say, the Neolithic revolution. Then some of the very common diseases that we are handling today, so smallpox, influenza, measles, HIV… they are actually all really quite recent.
So, there's really no doubt that infectious diseases have had an enormous impact on our human genomes. They are probably the biggest selective force that we've experienced and have wiped out a huge number of humans through history. But actually, knowing what some of these pathogens were through time and how they might have impacted on us, is really a very active and ongoing field of research.
We don't see as much evidence in the human genome as we might expect for the legacy of these kinds of infections that we know are really common through time.
Kat: Given that these pathogens have been around for a very long time, in some cases many many thousands of years, what kind of influence might they have they had on our evolutionary history as a species?
Lucy: My feeling is that throughout our history, infectious diseases are probably the biggest selective pressure that we've experienced. They have wiped out huge populations. You only have to look at for example, the Black Death or even the 1918 influenza pandemic, to see that many, many populations have been decimated through time because of infectious diseases.
Even today, we're still really struggling with malaria, tuberculosis and many other infectious diseases, despite the fact that we are now in the antibiotic era and potentially we have some therapies at our disposal, and more sophisticated healthcare systems. So it really isn't a long stretch of the imagination to assume that through time, diseases have really had an enormous impact.
One thing that's really very interesting is if we look at human genomes, we find that we don't see very much evidence for selection driven by infectious diseases, certainly not as much as we would expect.
There's a couple of reasons why this might be the case. It could be that we're being infected by slightly different organisms, we've been evolving but our pathogens and our bugs have also been evolving in different and mysterious ways, to try and evade our immune defences.
Also, the kinds of statistical methods that we use for inferring selection are not well designed for infectious diseases, because they infect in very different ways, people present in very different ways. Certainly, any disease which affects someone after reproductive age, we likely won't see a legacy of in their genome.
So it's a little bit of a mystery why we don't see more evidence in the human genome for the impact of disease, but we really do think it has been incredibly important.
Kat: But here’s a curious thing - while some very strongly selected advantageous human traits like lactase persistence (the ability to drink milk beyond infancy) have left signatures of selection in the human genome, we don’t see the same signatures when it comes to genes involved in fighting infection.
Lucy: It is a bit of a mystery. If we look at lactose persistence, we see it's been under a huge selective pressure. It's difficult to imagine the multitude of reasons that could be responsible for why drinking milk was just so important to your survival and your fitness.
Arguably, the ability to survive a plague pandemic or a similar large-scale infectious disease agent should have exerted just as much of a selective pressure, but we don't see it. I think it's a real challenge.
I would love to be able to get in a time machine and go back in time and say what was happening, back through time, with our interactions with disease. How were we evolving? What were we doing? One of the nice things about genetics is it gives you an opportunity to start to have a bit of a pseudo-time machine and start to be able to tease apart some of these signals.
But actually understanding what has been selected for and what hasn't, particularly in the context of disease but also in the context of some of these cultural traits like drinking milk, is something that is really incredibly interesting.
Kat: It’s not just human genomes that can be analysed in ancient remains, there’s plenty more in there, which can shed light on the diseases that killed our ancestors.
Lucy: So, DNA is really just a string of letters of As, Ts, Cs and Gs. The kinds of methods that we use to infer how people have moved and migrated in the past are directly transferable to many other different species. Some of the species that I'm most interested in are common pathogens, in particular tuberculosis and malaria.
It's possible to use exactly the same methods to ask how to have our bugs changed and moved and adapted through time, in just the same way as we've been thinking about human genomes.
So when you take an ancient sample, for example sampling the archaeological remains of an individual who died, quite often, the amount of DNA that you get back is very little of the human content and is actually a lot of everything else. I really mean everything else. There's a real soup of information there. But if you get lucky you might find that you can sequence the pathogen that may have killed this person at the time of their death.
In this way, we can start to ask questions about what diseases have occurred at different time points and we can extract the genomes of these pathogens and say how they have evolved and move through time. This is something we care about in very ancient timescales, but also we need to care about them quite recently, for example in the pre-antibiotic era, to see how our pathogens have been changing in response to us using different treatments.
In terms of historic pathogen genomes, some work which I've been involved in which I found really exciting, is working on the genomes of Plasmodium vivax and Plasmodium falciparum. These are two of the pathogens that cause human associated malaria. Malaria was actually quite common; it was really a truly global disease until quite recently.
In particular, we have malaria in Europe, stretching from Britain and the Mediterranean through to European Russia, until about the 1960s. One question is: How important are these eradicated and historic malarias in understanding the disease?
I was lucky to work in a collaboration where we sequenced DNA of some of these eradicated European Plasmodium of these malaria species from a fairly unique resource. This was the resource of some antique medical microscopy slides which were sampled from patients in Spain's Ebro Delta in the 1940s.
