Speaker 1: Hi, I'm Aaron Welsh and this is this podcast will
Speaker 1: kill You. I'm back with another bonus episode in our
Speaker 1: mini series of bonus content that will be releasing over
Speaker 1: the next few months. In case this is the first
Speaker 1: bonus episode you're tuning into and you're wondering what the
Speaker 1: heck is going on, I'm using these episodes as an
Speaker 1: opportunity to explore more about whatever disease or topic we
Speaker 1: covered in our previous week's episode, and also to get
Speaker 1: to chat with experts about their jobs, their hopes, their dreams,
Speaker 1: whatever comes to mind. If you've listened to the podcast before,
Speaker 1: you know that I'm kind of a relentless question asker,
Speaker 1: and so instead of just pestering Aaron Updyke with all
Speaker 1: the questions, I'm saving some for these episodes, and so
Speaker 1: far I've gotten to have some great conversations with people
Speaker 1: in very different careers, studying or working on very different problems.
Speaker 1: And this week I am so excited to have yet
Speaker 1: another fun conversation and learn a whole lot more about
Speaker 1: another topic. So what am I going through be talking
Speaker 1: about today? This week really kind of picks up where
Speaker 1: we left off in our most recent regular season episode.
Speaker 1: Which covered a virus of rabbits called the Maxoma virus.
Speaker 1: If you haven't listened to that episode yet, I would
Speaker 1: recommend check it out before listening to this, just because
Speaker 1: there's so much more to that story, but I'll give
Speaker 1: a quick recap here. The Maxoma virus is a type
Speaker 1: of poxvirus that can cause severe disease in some species
Speaker 1: of rabbits, and it became internationally famous back in the
Speaker 1: nineteen fifties when it was introduced to Australia as part
Speaker 1: of efforts to control the invasive European rabbit population. What
Speaker 1: had started out as a handful of European rabbits introduced
Speaker 1: to Australia in eighteen fifty nine had within a few
Speaker 1: decades grown to an absolute ecological and agricultural menace. Entire
Speaker 1: ecosystems were disrupted, native animals experienced tremendous population declines, many
Speaker 1: plant species were driven locally or regionally extinct, and huge
Speaker 1: tracts of land could no longer be used for agriculture.
Speaker 1: The introduction of the Maxoma virus did help to drive
Speaker 1: down or stabilize rabbit populations, but over generations the virus
Speaker 1: lost a bit of its impact. As both rabbit and
Speaker 1: mixomavirus adapted to one another, the deadly virus was no
Speaker 1: longer as deadly as it once was, and the rabbit
Speaker 1: was no longer as susceptible as it used to be.
Speaker 1: So when another lethal virus of European rabbits was identified
Speaker 1: in the nineteen eighties, the rabbit hemorrhagic disease virus or RHDV,
Speaker 1: it was explored as another possible form of biocontrol for
Speaker 1: rabbits in Australia, and RHDV was introduced in the mid
Speaker 1: nineteen nineties, again helping to keep rabbit populations under control.
Speaker 1: But the story of rabbits in Australia doesn't end there,
Speaker 1: and neither does the story of the rabbit hemorrhagic disease virus.
Speaker 1: In twenty ten, a new type of the virus was
Speaker 1: discovered in France, the aptly named rabbit hemorrhagic disease virus
Speaker 1: type two, and this one doesn't seem limited to just
Speaker 1: European rabbit populations. Since its discovery, RHDV two has spread
Speaker 1: around the world and has led to concerns for demmestic
Speaker 1: pet rabbits as well as the wild rabbits and hairs
Speaker 1: that are susceptible, especially in places which have already seen
Speaker 1: damaging ecological cascades from RHDV one. So what I really
Speaker 1: wanted to explore in this bonus episode was these two viruses.
Speaker 2: RHDV one and rhdv two.
Speaker 1: Where did they come from? What effects have they had
Speaker 1: on rabbit populations? Are they following the same evolutionary patterns
Speaker 1: as maxomavirus, How worried should we be? And to help
Speaker 1: me answer these questions and so many more, is doctor
Speaker 1: Robin Hall, veterinary virologist and team leader for the rabbit
Speaker 1: Biocontrol team at CSIRO, the Commonwealth Scientific and Industrial Research Organization,
Speaker 1: which is a government agency in Australia. I am super
Speaker 1: excited to jump into this interview, so I'll just take
Speaker 1: a quick break here and then we'll get started.
