Ep 41: Coronavirus II (with Andy Dobson)
Where did the new coronavirus come from? How can we be on the lookout for new diseases emerging from animals? Now that the coronavirus has infected humans, what’s the best path forward?
In this episode of Big Biology, we talk with Andy Dobson, a disease ecologist at Princeton University who studies epidemics like the current COVID-19 outbreak. We talked with him about the possible animal origins of the virus, the best way to control its spread and strategies to avoid the next pandemic. Andy emphasizes that we shouldn’t blame wildlife for the coronavirus outbreak. It’s human behavior that led to this problem, and it’s human behavior that’s going to have to change to avoid the next ones.
This episode is dedicated to Robert May,
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AW = Art Woods
MM = Marty Martin
AD = Andy Dobson
00:08
MM: The new coronavirus probably jumped into humans from wild animals. This type of event isn't uncommon. Viruses like Ebola, Hendra, Nipah, and Hunter virus, and even the first SARS virus, which caused an epidemic back in the early 2000s, came from wildlife. In fact, the Centers for Disease Control and Prevention estimates that more than half of the infectious diseases infecting humans come from animals.
AW: Over the past several months, scientists have been working to determine exactly where SARS-COVID 2 came from, and that's the virus that causes COVID-19. The final word isn't in, and probably won't be for some time, but one likely candidate is bats. Bats are the known or suspected source hosts of many of the viruses Marty just listed, and they're the most likely source of the novel coronavirus.
MM: As we continue to zero in on the host, we also need to learn exactly how the virus moved to humans. Even if bats are the source of the spillover, why are their viruses starting to spill over more into human populations? Is there anything special about bats that makes them especially prone to infect us?
AW: In part, bats are problems for us because they and we are mammals. Viruses are simple, so they need specific conditions to infect host cells. Mammalian cells are more like each other than say, bat and bird cells, but it might go beyond our shared mammalian ancestry. Surprisingly, one key trait of bats that may make them good reservoirs for zoonoses is their ability to fly.
MM: On this bonus episode of Big Biology, we talk to Andy Dobson, a disease ecologist at Princeton University, who studies epidemics like the current COVID-19 outbreak.
AW: We talked about the possible bat origins of the virus, but also spend a lot of time on what life will look like over the next several months, as many places across the US and the world start to flatten the curves. One point that Andy emphasizes is that we shouldn't blame wildlife for the coronavirus outbreak. It's human behavior that led to this problem, and it's human behavior that is going to have to change to avoid the next crisis.
MM: I'm Marty Martin.
AW: And I'm Art Woods.
MM: You're listening to Big Biology.
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02:13
AW: So, Andy, we're thrilled to have you on the show, and delighted to be able to talk about this topic at this time. We wanted to talk a little bit about just first of all, evidence for where COVID came from, so what's the source of COVID, and what's the route by which it got into humans?
AD: Well, the evidence, the best evidence of that obviously is the genetic evidence, and the person who's done the definitive work on that is Eddie Holmes, who's at the University of Sydney in Australia. He, and along with Peter Daszak, who'd actually been as part of the EcoHealth Alliance working with people in China, looking for different viruses. Mainly in their reservoir hosts, which would be bats, but other things that get sold in the wet food markets. And so all the genetic evidence, and they were very good, the Chinese were very good about getting the genetic tissue available and put on the web. All of that points to the coronavirus 19 having bats as their origin. There may have been some transit through a pangolin, but it mainly looks as if it was bats that were maybe brought into the food market or kept with one of the sort of whole wild food farms and infected animals there that were then sold in the market.
AW: And just in terms of evidence, so how do we know it's bats, and you know, why is there this sort of hovering question about pangolins? Why isn't it a sure thing?
AD: It's partly because, you know, most of our understanding of viral diversity comes from looking at humans and domestic livestock. It's only recently that people have been going out and looking at a whole range of other species, but largely because of worries about diseases jumping across. So, doing large-scale surveys to see what's the diversity of viruses out there. I mean, we know that one of the big things, what is global biodiversity of free-living species, we don't particularly know that to within a million species. But if each one of those species has 10 to 20 viruses in there, then there's a huge amount of viral biodiversity we don't know enough about. So, going and looking for these things we begin to get the beginnings of a phylogeny for the viruses that are pathogens and parasites in the free living things, so once we get genetic material we can say, that's from that particular branch of the tree that's mainly in bats, it's got some odd bits in it that it may have picked up when it got into the wrong host but managed to keep going before getting into something and spilling into humans.
