Hi, I'm Aaron Welsh and this is this podcast will kill You. I'm back with another bonus episode in our mini series of bonus content that will be releasing over
the next few months. In case this is the first bonus episode you're tuning into and you're wondering what the heck is going on, I'm using these episodes as an opportunity to explore more about whatever disease or topic we covered in our previous week's episode, and also to get to chat with experts about their jobs, their hopes, their dreams,
whatever comes to mind. If you've listened to the podcast before, you know that I'm kind of a relentless question asker, and so instead of just pestering Aaron Updyke with all the questions, I'm saving some for these episodes, and so far I've gotten to have some great conversations with people in very different careers, studying or working on very different problems. And this week I am so excited to have yet another fun conversation and learn a whole lot more about
another topic. So what am I going through be talking about today? This week really kind of picks up where we left off in our most recent regular season episode. Which covered a virus of rabbits called the Maxoma virus. If you haven't listened to that episode yet, I would recommend check it out before listening to this, just because there's so much more to that story, but I'll give
a quick recap here. The Maxoma virus is a type of poxvirus that can cause severe disease in some species of rabbits, and it became internationally famous back in the nineteen fifties when it was introduced to Australia as part of efforts to control the invasive European rabbit population. What had started out as a handful of European rabbits introduced to Australia in eighteen fifty nine had within a few
decades grown to an absolute ecological and agricultural menace. Entire ecosystems were disrupted, native animals experienced tremendous population declines, many plant species were driven locally or regionally extinct, and huge tracts of land could no longer be used for agriculture. The introduction of the Maxoma virus did help to drive down or stabilize rabbit populations, but over generations the virus
lost a bit of its impact. As both rabbit and mixomavirus adapted to one another, the deadly virus was no longer as deadly as it once was, and the rabbit was no longer as susceptible as it used to be.
So when another lethal virus of European rabbits was identified in the nineteen eighties, the rabbit hemorrhagic disease virus or RHDV, it was explored as another possible form of biocontrol for rabbits in Australia, and RHDV was introduced in the mid nineteen nineties, again helping to keep rabbit populations under control. But the story of rabbits in Australia doesn't end there, and neither does the story of the rabbit hemorrhagic disease virus.
In twenty ten, a new type of the virus was discovered in France, the aptly named rabbit hemorrhagic disease virus type two, and this one doesn't seem limited to just European rabbit populations. Since its discovery, RHDV two has spread around the world and has led to concerns for demmestic pet rabbits as well as the wild rabbits and hairs that are susceptible, especially in places which have already seen
damaging ecological cascades from RHDV one. So what I really wanted to explore in this bonus episode was these two viruses.
RHDV one and rhdv two.
Where did they come from? What effects have they had on rabbit populations? Are they following the same evolutionary patterns as maxomavirus, How worried should we be? And to help me answer these questions and so many more, is doctor Robin Hall, veterinary virologist and team leader for the rabbit Biocontrol team at CSIRO, the Commonwealth Scientific and Industrial Research Organization,
which is a government agency in Australia. I am super excited to jump into this interview, so I'll just take a quick break here and then we'll get started.
Hi. I'm Robin Hall.
I'm a veterinary virologist and epidemiologist at the Commonwealth Scientific and Industrial Research Organization or CSIRO, based in Canberra, Australia, team leader for the rabbit buyer Control team here, and I have a special interest in host pathogen interactions, management of invasive species and viral evolution.
Awesome.
Thank you so much for taking the time to chat with me today.
I am thrilled thanks for the opportunity. It's really exciting for me.
So in our episode on mixed and mitosis, Erin and I talked a lot about the long history of European rabbits in Australia and how this invsive species has been incredibly damaging both ecologically and economically, and I was wondering if you could bring us up to speed on the current situation with rabbits in Australia, like what do we know about the impact that they're still having and where does their continued presence seem to be the most problematic.
You know, back in the nineteen fifties, rabbits were at massive plague proportions throughout Australia, and then with the introduction of mixomavirus, it was incredibly effective in reducing population numbers, but of course populations begin to recover over time, and so in the mid nineties RHDV or rabbit hemorrhagic disease virus was released again with massive declines in rabbit populations,
but over time. You know, bio controls are not a silver bullet, and once more rabbit populations began to increase, and so that led to in twenty seventeen, the release of a new variant of RHDV, which we call K five in Australia, and again we're still seeing the impacts from both the K five release and the arrival of this new virus, rhdiv two in Australia which was not deliberately released but has spread here as it has globally.