Speaker 3: Hi. I'm Robin Hall.
Speaker 4: I'm a veterinary virologist and epidemiologist at the Commonwealth Scientific
Speaker 4: and Industrial Research Organization or CSIRO, based in Canberra, Australia,
Speaker 4: team leader for the rabbit buyer Control team here, and
Speaker 4: I have a special interest in host pathogen interactions, management
Speaker 4: of invasive species and viral evolution.
Speaker 2: Awesome.
Speaker 1: Thank you so much for taking the time to chat
Speaker 1: with me today.
Speaker 3: I am thrilled thanks for the opportunity. It's really exciting
Speaker 3: for me.
Speaker 1: So in our episode on mixed and mitosis, Erin and
Speaker 1: I talked a lot about the long history of European
Speaker 1: rabbits in Australia and how this invsive species has been
Speaker 1: incredibly damaging both ecologically and economically, and I was wondering
Speaker 1: if you could bring us up to speed on the
Speaker 1: current situation with rabbits in Australia, like what do we
Speaker 1: know about the impact that they're still having and where
Speaker 1: does their continued presence seem to be the most problematic.
Speaker 4: You know, back in the nineteen fifties, rabbits were at
Speaker 4: massive plague proportions throughout Australia, and then with the introduction
Speaker 4: of mixomavirus, it was incredibly effective in reducing population numbers,
Speaker 4: but of course populations begin to recover over time, and
Speaker 4: so in the mid nineties RHDV or rabbit hemorrhagic disease
Speaker 4: virus was released again with massive declines in rabbit populations,
Speaker 4: but over time. You know, bio controls are not a
Speaker 4: silver bullet, and once more rabbit populations began to increase,
Speaker 4: and so that led to in twenty seventeen, the release
Speaker 4: of a new variant of RHDV, which we call K
Speaker 4: five in Australia, and again we're still seeing the impacts
Speaker 4: from both the K five release and the arrival of
Speaker 4: this new virus, rhdiv two in Australia which was not
Speaker 4: deliberately released but has spread here as it has globally.
Speaker 4: And so currently rabbit populations are relatively suppressed to comparatively
Speaker 4: to what they have been in the past, but we
Speaker 4: do still see considerable impacts, and these fluctuate on a
Speaker 4: bit of a boom and bust cycle. You know, when
Speaker 4: conditions are good, the populations will breed very rapidly and
Speaker 4: increase in size, and if we go into a period
Speaker 4: of drought, then populations can decline again. So the impacts
Speaker 4: we see are really most obvious in environmentally sensitive areas,
Speaker 4: so particularly in the arid and semi arid zones where
Speaker 4: rabbits compete with native species for food and shelter, and
Speaker 4: they eat native plants that are already finding it difficult
Speaker 4: to grow in these arid conditions. And then obvious course
Speaker 4: in agricultural industries as well, where they impact crops through grazing,
Speaker 4: they damage the soil, they compete with livestock for food,
Speaker 4: and again particularly in drought conditions, those impacts are more severe.
Speaker 4: And they also Rabbits also have some perhaps less considered impacts,
Speaker 4: so things like they impact our indigenous cultural heritage sites
Speaker 4: by damaging these artifacts and sacred sites and things, and
Speaker 4: even the impact of reducing the vegetation. I mean that
Speaker 4: then exposes more soil, and the soil can then blow
Speaker 4: into the.
Speaker 3: Fleece of sheep which reduces fleace quality.
Speaker 4: So there's this really sort of lead on effects and
Speaker 4: they really have dramatic impacts that are quite wide ranging
Speaker 4: and both direct and indirect.
Speaker 1: Our last episode focused on one of the most impactful
Speaker 1: tools for rabbit control in Australia, of course, the maxomavirus,
Speaker 1: and we also briefly mentioned the rabbit hemorrhagic disease virus,
Speaker 1: which I cannot wait.
Speaker 2: To ask you more about.
Speaker 1: But these two biocontrol agents, they're not the only tools
Speaker 1: used to try to suppress rabbit population, So can you
Speaker 1: talk about the other methods that are used.