04:58
AW: And so you're talking about chunks of the genome, the viral genome that come from somewhere else.
AD: Yeah. And viruses don't have particularly good correction mechanisms such as things like you and I have for if there's a dodgy bit of genetic tissue in there, it might not be particularly good at clearing it out.
MM: Andy, the surveillance that's happened so far for COVID-19, has that mostly happened from animals that are in these wet markets, or is some of this information coming from wild populations, wildlife out in the field?
AD: I think it comes from three sources. You could, people have been going around the various wet markets to collect tissue, but obviously people are slightly concerned if you're taking tissue, and that you're just sort of surreptitiously ordering some food and then taking the tissue sample with you, which always looks a bit dodgy. People are also going into the wild, just if you want to get an overview, not everything in the wild gets into the whole food markets, the wet food markets. I shouldn't call them whole foods, the wet food markets. So, getting a broad perspective on how much viral diversity out there requires you to go and sample species in the wild. I mean, people go out and sample birds, bats, small mammals, to try and see just how much is out there and how similar are what's in the bats to what's in the small mammals, or is it more similar to what's in the birds, and trying to get a picture of this because it's trying to understand the diversity of life on this planet is still the greatest scientific challenge in this century, and a huge amount of that biodiversity is the parasites that live in the things that we are focused on.
06:39
MM: Right. Do we have a sense yet of which bats or which group of bats? I mean bats are, like you're talking about, they're an incredibly diverse group of animals.
AD: Yeah. I mean bats are one of the most diverse mammal groups, along with the sort of small mammals. They are essentially divided into two major groups, the bigger fruit bats, and anything that's bigger is more appealing for people to eat, because you got a meal for a family of it rather than a small snack for a sort of hungry person. So it tends to be the larger bats that get eaten, but there is as much of a radiation of these parasites across the bats as there is across the small mammals. There's a huge diversity of, you know, some bat families have lots of different species in them, some bat families have one or two species in them, and the diversity of the parasites in the bats reflects the diversity of bat species within the families.
07:38
MM: Hm okay. So there has been a lot of conversation in the scientific literature for quite a while but especially in the last 20 to 25 years about whether bats are special, and the way that you articulated that there are certain families of bats that are more speciose, and in those families there are not surprisingly more viruses and other microbes to be found. It was in fact there was just a paper in PNAS today that's generated a lot of attention on that front. But in a broad way, are bats special? What evidence do we have that bats are different than other mammals?
AD: Well, as a generality, everything is special in one way or another. We have an understanding of immunology that comes the distorted perspective of mainly having looked at humans, having looked at mice, because that's a handy laboratory model, so that also reflects a lot of what may be going on in other small mammals, but not necessarily the full diversity of things that are out there, and then the veterinary things we look at -- dogs, cats, sheep, horses, pigs. There is a huge amount of mammalian diversity. The thing that makes bats unusual is that they fly, which is a sort of trivial statement, but the difference between flying and non-flying is that you have hollow bones to be able to fly. So birds have hollow bones, bats have hollow bones. The cows, sheep, dogs, zebras, elephants, have bones that are full of bone marrow. And where you produce a significant amount of your immune cells is in your bone marrow, so if you have hollow bones, how does your immune system work, or does it work in a different way? And if your immune system is working in a subtly different way, does that mean that it's really good at fighting some types of pathogens, but not very good at fighting others? And if those pathogens that you fight really well as a bat get into something else, do they go around and cause much more damage because the immune system of those other things isn't as well geared up to fight them? And again, it's part of this huge desire to understand biological diversity. Moving away from our human-centric view of it will give us many more perspectives on how these things evolved and how different groups of species interact with each other.