And so currently rabbit populations are relatively suppressed to comparatively to what they have been in the past, but we do still see considerable impacts, and these fluctuate on a bit of a boom and bust cycle. You know, when conditions are good, the populations will breed very rapidly and increase in size, and if we go into a period
of drought, then populations can decline again. So the impacts we see are really most obvious in environmentally sensitive areas, so particularly in the arid and semi arid zones where rabbits compete with native species for food and shelter, and they eat native plants that are already finding it difficult
to grow in these arid conditions. And then obvious course in agricultural industries as well, where they impact crops through grazing, they damage the soil, they compete with livestock for food, and again particularly in drought conditions, those impacts are more severe. And they also Rabbits also have some perhaps less considered impacts, so things like they impact our indigenous cultural heritage sites by damaging these artifacts and sacred sites and things, and
even the impact of reducing the vegetation. I mean that then exposes more soil, and the soil can then blow into the.
Fleece of sheep which reduces fleace quality.
So there's this really sort of lead on effects and they really have dramatic impacts that are quite wide ranging and both direct and indirect.
Our last episode focused on one of the most impactful tools for rabbit control in Australia, of course, the maxomavirus, and we also briefly mentioned the rabbit hemorrhagic disease virus, which I cannot wait.
To ask you more about.
But these two biocontrol agents, they're not the only tools used to try to suppress rabbit population, So can you talk about the other methods that are used.
When we talk about a control tool, you really want something that's going to be effective, relatively cheap or easy to distribute, and viruses are really the only thing that we have that are self disseminating that work on a landscape scale with the existing technologies. However, certainly at local levels there are a lot of other tools that can
be used. So particularly poisons are used quite heavily, so pindone, but also ten eighty so pin done is an anticoagulant, so it's like rat baits sort of, and ten eighty as a metabolic topsin. We also focus a lot on habitat removal, so destroying the warrens or if they're harboring in you know, shrubs, removing the shrubbery where possible shooting
and trapping can be employed. On a local level, exclusion fencing has been applied so where you you know, put up fences that keep the rabbits out, but again you have to dig it down and put it up relative high. And then warren fumigation where you introduce like a gas
into the warren to kill them. So all of those other methods they are very effective at local levels, but as you can imagine, they're quite labor intensive and certainly, you know we can't use them across the landscape scale of Australia.
So now I am so excited because I get to ask about rabbit hemorrhagic disease virus.
I read that this is a calisivirus.
What does that mean?
Like, are there other types of callisi viruses?
Yep, I'm very happy to talk about URHDV as well. So yeah, RHDV is a kalisivirus. These are small RNA viruses. So like the coronavirus is an RNA virus as well, it has an RNA genome, but coronaviruses have like thirty thousand letters in their genetic code, whereas these caliciviruses have like seven and a half thousand letters, So we call them small RNA viruses.
The shell or the.
Capsid that the genome is packaged into is non enveloped, and so that means that they're incredibly environmentally resistant. So like I think, again, we hopefully all know now with coronavirus that you know, it doesn't survive particularly long on surfaces, and it does use droplets and things like that, it's protected in that moist droplet environment, whereas kalisivirus is because they're non enveloped, they can survive on surfaces or in
soil or something for months. Chalciviruses are pretty common and probably occur in most, if not all, vertebrate species, although we are really only starting to look at the virus sphere more broadly, but some that you may have heard of would include like human neurovirus, feline chalicivirus, so it's
something that we vaccinate our pet cats for. And then there are kalsiviruses of you know, cows, mice, pigs, chickens, atlantic salmon, so yeah, it's a big family, and the rabbit and hair ones there as well.
How are these viruses transmitted, or maybe in particular, how is RHDV transmitted?
A lot of the calisi viruses are transmitted by the fecal oral roots, so you know, you ingest them either from a contaminated surface or something like that, and then they replicating the body they're passed out in the feces and then contaminate their environment, and so RHDV broadly follows that process. However, because again this environmental stability, RHDV can also get picked up mechanically by insects, so particularly carryon flies.
The typical life circle for an rhdv virus is it's ingested somehow, so either you know, the grass is contaminated and the rabbit eats it, or the rabbit sniffs a dead rabbit and gets it in that way, or a blowfly comes and lands on like the eyelids of a healthy rabbit and deposits some virus there, and then the rabbit rooms itself and eats it the virus that way.
The virus then go into the gut, enters the animals systemically and causes this major infection that we can talk about in the second and then the rabbit dies typically within forty six to seventy two hours post infection, so this thing is incredibly incredibly fast. And then the carcass starts to break down and contaminates the environment and the flies can come in and pick it up and move it between populations.
What's going on at the path of physiological level, and like, what's a typical course of infection?
What does that look like?