Speaker 4: When we talk about a control tool, you really want
Speaker 4: something that's going to be effective, relatively cheap or easy
Speaker 4: to distribute, and viruses are really the only thing that
Speaker 4: we have that are self disseminating that work on a
Speaker 4: landscape scale with the existing technologies. However, certainly at local
Speaker 4: levels there are a lot of other tools that can
Speaker 4: be used. So particularly poisons are used quite heavily, so pindone,
Speaker 4: but also ten eighty so pin done is an anticoagulant,
Speaker 4: so it's like rat baits sort of, and ten eighty
Speaker 4: as a metabolic topsin. We also focus a lot on
Speaker 4: habitat removal, so destroying the warrens or if they're harboring
Speaker 4: in you know, shrubs, removing the shrubbery where possible shooting
Speaker 4: and trapping can be employed. On a local level, exclusion
Speaker 4: fencing has been applied so where you you know, put
Speaker 4: up fences that keep the rabbits out, but again you
Speaker 4: have to dig it down and put it up relative high.
Speaker 4: And then warren fumigation where you introduce like a gas
Speaker 4: into the warren to kill them. So all of those
Speaker 4: other methods they are very effective at local levels, but
Speaker 4: as you can imagine, they're quite labor intensive and certainly,
Speaker 4: you know we can't use them across the landscape scale
Speaker 4: of Australia.
Speaker 1: So now I am so excited because I get to
Speaker 1: ask about rabbit hemorrhagic disease virus.
Speaker 2: I read that this is a calisivirus.
Speaker 3: What does that mean?
Speaker 2: Like, are there other types of callisi viruses?
Speaker 4: Yep, I'm very happy to talk about URHDV as well.
Speaker 4: So yeah, RHDV is a kalisivirus. These are small RNA viruses.
Speaker 4: So like the coronavirus is an RNA virus as well,
Speaker 4: it has an RNA genome, but coronaviruses have like thirty
Speaker 4: thousand letters in their genetic code, whereas these caliciviruses have
Speaker 4: like seven and a half thousand letters, So we call
Speaker 4: them small RNA viruses.
Speaker 3: The shell or the.
Speaker 4: Capsid that the genome is packaged into is non enveloped,
Speaker 4: and so that means that they're incredibly environmentally resistant. So
Speaker 4: like I think, again, we hopefully all know now with
Speaker 4: coronavirus that you know, it doesn't survive particularly long on surfaces,
Speaker 4: and it does use droplets and things like that, it's
Speaker 4: protected in that moist droplet environment, whereas kalisivirus is because
Speaker 4: they're non enveloped, they can survive on surfaces or in
Speaker 4: soil or something for months. Chalciviruses are pretty common and
Speaker 4: probably occur in most, if not all, vertebrate species, although
Speaker 4: we are really only starting to look at the virus
Speaker 4: sphere more broadly, but some that you may have heard
Speaker 4: of would include like human neurovirus, feline chalicivirus, so it's
Speaker 4: something that we vaccinate our pet cats for. And then
Speaker 4: there are kalsiviruses of you know, cows, mice, pigs, chickens,
Speaker 4: atlantic salmon, so yeah, it's a big family, and the
Speaker 4: rabbit and hair ones there as well.
Speaker 1: How are these viruses transmitted, or maybe in particular, how
Speaker 1: is RHDV transmitted?
Speaker 4: A lot of the calisi viruses are transmitted by the
Speaker 4: fecal oral roots, so you know, you ingest them either
Speaker 4: from a contaminated surface or something like that, and then
Speaker 4: they replicating the body they're passed out in the feces
Speaker 4: and then contaminate their environment, and so RHDV broadly follows
Speaker 4: that process. However, because again this environmental stability, RHDV can
Speaker 4: also get picked up mechanically by insects, so particularly carryon flies.
Speaker 4: The typical life circle for an rhdv virus is it's
Speaker 4: ingested somehow, so either you know, the grass is contaminated
Speaker 4: and the rabbit eats it, or the rabbit sniffs a
Speaker 4: dead rabbit and gets it in that way, or a
Speaker 4: blowfly comes and lands on like the eyelids of a
Speaker 4: healthy rabbit and deposits some virus there, and then the
Speaker 4: rabbit rooms itself and eats it the virus that way.
Speaker 4: The virus then go into the gut, enters the animals
Speaker 4: systemically and causes this major infection that we can talk
Speaker 4: about in the second and then the rabbit dies typically
Speaker 4: within forty six to seventy two hours post infection, so
Speaker 4: this thing is incredibly incredibly fast. And then the carcass
Speaker 4: starts to break down and contaminates the environment and the
Speaker 4: flies can come in and pick it up and move
Speaker 4: it between populations.
Speaker 1: What's going on at the path of physiological level, and like,
Speaker 1: what's a typical course of infection?