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10:08
MM: So let's, I don't really know how much our audience really loves immunology, but I think everybody listening knows now that it's one of my favorite things, so if you'll indulge one little nuance about the immune system that's really fascinated me. I guess it's two dimensions though, Andy. It's crazy that we don't know more about bat immune systems, right. I mean I think, you know, to represent, they fly and they probably don't have parts of their immune system because they don't have places to make it, that's true, but my gosh these things are conspicuous for causing so much problems for people. It would seem to be the first thing that we would go and look at, so A. why don't we have more of an immunology for bats, and B. this neat thing that we seem to have discovered that their interferon response is not like most other mammal species that we've studied before?
AD: Well, I think there's a couple of things there. You know, when we first, twenty years ago, twenty-five years ago when people started getting really worried about emerging diseases, largely the appearance of HIV and they realized there are going to be other things coming across. People began to get concerned about bats. We had one person who was a bat immunologist. I mean A. they're very hard to keep as laboratory models, B. there was much more money if you've done the sort of veterinary or medical training to work on immunology. All the money is in mice and humans and domestic livestock. You were regarded as eccentric if you went off and worked on bats, and who's going to give you money for that? And if you put a grant in, most of the time people would say, "That's very interesting, but you know much better to this research on a mouse system than on a bat system." So it took a while for people to say, actually, there's a big thing different here, you know, people being lucky if you use your startup money you don't have to do a whole NSF grant where they persuade you to work on mice or Drosophila, you can actually go and do something creative and new. So, few people doing that began to discover things that said actually we really need to look at this more seriously.
12:15
MM: And one of those was this sort of interferon response, where, as I understand it, multiple bat species now have this kind of high-standing level of interferons that you don't usually see. It's one of those protein cysitic (spelling?) kinds, it's kind of turned on when bad guys like viruses show up on the scene, but otherwise it's at relatively low levels.
AD: The other thing about the immune system, I was thinking, go back to the very early immunology lectures I had is that I always think of it as being most similar to the "Tom and Jerry" cartoons, where you have the small mouse that comes in and is the pathogen, and your immune system is the cat that's trying to catch it. And although we think of the virus as being the mouse, as being the bad thing, the cat which is the immune system is doing as much damage to you as the mouse is. Because it's like, "What is this thing, I'm trying to get rid of it" but you know it's rushing around with a broom breaking things. And that's a lot of what we're seeing with COVID. Lots of these people who are getting really sick and dying, that's because their immune system is overreacting to this weird thing, and that virus would much rather be in a bat, where an immune system that is used to dealing with something like that would deal with it. So it's these things that are jumping across that create chaos because the cats that's the immune system don't know how to deal with these particular types of mice.
MM: Right, yeah. And there's one dimension of, I guess a paper that you and Cara Brook wrote, I think it was intrinsic microbiology a few years back, that extends off of your arguments about flight that, you know, bats live so much longer than mammals of similar body size, and one of the ways that they do that may be sort of an extension that comes off of their flying. When things fly, they're metabolizing a lot of energy, a lot of that metabolism generates all of these kind of flying vases and broken toasters and all of the other stuff that the mice knock over, or the cat's knocking over as it's running around the immune system. So bats seem to have evolved this kind of strong antioxidant protection that's not in other places. So, like you say, the viruses can sort of hang out there, do their thing, and not wreak the havoc that they seem to be doing with humans.
14:20
AD: I mean, same with viruses and any other type of pathogen. It's used to being in a particular type of host, and when it gets into something that it hasn't been in before, it's not particularly sentient but it's wandering around trying to locate the cues or being driven by the wrong cues to do the wrong thing. And you know, it's as unhappy as you are for having you in it.
AW: I want to riff off of that idea and bring up the sort of parallel idea that you talked about in a recent transmission essay, a set of essays put out by the Santa Fe Institute, and you said a lot of interesting things in this essay, but you had a thing that caught my eye about interspecies transmission of pathogens and viruses and the effects of body size and sort of relative rates of transmission among species of different body size. And you said if we increase between species transmission to levels where it matches within species transmission, then the small species can use the pathogen to drive the larger species extinct. So, maybe explain those dynamics, and what are the risks for the large bodied species out there?