It was possible, by taking the blood smears on these slides, to generate enough DNA to sequence the first semi-complete genomes of these eradicated malaria parasites. This suddenly allows us to ask questions. It allows us to ask how common was disease before the eradication in Europe?
It allows us to ask where there may have been some historic spreads in transmissions of malaria and it also allows us to ask whether we see any evidence for resistance for some of the antimalarials we use to day in those historic genomes.
In particular, we focused on plasmodium vivax malaria. We were able to infer that this European eradicated strain revealed the legacy of this migration and spread from Europe to the America's, taking place in around about the 15th Century. This gives us the tantalising insight that malaria caused by the vivax parasite was not that common or didn't exist in the Americas pre-this 15th Century period.
Of course, this date coincides very nicely with our knowledge of European colonial expansions. So, it's one of these cases where we think actually, malaria may well have been spread with colonialism, right across the sea.
Kat: So that’s the bad bugs that infected people in the past and made them sick (and the bad colonialism that didn’t help), which is fascinating for historians. But why should the rest of us care about studying these ancient diseases in today’s modern era, particularly when we’ve got a brand new pandemic to worry about.
Lucy: I think a lot of these methods are ones we really should be caring about now. That's because understanding the spread, movement and migration of humans and their pathogens is something that continues to happen and will continue to happen. Particularly for understanding the movement of different pathogen species, there are large scale efforts now to reconstruct epidemics and outbreaks using genetic data in conjunction with epidemiological data.
This is allowing us to infer what factors might be important in for example a hospital outbreak and understand how genomes are either expanding or contracting as we as a society change around them. This is really important, particularly for pathogens, as we have the potential to inform public health interventions and certainly to use what I term 'genomic surveillance' to understand what variants and what parts of the genome we need to be worried about.
Kat: And as you might expect, bringing us full circle, Lucy and her team at UCL have been very busy analysing the genomes of the various strains of SARS-CoV-2 in existence around the world, particularly in order to understand how the virus is mutating and evolving as the pandemic spreads. But that’s a topic for another time, if I can face it.
Evolution in reverse?
Kat: And finally, it’s time for a quick look at what’s in the latest episode of the podcast from Heredity, the journal of The Genetics Society. The evolutionary splitting of one species into two - a process called speciation - is usually thought of as a one-way street. However, this isn’t entirely true.
In this episode Dr Jente Ottenburghs from Wageningen University discusses the curious case of the wonderfully-named bean geese: where his analysis of goose genomes shows that the process of splitting into two different species, Taiga and Tundra geese, appears to have slowed or perhaps stopped altogether
Jente: I think I would highlight this idea of -- I'm a bit reluctant to say speciation in reverse, because then you imply that they were different species and they are now merging. So, I would say that they were in the process of becoming different species, and that this process has now been reversed.
Because if you look at a lot of the literature on speciation, often people see it as the speciation continuum, where you go from two populations that can hybridise, all the way to complete reproductive isolation.
You get this feeling that this reproductive isolation is the goal of speciation, the goal of evolution in getting different species. But I think it's important to realise that this process can stop. For example, when you get a hybrid zone. But it can also reverse as we have shown with the bean geese.
So, I think we need to step away a bit from this idea that speciation always leads to complete reproductive isolation, but that there is a whole continuum in between.
Kat: You can find the full interview in the latest Heredity podcast - just search for Heredity in your favourite podcast app, or follow the link on the page for this podcast at Geneticsunzipped.com
Recent introgression between Taiga Bean Goose and Tundra Bean Goose results in a largely homogeneous landscape of genetic differentiation https://www.nature.com/articles/s41437-020-0322-z
That’s all for now. Thanks to my guests Claire Steves, Christiana Scheib and Lucy van Dorp. In two weeks you’ll get the chance to hear so exclusive excerpts from my upcoming book, Rebel Cell, and next week will be the next bonus episode in the Genetics Shambles series, brought to you by the Cosmic Shambles team, in association with the Genetics Society and the Milner Centre for Evolution at the University of Bath.
In the meantime, you can find us on Twitter @geneticsunzip and please do take a moment to rate and review us on Apple podcasts - it really makes a difference and helps more people discover the show.
Genetics Unzipped is presented by me, Kat Arney, and produced by First Create the Media for The Genetics Society - one of the oldest learned societies in the world dedicated to supporting and promoting the research, teaching and application of genetics.
You can find out more and apply to join at genetics.org.uk Our theme music was composed by Dan Pollard, and the logo was designed by James Mayall, transcription is by Viv Andrews and production was by Hannah Varrall. Thanks for listening, and until next time, goodbye.
Image: Colourised scanning electron micrograph of a cell (blue) heavily infected with SARS-CoV-2 virus particles (red), isolated from a patient sample. Image captured at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland. Credit: NIAID/NIH via Flickr