Speaker 2: What does that look like?
Speaker 4: So from the outside you frequently don't see clinical signs,
Speaker 4: which I guess is great from a by control perspective,
Speaker 4: because the welfare is actually I mean, anything that kills
Speaker 4: something you don't want to say welfare is good, but
Speaker 4: it certainly has less impact on the animal than something
Speaker 4: like say mixomavirus. So many pet owners, you know, we
Speaker 4: often hear that, oh, it was fine, it was eating
Speaker 4: the night before I came in in the morning it
Speaker 4: was and so you often find them still with food
Speaker 4: in their mouth. And so it does happen very quickly,
Speaker 4: and frequently you don't see any clinical signs in the
Speaker 4: rabbit unless you're sort of taking temperatures every few hours
Speaker 4: or something at the path of physiological level. Basically, what
Speaker 4: happens is the virus goes in. It targets the liver,
Speaker 4: so it starts to replicate in the liver, and it
Speaker 4: causes this massive hepatitis that all a liver cell start
Speaker 4: to bust open and the liver just pretty much disintegrates,
Speaker 4: I guess, And so that leads to you know, a
Speaker 4: cytokine storm as such, and so you get this massive
Speaker 4: systemic inflammatory response syndrome, disseminated intravascular coagulation and you know,
Speaker 4: circulatory shock and death. And so that sounds all very
Speaker 4: awful and it is, I guess, but it's a fairly
Speaker 4: typical hemorrhagic fever virus so you know, some people have
Speaker 4: referred to it as bunny a bola and things like that,
Speaker 4: But basically, the virus goes in, causes a lot of
Speaker 4: damage to the internal organs, sets up this massive inflammatory response,
Speaker 4: and then the body's just overwhelmed.
Speaker 2: And so is that courus of infection?
Speaker 1: Is that fairly consistent across individuals within a population.
Speaker 2: Or within a species?
Speaker 1: And how variable is that a cross species as well?
Speaker 4: So RHDV is incredibly species specific. So there's a couple
Speaker 4: of different variants of RHDV. RHDV one was like the
Speaker 4: original RHDV that was first reported in sort of the
Speaker 4: nineteen eighties, and that RHDV one only affect European rabbits,
Speaker 4: so there's no definitive evidence that it can replicate in
Speaker 4: any other species. Then in twenty ten, a new variant
Speaker 4: called RHDV two emerged, and what we saw with RHGV
Speaker 4: two is that it can also infect other lagomorph species,
Speaker 4: so hares or jack rabbits, the Lepis species, and then
Speaker 4: also the cottontails or the silver lagas species. But still
Speaker 4: people are looking and have looked, and there's no evidence
Speaker 4: of any disease outside of those lagomorph species, within a species,
Speaker 4: or within individuals, within naive individuals. Certainly, the disease courses
Speaker 4: is pretty typical, and we see a case fatality rate,
Speaker 4: you know, upwards of ninety five percent, ninety nine percent,
Speaker 4: So it's it is very very consistent. In animals that
Speaker 4: have some degree of pre existing immunity, then the infection
Speaker 4: can look quite different. So you may get prolonged infections,
Speaker 4: they may get a subclinical heptitis with jaundice and things
Speaker 4: like that, and then secondary liver disease. But again that
Speaker 4: sort of depends on the level of immunity. But in
Speaker 4: naive individuals, it's very very consistent with an extraordinarily high
Speaker 4: case fatality rate.
Speaker 1: Where did these viruses come from? What do we know
Speaker 1: about the origins either of RHGV one or RHDV two.
Speaker 3: Yeah, I mean, where the viruses come from, that's the question.
Speaker 4: It is so certainly, you know, when i HGV one
Speaker 4: emerged in the nineteen eighties, it was reported in Angora
Speaker 4: rabbits in China. These rabbits are being bred for and
Speaker 4: they just observed these mass mortality events, so it was
Speaker 4: pretty clear that something was going on, and they identified
Speaker 4: this virus and later it was found to be a
Speaker 4: Callesi virus and things like that. So we're fairly confident that,
Speaker 4: you know, it wasn't around beforehand or for a long
Speaker 4: period of time beforehand, because we would have seen these
Speaker 4: math mortality events. A couple of hypotheses as to how
Speaker 4: that virus emerged. It could have either been a species jump,
Speaker 4: so the same thing as mixomavirus. You know, it's completely
Speaker 4: subclinical in its natural reservoir host, but when it transmits
Speaker 4: to European rabbits, it becomes highly virulent in that species,
Speaker 4: and so that is one hypothesis. Or it could be recombination.