AD: Well, that was the, I mean, one of the things I've been interested in for 10 to 20 years. It's what happens if you have systems where you've got multiple hosts and a single species of pathogen, or multiple pathogens in a single species of host, moving beyond our sort of standard way where we've learned a lot is looking at one parasite - one host type models. Now if you start looking at shared pathogens, that is the sort of general case of what happens when one pathogen jumps from one host species to another. So can we try and understand the dynamics of that? Now, the dynamics for one of the things I'm going to get at is that if we look at pathogens in different populations, those can be different populations and different species, or they can be different populations of the same species that are isolated from each other in different ways. So one of the things I think is important with COVID is it may well be circulating, or once it gets established it'll circulate in younger people, initially we thought without causing much damage, but increasingly we're seeing worrying signs of damage even in young people. The people who are most at risk are the older people, how connected are the younger people to the older people, and could it continue circulating quite happily in the younger people but cause catastrophe once it gets into the older people. And so trying to understand how different subpopulations are coupled together and that again get some of the things we are seeing at the moment, once COVID gets into the United States or China, it takes off in the bigger cities, and we've seen the sort of tragic things like we're seeing in New York, San Francisco, New Orleans, where you get a huge epidemic in the city and then everyone in the rural areas is saying, well, you know, it's not affecting us, hardly anybody out here is sick, but that's because the rural areas are only weakly coupled to the larger cities. Once it spreads into the rural areas, the same thing'll happen. It'll just take longer and spread more slowly in those rural areas, but then you get the problem is that the cities will begin, they'll have created some level of immunity where infections goes down in the city, and they're just thinking that everybody's fine, when it drifts back from the rural areas again. So, getting at how different populations and sections of the populations are coupled together is vital to understand the dynamics of this. So in that essay for Santa Fe Institute, I was pointing out that if we look at different species, because different species have different birth and death rates, if you've got a fast birth rate, you can recover quickly from infection. If you have a slow one, you recover more slowly, but if you get reinfected from the larger numbers of the smaller species, that can eventually drive you extinct.
18:23
AW: So the evolutionary dynamics of the pathogens of the small species, those evolve characteristics that make them particularly dangerous to the large-bodied, slow lifestyle species.
AD: And then the sort of scary analogy to that is the sort of rapid growth of younger people in the human population where they're able to withstand the disease, will that cause it to spill over into the older people where they don't come back from being infected as well?
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18:58
MM: So, you mentioned Peter Daszak earlier, so there was an article in Politico this morning that said that the NIH pulled money from collaboration that EcoHealth Alliance had ongoing, I think it was NIH supporting collaboration with one of the Chinese research institutes in Wuhan. Do you know anything about this? It was on bats, I believe.
AD: It was. Well, the EcoHealth Alliance, as part of program, has been doing surveys of bat pathogens throughout Southeast Asia and other parts of the world, training lots of people, so we have more people out there who could do this work of identifying viruses, the labs in Wuhan as well as several other labs in Wuhan were obvious people to develop collaborations with, because it's in an area of China where you can get out into the rural areas, you also have markets you could sample. And the basis of science is building collaborations, particularly across countries, to areas where different people are working on different things. And so I think Peter had actually been doing a phenomenally good job at developing relationships with the Chinese. He also, when this whole virus first appeared, and there was this tendency for people to blame the Chinese, Peter got together a group of people who wrote a high level letter to the Lancet to say actually we need to collaborate with China on this, and there are excellent Chinese scientists who've been very good from the beginning, of sharing their genetic material and putting it out there for different people around the world to use so we could begin to develop A. the vaccines and B. the serology test. So the Chinese got on top of that very very quickly, largely thanks to Peter working with them and developing good relationships with them. So to have him sort of have that funding withdrawn, I think is very short sighted
MM: And the funding withdrawal, I mean I haven't had a lot of funding from NIH myself, but it's fairly atypical from federal agencies this far along on a project to have funding pulled. I mean that's a pretty specific type of an approach, no?
AD: Well, spiteful might be the word you're looking for. But it's also that grant, I think, had ended, and always when you have a grant you have a, usually an extra year, you get a what's called a no cost extension to spend out whatever funds are still available, usually so as you can put, pull things together to apply for your next round of funding. And that's what Peter was using it for. And in fact, he had been writing a grant before this all happened, to look at coronaviruses across Southeast Asia, because people have consistently felt for about the last decade, that if we're going to get a major pandemic, it might well be influenza, but it could also be a coronavirus. And so having that bigger understanding and going to the parts of the world where it was likely to emerge, is the most sensible thing you can do. So coming off that makes this much more susceptible, I mean, this isn't the last virus that's going to come over, they're coming over about once every five years. We really need to know what's out there and be better prepared next time, and the way to do that is to have people like Peter going out and doing those surveys. So it's a spectacular way for NIH to shoot itself in the other foot.