So from the outside you frequently don't see clinical signs, which I guess is great from a by control perspective, because the welfare is actually I mean, anything that kills something you don't want to say welfare is good, but it certainly has less impact on the animal than something like say mixomavirus. So many pet owners, you know, we often hear that, oh, it was fine, it was eating the night before I came in in the morning it was and so you often find them still with food
in their mouth. And so it does happen very quickly, and frequently you don't see any clinical signs in the rabbit unless you're sort of taking temperatures every few hours or something at the path of physiological level. Basically, what
happens is the virus goes in. It targets the liver, so it starts to replicate in the liver, and it causes this massive hepatitis that all a liver cell start to bust open and the liver just pretty much disintegrates, I guess, And so that leads to you know, a cytokine storm as such, and so you get this massive systemic inflammatory response syndrome, disseminated intravascular coagulation and you know,
circulatory shock and death. And so that sounds all very awful and it is, I guess, but it's a fairly typical hemorrhagic fever virus so you know, some people have referred to it as bunny a bola and things like that, But basically, the virus goes in, causes a lot of damage to the internal organs, sets up this massive inflammatory response, and then the body's just overwhelmed.
And so is that courus of infection?
Is that fairly consistent across individuals within a population.
Or within a species?
And how variable is that a cross species as well?
So RHDV is incredibly species specific. So there's a couple of different variants of RHDV. RHDV one was like the original RHDV that was first reported in sort of the nineteen eighties, and that RHDV one only affect European rabbits, so there's no definitive evidence that it can replicate in
any other species. Then in twenty ten, a new variant called RHDV two emerged, and what we saw with RHGV two is that it can also infect other lagomorph species, so hares or jack rabbits, the Lepis species, and then also the cottontails or the silver lagas species. But still people are looking and have looked, and there's no evidence of any disease outside of those lagomorph species, within a species,
or within individuals, within naive individuals. Certainly, the disease courses is pretty typical, and we see a case fatality rate, you know, upwards of ninety five percent, ninety nine percent, So it's it is very very consistent. In animals that have some degree of pre existing immunity, then the infection can look quite different. So you may get prolonged infections, they may get a subclinical heptitis with jaundice and things like that, and then secondary liver disease. But again that
sort of depends on the level of immunity. But in naive individuals, it's very very consistent with an extraordinarily high case fatality rate.
Where did these viruses come from? What do we know about the origins either of RHGV one or RHDV two.
Yeah, I mean, where the viruses come from, that's the question.
It is so certainly, you know, when i HGV one emerged in the nineteen eighties, it was reported in Angora rabbits in China. These rabbits are being bred for and they just observed these mass mortality events, so it was pretty clear that something was going on, and they identified this virus and later it was found to be a
Callesi virus and things like that. So we're fairly confident that, you know, it wasn't around beforehand or for a long period of time beforehand, because we would have seen these math mortality events. A couple of hypotheses as to how that virus emerged. It could have either been a species jump, so the same thing as mixomavirus. You know, it's completely subclinical in its natural reservoir host, but when it transmits to European rabbits, it becomes highly virulent in that species,
and so that is one hypothesis. Or it could be recombination. So these viruses recombined, so basically different parts the genome sort of switch in and switch out, and that can give the virus different characteristics. And so it could be that, you know, if there was a benign kalisivirus present in rabbits, which we know rabbits do have several benign rabbit Colisi viruses that just infect the gut, they don't cause that
systemic disease. And if that benign virus then acquired virulence, either through just standard viral evolution or probably more likely through a recombination event with something, then that could have led to the emergence of this highly virulent rabbit calisi virus. Similarly with RHDV two, all known RHDV twos actually contain part of their genome from other rabbit calisi viruses, and then it's the RHDV two capsid that's the new part and that gives it the broader host range and things
like that. So the capsid is the shell of the virus. And so where those capsid genes came from again, we don't know. Was it just through natural evolution or was it a recombination event with another calicivirus. So two main hypotheses cross species jump or evolution from a benign ancestor.
So how did RHDV two get to be globally distributed because it was only found in twenty ten, but now it has this global distribution, So what do we know about how that happened.
That's been the really incredible thing is seeing the how RHDV two has become globally distributed so rapidly. It's really been incredible observing this sort of in real.
Time and a bit horrifying.