Speaker 4: So these viruses recombined, so basically different parts the genome
Speaker 4: sort of switch in and switch out, and that can
Speaker 4: give the virus different characteristics. And so it could be that,
Speaker 4: you know, if there was a benign kalisivirus present in rabbits,
Speaker 4: which we know rabbits do have several benign rabbit Colisi
Speaker 4: viruses that just infect the gut, they don't cause that
Speaker 4: systemic disease. And if that benign virus then acquired virulence,
Speaker 4: either through just standard viral evolution or probably more likely
Speaker 4: through a recombination event with something, then that could have
Speaker 4: led to the emergence of this highly virulent rabbit calisi virus.
Speaker 4: Similarly with RHDV two, all known RHDV twos actually contain
Speaker 4: part of their genome from other rabbit calisi viruses, and
Speaker 4: then it's the RHDV two capsid that's the new part
Speaker 4: and that gives it the broader host range and things
Speaker 4: like that. So the capsid is the shell of the virus.
Speaker 4: And so where those capsid genes came from again, we
Speaker 4: don't know. Was it just through natural evolution or was
Speaker 4: it a recombination event with another calicivirus. So two main
Speaker 4: hypotheses cross species jump or evolution from a benign ancestor.
Speaker 1: So how did RHDV two get to be globally distributed
Speaker 1: because it was only found in twenty ten, but now
Speaker 1: it has this global distribution, So what do we know
Speaker 1: about how that happened.
Speaker 4: That's been the really incredible thing is seeing the how
Speaker 4: RHDV two has become globally distributed so rapidly. It's really
Speaker 4: been incredible observing this sort of in real.
Speaker 3: Time and a bit horrifying.
Speaker 4: But so again we know that it's an incredibly environmentally
Speaker 4: resistant virus, and so it can survive and remain infectious
Speaker 4: for months in the environment. And then I think the
Speaker 4: other thing that's contributed to that is that because there's
Speaker 4: not a lot of cross protection or imminological cross protection
Speaker 4: between RHDV one and RHDV two, RHDV two very rapidly
Speaker 4: replaced rh tov one. So I guess the analogy here
Speaker 4: would be the RTV two is the omicron of rabbit
Speaker 4: caliciviruses replacing delta. And so you know, there was this
Speaker 4: huge surge in cases because it swept through an effectively
Speaker 4: naive population, so you had huge case numbers. The virus
Speaker 4: grows to extremely high levels and infected rabbits, and so
Speaker 4: there was just this massive virus load being shed into
Speaker 4: the European environment after the emergence and local Europeans spread
Speaker 4: and so then with global travel and globalization, you know,
Speaker 4: if people walked across a park where a rabbit had died,
Speaker 4: they pick it up on their shoes and then they
Speaker 4: travel and take it home, you know, and if it
Speaker 4: gets into a wild rabbit population anywhere, then it spreads
Speaker 4: that way. And I think we saw a similar thing
Speaker 4: with the emergence of canine pavovirus back in the mid seventies.
Speaker 4: Parvoviruses are also incredibly environmentally resistant, and we saw that
Speaker 4: spread globally within about six months actually, so we know
Speaker 4: that environmentally resistant viruses just through bomite transmission, can you know,
Speaker 4: transmission on shoes and things like that. I think the
Speaker 4: other thing that I don't have a lot of data on,
Speaker 4: but I really didn't appreciate. I guess so much before
Speaker 4: RHGV two how much trade of rabbits and rabbit equipment
Speaker 4: particularly there are. So I think, you know, it could
Speaker 4: be that if somebody's pet rabbit dies, they then put
Speaker 4: the cage on eBay or something, and somebody else orders
Speaker 4: the cage and then the cage is contaminated. And so
Speaker 4: again I certainly don't have direct evidence for that, but
Speaker 4: I think it's it's easy to sell stuff internationally these
Speaker 4: days and ship stuff, and so I suspect that there
Speaker 4: may be some of that as well.
Speaker 1: I want to talk about sort of the impact of
Speaker 1: RHDV two in Australia in a minute, but I want
Speaker 1: to first ask about some of these places where RHDV
Speaker 1: one or RHDV two has spread and where rabbits are
Speaker 1: not considered invasive where they're, you know, just a part
Speaker 1: of the natural ecosystem. What have we seen in terms
Speaker 1: of the impact on the local rabbit populations there, and
Speaker 1: what kind of downstream effects have there been on the
Speaker 1: other members of that ecosystem.