22:27
AW: Well, let's come back to the situation in the US. And let me preface this by saying, we talked to John Drake from the University of Georgia about six weeks ago, and I was just listening to the intro of that again, and Marty and I were summarizing the caseloads and deaths from COVID in the US, and at that point there were about 1,500 infections and 40 deaths in the US. And it was just very strange to hear this because, you know, so much has happened in six weeks, and it feels like it's six months or six years later, and here we are, just a few weeks later, you know, a million plus cases and 50,000 plus deaths. So what, just from your point of view, what happened and what is going to happen going forward, and are we successfully flattening the curve?
AD: It has certainly been a strange spring. It's literally, I, first heads-up I got on this was actually the 30th of December last year. My son was putting together his annual New Year's Eve party in the house, which is full chaos. So I was quietly sitting, literally at this computer, looking at things and there was a report that came through on ProMed that actually Peter Daszak had [couldn't distinguish here] to me and says, this looks weird, and it was a report of this thing in Wuhan and I thought, "Huh, that is kind of strange." So I sort of printed it out and kept it. And then as things became to take off, I did what any nerd does, I just copied down the data coming out every day and was sort of plotting it out for Wuhan, then for China, and for the rest of the world, going, "This is really not good news." And you know, a bunch of us started talking about it, and then I teach my course which I've taught for about 20 years now on the ecology and evolution of parasites, and I now teach that in Panama, I think Marty took maybe when it was on campus. But I always have this sort of lecture where I sort of say at the beginning of the course, "Usually when we teach this course in the spring, there's some global disease outbreak somewhere." It was foot-in-mouth one year, and it was bovine spongiform encephalitis, it was SARS, it was Zika. And I said, "This year looks really serious, so we should monitor this in the course of the class, because I'm worried it might sort of affect your ability to sort of stay on down in Panama for the other two courses." By the last week, we realized that the students were going to have to get out of Panama and come back, and we just are going to have to come back and probably the university was going to shut down, so it happened really really quickly.
AW: So in terms of just responses within the US, what do you think we've done right, and what have we done wrong? And how important are these university closures, right? I mean, that to me, that hits home too, because obviously University of Montana has been shut down also, but you know, what does that do to the dynamics of transmission?
25:17
AD: I mean, transmission is always contacts between people. And I guess, when I was, I guess I was in Panama from the 24th of February until the 13th of March, the end of the first week when I was there, there was a paper that came out in the Lancet saying for people in Imperial College had been using a model that then Roy Anderson who trained a lot of those people published a paper in the Lancet saying, "We really have to massively social distance people if we are going to flatten this epidemic curve out, because the current trajectory suggests it will overwhelm the health services we have to be able to deal with it." So that I think came out on the Friday, by the Monday or Tuesday people realized we were going to have to do something serious about slowing the economy down by way of reducing interactions between people. It's always easy to say we didn't do things quickly enough, but you know, as I said, the 30th of December we noticed something weird was happening. And it's a sort of how long does it take, you know, me plotting out data from Johns Hopkins coming in, other people, when did we get to feel nervous? And I think people have different levels of nervousness when they begin to think this is something we have to do something about, and when will people believe that we really have to do something? So it was always going to be that different countries were going to react to different speeds. People can blame people later, but I don't think that's what we should be thinking about in the moment. It's like, what can we do, how long do we have to sustain that for, and then plainly we can't completely sacrifice the economy. We have to start thinking of how can we logistically get different groups of people back to work to get things going again in a way that we can stop all that if it looks as if the number of cases start going up again. And we've got to do that against this sort of background of the different populations that maybe it's gone through the big cities and has moved into rural areas and is spreading more slowly. There's different levels of hospital capacity out there. We've also taken lots of medical people, nurses from the rural areas, into the cities. They've now got to go back and keep fighting this as the cities come down. As with all these things, we have to experiment, but we have shut down that experiment of getting things going again if it just increases the scale of the epidemic again. You know, in your dream world you'd want to be like New Zealand, to have done everything really efficiently, have closed it down and say, "Now, we're now getting less than one case a day. With luck, we will get rid of it within New Zealand within a month, but then what does New Zealand do about reconnecting itself to the rest of the world?