But so again we know that it's an incredibly environmentally resistant virus, and so it can survive and remain infectious for months in the environment. And then I think the other thing that's contributed to that is that because there's not a lot of cross protection or imminological cross protection between RHDV one and RHDV two, RHDV two very rapidly replaced rh tov one. So I guess the analogy here would be the RTV two is the omicron of rabbit
caliciviruses replacing delta. And so you know, there was this huge surge in cases because it swept through an effectively
naive population, so you had huge case numbers. The virus grows to extremely high levels and infected rabbits, and so there was just this massive virus load being shed into the European environment after the emergence and local Europeans spread and so then with global travel and globalization, you know, if people walked across a park where a rabbit had died, they pick it up on their shoes and then they travel and take it home, you know, and if it
gets into a wild rabbit population anywhere, then it spreads that way. And I think we saw a similar thing with the emergence of canine pavovirus back in the mid seventies. Parvoviruses are also incredibly environmentally resistant, and we saw that spread globally within about six months actually, so we know that environmentally resistant viruses just through bomite transmission, can you know, transmission on shoes and things like that. I think the other thing that I don't have a lot of data on,
but I really didn't appreciate. I guess so much before RHGV two how much trade of rabbits and rabbit equipment particularly there are. So I think, you know, it could be that if somebody's pet rabbit dies, they then put the cage on eBay or something, and somebody else orders
the cage and then the cage is contaminated. And so again I certainly don't have direct evidence for that, but I think it's it's easy to sell stuff internationally these days and ship stuff, and so I suspect that there may be some of that as well.
I want to talk about sort of the impact of RHDV two in Australia in a minute, but I want to first ask about some of these places where RHDV one or RHDV two has spread and where rabbits are not considered invasive where they're, you know, just a part of the natural ecosystem. What have we seen in terms of the impact on the local rabbit populations there, and what kind of downstream effects have there been on the other members of that ecosystem.
You know.
The impacts of RHDV first RGV one are now URHDV two on rabbit populations in their native home range is really concerning and it's actually caused them to be their threat category to be upgraded in terms of the IC and Red List. So it really is a major concern
for native rabbit populations. And so rabbits are native to the Iberian Peninsula, so Portugal and Spain, and they've certainly observed sixty to seventy percent declines in rabbit populations, and then they've also observed similar reductions on their apex predators, so the Iberian links in the Spanish Imperial Eagle, particularly because those animals don't have the food source, and that then effects for tea of those populations and so they're
not breeding as effectively, and so rabbits really are keystone species.
In their native environment.
Similarly, RGB two arrived in the US in early twenty twenty and we've seen quite dramatic impacts on cottontail and jack rabbit populations in the US, and certainly there are several endangered species over there, and so there's quite grave concerns about the impacts of RHGB two on those already threatened populations. Likely there'll be similar lead on effects on
their predators as well. I don't know that the reductions have actually been quantified at this point in the US, and I think the other thing, you know, I've had some conversations with colleagues in the US and they've sort of said, we haven't really seen the knockdowns that we you know, you've reported in Australia that we're seen in Europe. And I think that's probably at least partially due to the different ecology of the cottontails and jack rabbits over there.
So I believe that they don't form these massive warren systems same way that rabbits do. The contact densities are probably lower, and things like that.
A lot of people who are concerned about this are not just concerned about the wild rabbits but also sort of domestic pet owners. Is there anything good on the horazon or is there any good news on the horizon potentially for a vaccine or any sort of control, I guess either for both the wild rabbits or people who have domestic pets.
Certainly for domestic pets, good news with RHDV or caliciviruses is that really there's only those two types, so RHDV one and then RHDV two, and the immunity induced if you do stuff I have infection or after vaccination is pretty much lifelong. Like it's really durable. It's a really strong induction of immunity. And so RHDV two vaccines have been developed and are available in many parts of the world, and so for pet rabbits, if they're vaccinated, really not likely.
To be an issue.
Unfortunately, in Australia we don't currently have an RHDV two vaccine and that is a problem and something that is being worked on. In terms of wild rabbits, I think that's a bit harder. You know, how do you vaccinate wild populations, I think is an ongoing concern in multiple from multiple disease perspectives. You know, certainly in the Iberian Peninsula they're doing a lot of habitat management to try to help support rabbit populations. They're actually restocking wild populations,
so moving animals from high density to impacted areas. And I think we now know so in the last couple of years, it's clear that maternal antibodies, so if the mum has antibodies to RHDV two, then the kittens will be protected for you know, sort of around an eight week period, and if the kittens are infected during that time, then they don't die, they effectively get vaccinated. And so
there was a really interesting paper out recently. They actually spread URHDV two baits in an enclosed population in a control population, but they actually spread URHDV two brates during breeding periods and they actually showed that there was a reduction in young rabbit mortality by a third and there were actually more immune juveniles recruited into the adult population.
And so I think as RHDV two becomes endemic and imminity levels increase, that maternal antibody protection will help buffer those impacts on rabbit populations moving forward, which is good for native populations, but again in Australia it's going to be an issue for bio control.