Speaker 3: You know.
Speaker 4: The impacts of RHDV first RGV one are now URHDV
Speaker 4: two on rabbit populations in their native home range is
Speaker 4: really concerning and it's actually caused them to be their
Speaker 4: threat category to be upgraded in terms of the IC
Speaker 4: and Red List. So it really is a major concern
Speaker 4: for native rabbit populations. And so rabbits are native to
Speaker 4: the Iberian Peninsula, so Portugal and Spain, and they've certainly
Speaker 4: observed sixty to seventy percent declines in rabbit populations, and
Speaker 4: then they've also observed similar reductions on their apex predators,
Speaker 4: so the Iberian links in the Spanish Imperial Eagle, particularly
Speaker 4: because those animals don't have the food source, and that
Speaker 4: then effects for tea of those populations and so they're
Speaker 4: not breeding as effectively, and so rabbits really are keystone species.
Speaker 3: In their native environment.
Speaker 4: Similarly, RGB two arrived in the US in early twenty
Speaker 4: twenty and we've seen quite dramatic impacts on cottontail and
Speaker 4: jack rabbit populations in the US, and certainly there are
Speaker 4: several endangered species over there, and so there's quite grave
Speaker 4: concerns about the impacts of RHGB two on those already
Speaker 4: threatened populations. Likely there'll be similar lead on effects on
Speaker 4: their predators as well. I don't know that the reductions
Speaker 4: have actually been quantified at this point in the US,
Speaker 4: and I think the other thing, you know, I've had
Speaker 4: some conversations with colleagues in the US and they've sort
Speaker 4: of said, we haven't really seen the knockdowns that we
Speaker 4: you know, you've reported in Australia that we're seen in Europe.
Speaker 4: And I think that's probably at least partially due to
Speaker 4: the different ecology of the cottontails and jack rabbits over there.
Speaker 4: So I believe that they don't form these massive warren
Speaker 4: systems same way that rabbits do. The contact densities are
Speaker 4: probably lower, and things like that.
Speaker 1: A lot of people who are concerned about this are
Speaker 1: not just concerned about the wild rabbits but also sort
Speaker 1: of domestic pet owners. Is there anything good on the
Speaker 1: horazon or is there any good news on the horizon
Speaker 1: potentially for a vaccine or any sort of control, I
Speaker 1: guess either for both the wild rabbits or people who
Speaker 1: have domestic pets.
Speaker 4: Certainly for domestic pets, good news with RHDV or caliciviruses
Speaker 4: is that really there's only those two types, so RHDV
Speaker 4: one and then RHDV two, and the immunity induced if
Speaker 4: you do stuff I have infection or after vaccination is
Speaker 4: pretty much lifelong. Like it's really durable. It's a really
Speaker 4: strong induction of immunity. And so RHDV two vaccines have
Speaker 4: been developed and are available in many parts of the world,
Speaker 4: and so for pet rabbits, if they're vaccinated, really not likely.
Speaker 3: To be an issue.
Speaker 4: Unfortunately, in Australia we don't currently have an RHDV two
Speaker 4: vaccine and that is a problem and something that is
Speaker 4: being worked on. In terms of wild rabbits, I think
Speaker 4: that's a bit harder. You know, how do you vaccinate
Speaker 4: wild populations, I think is an ongoing concern in multiple
Speaker 4: from multiple disease perspectives. You know, certainly in the Iberian
Speaker 4: Peninsula they're doing a lot of habitat management to try
Speaker 4: to help support rabbit populations. They're actually restocking wild populations,
Speaker 4: so moving animals from high density to impacted areas. And
Speaker 4: I think we now know so in the last couple
Speaker 4: of years, it's clear that maternal antibodies, so if the
Speaker 4: mum has antibodies to RHDV two, then the kittens will
Speaker 4: be protected for you know, sort of around an eight
Speaker 4: week period, and if the kittens are infected during that time,
Speaker 4: then they don't die, they effectively get vaccinated. And so
Speaker 4: there was a really interesting paper out recently. They actually
Speaker 4: spread URHDV two baits in an enclosed population in a
Speaker 4: control population, but they actually spread URHDV two brates during
Speaker 4: breeding periods and they actually showed that there was a
Speaker 4: reduction in young rabbit mortality by a third and there
Speaker 4: were actually more immune juveniles recruited into the adult population.