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28:21
MM: Andy, what do you think, what's life going to be like over the next six weeks, and I mean maybe this whole, this talk that we constantly hear about, that it's going to go away in the summer, and then maybe it's going to come back with a vengeance in the fall?
AD: Well, I mean, the perception that this would go away in the summer I think comes from a perception that influenza and the common cold tend to die back in the summer. Similarly, measles, which is the sort of poster child for all the diseases like this, have very strong seasonal cycles. Those seasonal cycles are driven as much by the school terms as anything else, because it's kids getting together that give the system a kick out the [can't distinguish what he said] and make everything much bigger. For you to have seasonality though, you have to have high levels of herd immunity in the first place. So to get any pronounced seasonal signal, you have to have lots of people immune, so it's suddenly an increase in the numbers of susceptibles meeting together, usually new kids starting school, or mixing with different kids you haven't mixed with before that give you that seasonal signal. If you haven't got herd immunity, you're not really going to see a seasonal signal, because having a massive number of susceptible people out there, the epidemic's just going to keep growing and growing. So I think more what we're going to see is this moving out from the big cities and into large towns, cities in more areas away from the coasts, and then into rural areas. So it's just going to keep going and going. So it's like summer will appear, but we're not, the diminishing we're going to see is a flattening out spatially across the US with different little epidemics all sort of coupled together.
MM: And the appearance of herd immunity, I mean we're quite a ways from anything like that. Usually 60 to 70 percent of a population would have to be immune for that to be effective, correct?
AD: Yes. We think it would be, I mean people's estimates are of R0, the rate of spread of the disease that gives your relatively good rule of thumb for what the levels of herd immunity would be. So if R0 is about two, then it's 1 minus 1 over 2, so 50% of people would give you herd immunity. If R0 is 4, then it's 1 minus 1 over 4, which is like 75% of people. That also assumes that immunity lasts forever like it does for measles. You know, if it lasts for the rest of your life then that's good. You've got herd immunity where you could control the disease. We don't know how long herd immunity, how long immunity to people lasts for this. So if the immunity lasts for a year, then this thing will keep circulating and people will keep getting it again. If we have a vaccine, which we hope we will eventually get, but that vaccine immunity will probably only last for a year, so people will have to be vaccinated every year.
31:28
AW: Are you optimistic about vaccine development? I mean, do you think we have one on the horizon within some reasonable time frame?
AD: Well, what I first started out doing this, HIV appeared. We were told when HIV appeared, "We'll have a vaccine in two years." And then it was like 4 years, and then it was like 8 years... We haven't got an HIV vaccine. I've had colleagues who spend their whole career working on a malaria vaccine, we don't have a malaria vaccine. This, but those are more complicated pathogens. There are hundreds of drug companies that'll tell you "We'll have a vaccine within a year." But you know, we've only ever eradicated two diseases with vaccines -- smallpox and rinderpest. Well, you know, one domestic livestock pathogen, one human pathogen. The original vaccines for both of those were developed in the 1760s. So, time from initial vaccine trial to eradication was 250 years, plus or minus two years for those two things.
AW: So what about the biology of the pathogens affects how easy it is to get a vaccine developed?
AD: It's a mix of the delightful natural history of the, you know, which sites is it going to, and which parts of the immune system is it switching on. I personally think the physical size, which correlates massively with the genome size for pathogens is important. The bigger it is, the harder it is to produce a vaccine. But the other side of that is the bigger it is, maybe the easier it is to produce a treatment because you've got something you can physically hit. So washing your hands is really effective against this thing, because it's a big chunky thing that it has this sort of globular outside which just melts when exposed to, you know, the sort of soapy water. So although there's lots of talk of a vaccine, I actually think we should be having certainly as much discussion of potential treatments. Not the least, because if you come up with a vaccine, who's going to do a voluntary vaccine trial unless you've got a treatment to cure them once you've, you know, half the people get given the pathogen, half of them, then you give them the vaccine. You need to know you can treat them if they get sick from the vaccine, or you've got to give them the disease and hope the vaccine is protecting them. So you need some form of treatment, so going for a treatment first may be as powerful of a way to go as going for a vaccine.