In our mixomatosis episode, we talked a lot about the evolution of virulence, which is one of my all time favorite things to think about, and how selection pressures are super dependent upon the virus itself and the way it's transmitted, the host behavior, the environment, among many other things. In the case of maximatosis, of course there is this trend towards decrease veryviolence, and then more recently it seems like
a few more virulent streams have been selected for. And then of course genetic resistance among the rabbits played a large role, and so I was wondering, you know, what have we seen in terms of any virulence changes of RHDV one or two since these viruses were first discovered, and has there also been any genetic resistance among rabbits.
It's such a beautiful example of how each virus is perfectly adapted to maximize its transmission, right, And so mixomavirus is spread by biting insects, and so therefore it requires a live animal to transmit. So it's, you know, in the virus's best interest to keep the host alive for as long as possible to maximize the number of biting insects that can feed on that infected animal. And so prolonged disease duration is good, so hence the virus attenuates
to become less virulent. In the case of rhdv it's spread from that dead animal. Like I said, it's that carcass contaminating the environment and being exposed to blowflies that facilitates transmission. And so as long as they die at
the peak amount of infectious virus, that's going to optimize transmission. Hence, we really haven't seen attenuation of the virus with either RHDV one or RHDV two, because again, maximum transmission occurs by killing the rabbit at that you know, forty eight hour mark, when the entire liver is just packed full
of virus. And so I know there's been a lot of discussion about that virus has always evolved to be mild, and certainly I think this is the classic example of you know, it really depends on the root of transmission.
And so in terms of genetic resistance, mixomavirus is a pox virus, so it's a very large DNA virus, and so it encodes a whole bunch of genes, and I guess that also provides a lot of targets for the host immune system and so pox viruses have all of these really cool mechanisms of trying to counteract the host immune system, and therefore the host evolves to then counter the counteractions and etcetera, etcetera. And this really beautiful virus
host coevolution. Because calisi viruses are so tiny, they just kind of they get in, get it done, and that's it.
And so it's, yeah, a bit of a different story.
There are some studies suggesting the development of genetic resistance in some localized populations to RHDV one, at least in Australia, but certainly it doesn't seem to be a major driving force the way that mixomavirus was. And again, I think that's because rhdv is just so lethal so quickly that there's not really the opportunity to survive. And I think what's really intriguing is the RHDV one RHDV two differences here.
Because RHDV one, while it was able to infect, is able to infect young rabbits younger than about eight weeks of age, it doesn't tend to cause disease in young rabbits. It only kills adult rabbits, and that's independent of maternal antibodies.
There's just there's.
Something about young rabbits that leads them to not develop disease after rhgv one infection, whereas that's not true of RHGV two. RHGV two lethally kills both young and old rabbits, and so in the case of rhdv one, it was kind of a very stochastic or random event, Like if you happened to be five weeks old when you got infected, you survived, and if you happen to be nine weeks old, you know, you died, and so there's not.
Really a strong selection pressure there.
It was just a sort of a random event, whereas with RHDV two there's not that sort of age differential and so previously just being young enough to randomly avoid dying is not a thing anymore. And so the rabbits that survive RHDV two infection, if there is a genetic component there, it's potentially likely that there will be a lot more as strong a selection pressure for development of genetic resists to HGV two than there was to development
of rhgv one. So it's certainly something that people are very keen and actively investigating to try to see how this plays out as RHDV two becomes endemic.
Here in North America and in many other places where rabbits are considered like a keystone native species. The arrival of RHDV two has been met with these alarm bells, like you know, concern for the rabbits. This could be lead to a lot of ecosystem collapses. But in Australia, you know, where rabbits have been invasive for about one hundred and sixty years or so, has RHDV two been seen as a problem or more as a potential solution.
And do you think that these differences in perspectives across different countries, do you think that that changes the way that research is done or focused on the different types of research questions into this pathogen.