Speaker 4: And so I think as RHDV two becomes endemic and
Speaker 4: imminity levels increase, that maternal antibody protection will help buffer
Speaker 4: those impacts on rabbit populations moving forward, which is good
Speaker 4: for native populations, but again in Australia it's going to
Speaker 4: be an issue for bio control.
Speaker 1: In our mixomatosis episode, we talked a lot about the
Speaker 1: evolution of virulence, which is one of my all time
Speaker 1: favorite things to think about, and how selection pressures are
Speaker 1: super dependent upon the virus itself and the way it's transmitted,
Speaker 1: the host behavior, the environment, among many other things. In
Speaker 1: the case of maximatosis, of course there is this trend
Speaker 1: towards decrease veryviolence, and then more recently it seems like
Speaker 1: a few more virulent streams have been selected for. And
Speaker 1: then of course genetic resistance among the rabbits played a
Speaker 1: large role, and so I was wondering, you know, what
Speaker 1: have we seen in terms of any virulence changes of
Speaker 1: RHDV one or two since these viruses were first discovered,
Speaker 1: and has there also been any genetic resistance among rabbits.
Speaker 4: It's such a beautiful example of how each virus is
Speaker 4: perfectly adapted to maximize its transmission, right, And so mixomavirus
Speaker 4: is spread by biting insects, and so therefore it requires
Speaker 4: a live animal to transmit. So it's, you know, in
Speaker 4: the virus's best interest to keep the host alive for
Speaker 4: as long as possible to maximize the number of biting
Speaker 4: insects that can feed on that infected animal. And so
Speaker 4: prolonged disease duration is good, so hence the virus attenuates
Speaker 4: to become less virulent. In the case of rhdv it's
Speaker 4: spread from that dead animal. Like I said, it's that
Speaker 4: carcass contaminating the environment and being exposed to blowflies that
Speaker 4: facilitates transmission. And so as long as they die at
Speaker 4: the peak amount of infectious virus, that's going to optimize transmission. Hence,
Speaker 4: we really haven't seen attenuation of the virus with either
Speaker 4: RHDV one or RHDV two, because again, maximum transmission occurs
Speaker 4: by killing the rabbit at that you know, forty eight
Speaker 4: hour mark, when the entire liver is just packed full
Speaker 4: of virus. And so I know there's been a lot
Speaker 4: of discussion about that virus has always evolved to be mild,
Speaker 4: and certainly I think this is the classic example of
Speaker 4: you know, it really depends on the root of transmission.
Speaker 4: And so in terms of genetic resistance, mixomavirus is a
Speaker 4: pox virus, so it's a very large DNA virus, and
Speaker 4: so it encodes a whole bunch of genes, and I
Speaker 4: guess that also provides a lot of targets for the
Speaker 4: host immune system and so pox viruses have all of
Speaker 4: these really cool mechanisms of trying to counteract the host
Speaker 4: immune system, and therefore the host evolves to then counter
Speaker 4: the counteractions and etcetera, etcetera. And this really beautiful virus
Speaker 4: host coevolution. Because calisi viruses are so tiny, they just
Speaker 4: kind of they get in, get it done, and that's it.
Speaker 3: And so it's, yeah, a bit of a different story.
Speaker 4: There are some studies suggesting the development of genetic resistance
Speaker 4: in some localized populations to RHDV one, at least in Australia,
Speaker 4: but certainly it doesn't seem to be a major driving
Speaker 4: force the way that mixomavirus was. And again, I think
Speaker 4: that's because rhdv is just so lethal so quickly that
Speaker 4: there's not really the opportunity to survive. And I think
Speaker 4: what's really intriguing is the RHDV one RHDV two differences here.
Speaker 4: Because RHDV one, while it was able to infect, is
Speaker 4: able to infect young rabbits younger than about eight weeks
Speaker 4: of age, it doesn't tend to cause disease in young rabbits.
Speaker 4: It only kills adult rabbits, and that's independent of maternal antibodies.
Speaker 3: There's just there's.
Speaker 4: Something about young rabbits that leads them to not develop
Speaker 4: disease after rhgv one infection, whereas that's not true of
Speaker 4: RHGV two. RHGV two lethally kills both young and old rabbits,
Speaker 4: and so in the case of rhdv one, it was
Speaker 4: kind of a very stochastic or random event, Like if
Speaker 4: you happened to be five weeks old when you got infected,
Speaker 4: you survived, and if you happen to be nine weeks old,
Speaker 4: you know, you died, and so there's not.