34:07
MM: Hmm. And are there treatments of which you are aware that sort of seem suitable, promising, if we want to use a vaccine or just in general?
AD: I mean, there's plainly going to be lots of people working on this. I mean, the Chinese again, I thought even when I was still down in Panama, so that would be the very beginning of March, just looked at every single compound that they had and tried it against this thing in cell culture. So that sort of shotgun approach might well turn up something. And I think, you know, other nations should be doing similar things. We, as with all these things, we're seeing a sort of strange sort of correlations. There's this thing that people are noticing in African countries that people have had the BCG examination, which, vaccination, which some countries still do routinely, particularly if TB is a problem. People who have had the BCG vaccination don't seem to be as susceptible to COVID as other people, but that seems to be correlative evidence rather than any definitive test that people have done. But if it is something like that, then scaling up vaccine production of that would be good, because the other problem we have with a vaccine is the world has a finite vaccine production capability. If we suddenly had a vaccine for COVID and we had to vaccinate 9 billion people every year, our ability to produce influenza vaccines, measles vaccines, and other vaccines would plummet. So now we're going to need to invest in vaccine making companies and the technology to make vaccines more efficiently, so growing things up in chickens' eggs is a slow way to cure a disease. You know, have we got enough chickens to make that many eggs to grow that many vaccines in is a nontrivial problem.
MM: So, maybe that's a good transition, an opportunity for a transmission to the what does the world look like in the near future once we start to get, either we start to get COVID under control, or we're with it long enough that we just have to change the ways that we're doing things. I mean we're not going to be able to social distance to the extent that we are now.
36:29
AD: I, the optimist in me, thinks "Oh, maybe we'll be through this in a year, 18 months time." But the sort of pragmatist in me says, "No, actually I think we've really got to rethink lots of the way in which people socialize, which is a huge effect of how the economy is going to work." We've certainly got to prepare much more strongly against this type of thing happening again, both in terms of knowing more about what's out there, stopping the processes that allow things to come across, which is a mixture of closing down the food trade in species we really shouldn't be eating.You kind of, I think this, it's an exaggeration to say we need to close the wet markets. It's a bit like saying "We need to close the Trenton Farmers Market," where I go every week in New Jersey for my vegetables. That's effectively a wet market in New Jersey because it sells fish. Most people in China like to have fresh fish, fresh vegetables, that's the definition of a wet market. So you can't close down people's access to fresh food. That is totally bonkers. But we need to close down the aspects that are dealing with the trade in wildlife that's potentially harmful to human health. The other thing you have to do is go back up the pipeline from there. Most of these pathogens are coming from areas of broad-scale deforestation where people are going in and getting exposed to that thing and then coming into town sick with things. So we have to rescale what we are going to do about global deforestation, but that would have multiple other benefits. So that's one aspect of the world that's got to change, and we have to learn, maybe people will find that actually working from home is even nicer than working in an office, and the economy could work quite well like that. Much harder to teach students, or kids at school that way. You have to find some way of teaching people that's both safe for the children and safe for the people teaching.
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38:39
AW: It seems like, you know, somebody or some organizations or perhaps some governments are going to decide that bats themselves are too dangerous, and that we should do something, you know, to eradicate one or more species of bats. What would you say to people who make that argument?
AD: Bats are massively bringing more benefits to humans than they are causing harm. This problem with this farce emerging isn't a problem with the bats, it's a problem with people being stupid, and people being stupid at every chain along the way in many ways. So, having a better understanding of the way the natural world works and interfering in less of a belligerent and less edifying way would really make things much better. I don't, absolutely not say impossible to reduce the number of bats, but just totally stupid and totally counterproductive. And, you know, it's not necessarily true that the next pathogen that'll come along in 3 to 5 years will come from a bat. It's just as likely it could be influenza that comes from ducks. Are we going to eradicate all of the world's ducks? It could be another vector borne disease like Zika, though the potential for a vector borne disease to take off isn't as big as it is for one of these directly transmitted diseases. But it's better to learn how to manage the world, you know, and have those pathogens stay in different parts of it, and maybe have humans spend less time in those other parts of it than for us to think we know anything about managing as complex a system as the natural world.