Yeah. So RHGV two was first detected in Australia and probably arrived in Australia in around twenty fourteen. First detected in twenty fifteen, and at that time rabbit populations were so certainly increasing and we were actively investigating the release of a new buyer control of this K five variant that I mentioned briefly at the beginning, So you know, rabbit populations were increasing, it was seen to be a
problem and population densities were very high. So when RHDV two entered the Australian rabbit population, as we've observed elsewhere, there was this massive epizootic sweep through and we saw population reductions based on you know, serological data and spotlight counts and things like that, as an estimated to sixty reduction in rabbit abundance nationally, like sixty percent population level reduction,
so very considerable from our perspective. That dramatically interfered with all of the research that had been going on for the K five release, right because we'd put all this modeling and effort into looking at how K five would behave in the pre RHDB two rabbit population, and obviously once RHDV two swept through, population density were much lower, they were probably a lot more fragmented, and so you know,
the effective reproductive number is totally different in different population conditions, and so there was very confusing aspect between like was this the new buyer control that these scientists were talking about, and then we're trying to say no, it was a different strain that was just spontaneously came in and things like that. So overall, perspective, it's dramatically reduced rabbit numbers,
which has been very beneficial. However, it's certainly a problem for pet rabbit populations because, as I said, we don't have a vaccine here. We weren't expecting URHDV two and so like again for that K five virus, we've done a lot of research into making sure that the vaccines were appropriate for that release, and then RHDB two swept through and it's having really really dramatic impacts on pet rabbits, and so an RGB two vaccine is certainly needed for
Australian pet rabbits. In terms of the differences and research focuses between different countries, I think really it's all about understanding the pathogen right, and then you can either use that to your advantage as a bio control or to your advantage to counteract its impact. And so I think we're all actually doing quite similar research.
It's just how those findings are applied.
So the use of biocontrol is never without controversy. Can you talk about some of the reasons that people are opposed to the use of these rabbit viruses and is there a possible downside to reducing rabbit populations in Australia.
I mean, nobody likes killing animals, right like, nobody wants to be killing animals if there was a better way, you know, one hundred percent. So unfortunately, with the current technologies that we have, lethal control invasive species really is the only way to manage that. And even you know, you can't go around and surgically sterilize every rabbit in Australia and things like that, and even if you do, then they're still going to have those environmental impacts in
the meantime. So but of course, yeah, it certainly is controversial. There's a few different reasons why it's controversial. I mean, I guess obviously animal welfare particularly you know, as we said, RHDV is very quick and there are minimal clinical signs. You know, although the path of physiology sounds horrific, it's really your organs just pretty much go into organ failure and you die very quickly.
So the welfare is way better than something like mixo.
People have raised concerns about releasing viruses viruses of alve you know, will it spread to native species or other species or could it cross species? And certainly I guess with the many decades at least with RHDV one. These viruses appear to be incredibly species specific and we haven't seen any evidence of infection in non lagomorph species. Obviously, the impact on domestic rabbits is controversial, and for that, as we said, we need a vaccine, but the vaccines
are very effective when they're available. Possible downsides to reduce rabbit populations. I think one thing that's frequently raised is that if you reduce rabbit populations, that would lead to predators turning to native species. And again there's been quite a lot of research actually done investigating that, and there's been no direct evidence to actually support this prey switching by either feral or native predators in Australia, and so
actually it was the opposite. Reduced rabbit abundance was shown to actually reduce feral cat and fox abundance and reduce the predation of native fauna because you know, a large population of rabbits supports a large population of these predators, and so just by reducing the number of predators by reducing their food source was actually beneficial. But it is
something that's quite frequently raised. And then just briefly, I think the other thing that perhaps is not so frequently raised by opponents of bio control, but for users of the buyer control, I guess the efficacy of the agent
can be quite variable. So it depends on you know, the virus dose that the animal receives, the level of pre existing immunity, the maternal antibody status, and it really needs to be used at the right times, and so they're require a little bit more finesse than something like putting out a poison.
So one last question about r HGV two biology and so on before I get to ask a bunch of questions about you, and that is the impact of climate change. So what do we know or what is thought to be the potential impact of climate change on rabbit populations or on the distribution of these rabbit viruses in Australia.
You know, rabbits are known to be really adaptable their native range of that Mediterranean ecosystem, but they've really managed to adapt to a lot of Europe. There's feral rabbit populations in British Columbia and Canada. You know, they colonized
Australia within a seventy year period or so. They are really adaptable and so if the rabbit populations thrive and particularly in adverse environmental conditions, then this is going to really have more impacts on our native plant and animal species.
And so for the.
Viruses themselves, as we said, they're pretty environmentally resistant. But again, if we start to see these really prolonged periods of drought, then that's going to probably reduce the environmental burden of these viruses. And I think we're probably already seeing some of these impacts in terms of the variability that we've seen.
Over the last few years.
So last over the last couple of years, we've had a La Nina event in Australia, so a lot of warm, wet weather, and certainly the last two years we've seen really massive outbreaks of callicivirus in spring when those fly vectors start to increase. But I would assume that drought
may then reduce environmental survival. So there's probably arguments both ways on how that would affect the actual virus, But certainly I think rabbits will survive or adapt to climate change a lot more readily than our native species, which is a concern.
So we're going to take a quick break here and then when we get back. I want to ask you what it's like to work in the rabbit biocontrol program and what a veterinary virologist does.
I'm so excited.
Thanks, Welcome back everyone. Okay, So, I want to know, as the team leader on the rabbit biocontrol program, what do you end up doing on a day to day basis, or maybe it's more accurate to ask you how much does what you do change from d to day?
Yes, So, I think you know what's really exciting about our team or the research that we do is it spreads quite a few broad areas. So you know, we do animal experimental work, so infection trials, and then we do a lot of in vitro work policy viruses notoriously don't grow in cell culture, and so we're trying to
establish an organoid system for these viruses. So there's some you know, molecular biology, there's cell culture, there's animal experiments, and then there's field work as well, so we get to go out and sample rabbits in the field, which is lovely, and then there's a lot of molecular surveillance and diagnostic testing as well. So we really have broad techniques and are able to do a lot of variable things that that keeps life interesting for.
Me as team leader. I'm not really in the lab so much.
These days, which is quite sad, but you know, like many sort of pis, I guess, I'm working across several projects, you know, working on the next grant, working on the next publication. I'm also a facility veterinarian here, so I respond to animal emergencies and yeah, you know, life's never dull in science.
I think, Yeah, that's that's right.
You practiced as a veterinarian for a bit, it's and you are still practicing as a veterinarian, which is amazing. So can you take me through how you got from veterinarian to veterinarian and veterinary virologists.
Lots of views in that sentence, lots of made it through.
Yeah. So you know, I was one of those kids who was I always curious, you know, I was why but why?
But why? But why?
And you know, I love nature, I loved animals, and so I from a very young age, I said I'm going to be a vet and so that's what I did.
And I actually thought I was going to be in.
Small animal practice for the rest of my life, and I got into small animal practice, and you know, I think I found that I wasn't really asking why so
much on a day to day basis. There was a lot of routine and you know, there's a lot of other considerations, and so that sort of that curiosity wasn't satisfied the way I had expected it to be, I guess, and so to me that lent itself to going back to do a PhD. And when I was applying for PhD programs, you know, looking back, everything I applied for was an infectious disease of some sort, and so I'm guessing that infectious diseases piqued my interest somewhere along the line.
And yeah, ended up doing a virology project working on recombinant vaccines for the poultry industry. And yet from there I just fell in love with viruses, like they're just they're so cool and they're so diverse, and heaps of different opportunities have stemmed from that. So after my PhD, I worked for a period of time as a diagnostic virologist in one of the state labs, and then went to do a postdoc in rabbit callisi viruses, and you know, like we've just talked about.
They're so cool. How you know, there's so much to do, so I've stayed stayed. Since do you.
Have a favorite virus or bacterium, I'll allow that too, or parasite.
Well, I mean I probably have to say O HDV, don't I you.
Don't have to, but I would. I would think that that's a very strong contender.
Yeah, yes, I just you know, I think, yeah, viruses are also perfectly adapted to their niche, right, and so every single one of them has such a cool story to tell. So I mean, I think perhaps one of the coolest ones is, you know, since sittin. So since sittin gene, which is the gene that allows the development of placenta, right, it allows the cells to fuse, which is the basis for the you know, for placental development.
Since sittin is a captured retroviral gene from a human retrovirus, right, and that that allows the evolution of all placental mammals. So I guess I kind of have to say sincitan otherwise I wouldn't be here, you know, or whatever virus gave rise to sincitin. And also, you know, I would hate to live in a world without my dog, and so you know, but yeah, you know, viruses have just shaped evolutions so strongly, and so every single one of
them is just amazing. And that you know, there's those POLYDNA viruses in parasitoid wasps that they inject the virus along with their eggs that suppresses the caterpillar immune response so that the caterpillar immune system doesn't kill the egg and things like that. And then there's a microvirus that infects a fungus that infects rape seed, which turns the fungus from virulent to actually beneficial for the plant and things like that, and so they're just I mean, I
can't pick one. There are just there's so many cool examples.
You just give some of the most fascinating examples that I don't think I've heard of any of those. And so that is like I am about to go after this is over, I'm going to go like on a Wikipedia rabbit hole about every single one of those.
And I'm very excited.
Worth it, totally worth it.
So you work at CSIRO, which is a government institution, and what do you think are some of the pros and cons of working at a place like CSIRO versus like a university for instance.
Yeah, so I think, you know, one of the things about working for Sarah that I really enjoy and that really vibes with my values, I guess, is the really applied focus. You're doing research because someone or an industry body has said this is important to us, can you look into this? And so they're really applied outcomes that
end users really care about. It's really output driven and you really do get to work closely with stakeholders, so you know, setting the next research agenda, it's like, okay, well, how do you feel about what we've done so far? What like where we go from here? And so it's it's a real, really collaborateive approach with the end users, which is great.