MM: You mentioned a minute ago Andy that one of the really important things going forward is surveillance, looking for the next big one, and the gripe, somewhat reasonably, has been in the past that it's really difficult and it's very expensive to do it, I mean exhaustively for sure, but even well. So, what kind of perspective, what advice maybe, do you have for how we look for the next zoonotic threat?
40:46
AD: I think the expense, the relative cost of spending, 50 to 100 million a year, on programs sort of training up people to be experts on tropical diseases, versus the 5 to 10 trillion dollars we've lost this year already, is trivial. So the surveillance, you have the capacity building benefits, and I think part of the criticism of the surveillance stems from the fact that people said "We'll be able to identify the next disease." We won't be able to do that, and we will miss things. I mean, think of HIV. If you'd gone and taken this virus out of a monkey, you put it in people, nobody gets sick for 5 or 10 years, you wouldn't be worried about that. And then, when it comes across and you realize how it works, you realize that could have halved the population of Africa, it was such an unpleasant pathogen. It also tells you, yeah, these things aren't produced by weird people who hate society with lab coats, behind the scenes, because the smartest ones are so much smarter than the one [word was unclear here] people's perception that we make something really nasty and it kills people really quickly. You don't do it that way. You make something that operates really slowly. The other side to that is you don't want to predict exactly what the next one is. You want to do this thing of having a huge genetic library of what the different things are that are out there to being to get some understanding of how they function. Because, you know, once we've got the genetics, we don't really know which ones are going to be pathological, which ones are, how long they're going to transmit for, whether they're going to show symptoms. We haven't got the genetic machinery to do that. But when something appears, as happened this time, we need a big enough library to say, "This thing is from that type of species, from that particular region, what were we doing in that region that caused this to come across, because we need to stop doing that in that region." So the surveillance is building up that library, which is knowledge. And eventually, if we're around long enough, and it won't be tomorrow and it won't be this decade, we'll have the genetic techniques to be able to say, "Actually, those set of genetic signatures mean this is like going to be a much nastier pathogen than that." In another 50 years we'll be able to say, "Oh, those genetic things mean the incubation thing and time of that is going to be about 2 days, 3 days, 4 days." But that's a long, long way down the pipeline, so better to build up that library now.
43:28
AW: It's been total thrill to talk to you Andy, this is I think a good place to stop. But we also like to ask at the very end just if there's anything else you'd like to say, anything we didn't cover that's on your mind?
AD: Well, it's also been a great pleasure to talk with both of you. It's, the thing that constantly is in the back of my mind whenever we talk about this, this is something that we knew was going to happen. And scientists sort of warned against it and you know, we need to prepare ourselves for things like this. We've been saying exactly the same thing about climate change, and that's as big a worry still as this. Scientists with many many more people, scientists working on climate change and this, and we all know that that is an equally big problem. It may come in more slowly, but it's going to be just as devastating as this is. So, having the politicians listen a bit more to the scientists isn't going to harm at all.
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44:36
AW: This is the second episode we've released about the new coronavirus. In Episode 38, we talked to John Drake at the University of Georgia about the challenges of modeling the new disease and some of the best ways to slow down the spread.
MM: If you liked this episode, you might also want to check out our conversations with disease ecologist Barbara Han in Episode 5, and our chat with Felicia Keesing and Rick Ostfeld in Episode 32. Those shows too cover diseases we get from wildlife.
AW: We also want to remind you that we are in the middle of a fund drive for Season 3. We know it's a tough time to ask, but if you can, we really need your support. You can make a one-time donation on our webpage, www.bigbiology.org, or a recurring donation through our Patreon page, patreon.com/bigbio.
MM: Patrons also get to submit questions for our guests and get access to show notes and extra audio. If you can't afford to donate money right now, instead, please go to iTunes and give us a rating, or share Big Biology with your friends over social media.
AW: Thanks to Matt Blois for producing this episode, Mike Levine manages our social media accounts and produces the Student Spotlights, and Dana Baxter helps with background research. As always, Steve Lein manages the website.
MM: Thanks to the College of Public Health at the University of South Florida, and the Colleges of Humanities and Sciences at the University of Montana for support.
AW: Music on the episode is from Poddington Bear.