You know.
The flip side of that is that there are really strict milestones and deadlines and there's not so much of the opportunity to sort of just follow the science for the science's sake that perhaps you may get in an
academic institution. Similarly, it's a lot harder to I guess, pivot. So, for example, with the whole coronavirus situation, I know so many virology labs, you know just completely pivoted to SARS Kobe two and obviously like that was never going to be an option because you know, the agriculture industry isn't going to they have a rabbit problem. They still have a rabbit problem. So, yeah, the pros and cons, you know, they're both the same side of the coin. It's really
achievement focused. But then it's a little less curiosity driven.
I suppose on.
The podcast we're always talking about one health and how much we love it and how important it is for different fields to work together to consider the whole picture. And so do you feel as though so your experience as a veterinarian has given you more of an insight into the one health approach?
Yeah, I really do.
I think you know, at VET school well and in practice you have to have your head both around the individual level treating the individual animal, but also how that impacts the herd and the population and interspecies level as well. And so I think it's just drilled into us and we've never considered otherwise that you know, how does what I do here, how is that going to impact the
rest of the ecosystem? And you know, and again from the vetnory perspective, it incorporates nutrition, and in terms of large animals, that incorporates pasture, and so that involves drought because then different weeds will pop up with different climactic conditions and things like that.
So I think training as a veterinarian really gives.
You that broader perspective of the animal, but also the environmental and then the human and zenotic disease picture as well.
So can you tell me about a cool project that you're currently working on?
So perhaps I may have given away a bit earlier, but the whole recombination story has just over the last couple of years has really peaked my interest. So, as I mentioned, ERHDV two first arrived in Australia probably in twenty fourteen, and we've been tracking the genomic epidemiology of these viruses since it arrived. And what we've seen through the genomic surveillance is at least six independent recombination events
since the arrival of RHDV two in Australia. And that's just the recombination events that have generated epidemiologically fit viruses, right, not all the viruses that died out. So that's unprecedented or at least I didn't appreciate it prior to that how important recombination was, and then seeing these successive waves of epidemiological replacement by these variants, and sadly, I think it's been superseded now by the coronavirus variance.
And everybody's like, well, yeah, what did you expect? But for me, it was really striking when I saw this with Kaleci viruses.
And I think what's been really intriguing. So among those six recomninant variants that have arisen, they all contain almost identical capsid proteins or you know, effectively the spike protein to each other. So it's not immune escape that's driving this epidemiological replacement of these viruses. And so if it's not immune escape, like what is it? Because again there's
all this focus on immune escape. And so we recently had a got funding support for a postdoctoral position to start to try to look into what is driving the epidemiological fitness of these recombinant variants. So which of these non structural proteins and why if it's not immune escape, what is going on? And so I think that's really got my interest at the moment.
All Right, So I've got one last question for you, and that is an.
Advice seeking question.
What advice would you give to someone who is interested in pursuing this career or maybe you know, what type of advice do you wish you had received when you were just starting out?
You know, in hindsight looking back, you know, I think there's a lot of talk now about this fixed mindset versus growth mindset type thing. And I think, as I said, I decided from a really early age that I was going to be a vet, and so I guess my whole identity, as you know, through my school years and then going through vet school and everything was like I'm going to be a vet.
I'm going to be a vet. And that really fixed mindset.
I mean it was good obviously, like you need to have that the drive, but it also you know, it probably made me pass up or bypass other opportunities that may have popped up in the way along the way. So I think, in hindsight, you know, if I could have adopted more of a growth mindset instead of this focus on being a small animal practicing veterinarian, it could
have looked really different. So I would just say my advice based on that would be be open to opportunities, like you know, have a plan, but be prepared to adapt it.
Be curious.
And I think for me it was really important finding out what my values were and you know, as I sort of briefly mentioned, reconciling that practice wasn't satisfying that core curiosity value that is so strong for me, and knowing that there's other things out there where you will be a good fit sort of thing, and so yeah, be open to different directions and yeah, just be curious.
That was so fascinating.
Oh my goodness, Thank you so so much doctor Hall for chatting about rabbits and viruses and evolution. I had
such a great time. If you want to learn more about the work that doctor Hall is doing, I'll link to the project's website, as well as a bunch of cool articles related to doctor Hall's work on the post for this episode on our website, This podcast will Kill You dot com, speaking of which you can find all sorts of things on that website, including, but not limited to, the sources for all of our episodes, transcripts, our bookshop
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We've got another
Regular season episode coming out next week covering a whole new topic, so until then, keep washing those hands