Speaker 3: Really a strong selection pressure there.
Speaker 4: It was just a sort of a random event, whereas
Speaker 4: with RHDV two there's not that sort of age differential
Speaker 4: and so previously just being young enough to randomly avoid
Speaker 4: dying is not a thing anymore. And so the rabbits
Speaker 4: that survive RHDV two infection, if there is a genetic
Speaker 4: component there, it's potentially likely that there will be a
Speaker 4: lot more as strong a selection pressure for development of
Speaker 4: genetic resists to HGV two than there was to development
Speaker 4: of rhgv one. So it's certainly something that people are
Speaker 4: very keen and actively investigating to try to see how
Speaker 4: this plays out as RHDV two becomes endemic.
Speaker 1: Here in North America and in many other places where
Speaker 1: rabbits are considered like a keystone native species. The arrival
Speaker 1: of RHDV two has been met with these alarm bells,
Speaker 1: like you know, concern for the rabbits. This could be
Speaker 1: lead to a lot of ecosystem collapses. But in Australia,
Speaker 1: you know, where rabbits have been invasive for about one
Speaker 1: hundred and sixty years or so, has RHDV two been
Speaker 1: seen as a problem or more as a potential solution.
Speaker 1: And do you think that these differences in perspectives across
Speaker 1: different countries, do you think that that changes the way
Speaker 1: that research is done or focused on the different types
Speaker 1: of research questions into this pathogen.
Speaker 4: Yeah. So RHGV two was first detected in Australia and
Speaker 4: probably arrived in Australia in around twenty fourteen. First detected
Speaker 4: in twenty fifteen, and at that time rabbit populations were
Speaker 4: so certainly increasing and we were actively investigating the release
Speaker 4: of a new buyer control of this K five variant
Speaker 4: that I mentioned briefly at the beginning, So you know,
Speaker 4: rabbit populations were increasing, it was seen to be a
Speaker 4: problem and population densities were very high. So when RHDV
Speaker 4: two entered the Australian rabbit population, as we've observed elsewhere,
Speaker 4: there was this massive epizootic sweep through and we saw
Speaker 4: population reductions based on you know, serological data and spotlight
Speaker 4: counts and things like that, as an estimated to sixty
Speaker 4: reduction in rabbit abundance nationally, like sixty percent population level reduction,
Speaker 4: so very considerable from our perspective. That dramatically interfered with
Speaker 4: all of the research that had been going on for
Speaker 4: the K five release, right because we'd put all this
Speaker 4: modeling and effort into looking at how K five would
Speaker 4: behave in the pre RHDB two rabbit population, and obviously
Speaker 4: once RHDV two swept through, population density were much lower,
Speaker 4: they were probably a lot more fragmented, and so you know,
Speaker 4: the effective reproductive number is totally different in different population conditions,
Speaker 4: and so there was very confusing aspect between like was
Speaker 4: this the new buyer control that these scientists were talking about,
Speaker 4: and then we're trying to say no, it was a
Speaker 4: different strain that was just spontaneously came in and things
Speaker 4: like that. So overall, perspective, it's dramatically reduced rabbit numbers,
Speaker 4: which has been very beneficial. However, it's certainly a problem
Speaker 4: for pet rabbit populations because, as I said, we don't
Speaker 4: have a vaccine here. We weren't expecting URHDV two and
Speaker 4: so like again for that K five virus, we've done
Speaker 4: a lot of research into making sure that the vaccines
Speaker 4: were appropriate for that release, and then RHDB two swept
Speaker 4: through and it's having really really dramatic impacts on pet rabbits,
Speaker 4: and so an RGB two vaccine is certainly needed for
Speaker 4: Australian pet rabbits. In terms of the differences and research
Speaker 4: focuses between different countries, I think really it's all about
Speaker 4: understanding the pathogen right, and then you can either use
Speaker 4: that to your advantage as a bio control or to
Speaker 4: your advantage to counteract its impact. And so I think
Speaker 4: we're all actually doing quite similar research.
Speaker 3: It's just how those findings are applied.
Speaker 1: So the use of biocontrol is never without controversy. Can
Speaker 1: you talk about some of the reasons that people are
Speaker 1: opposed to the use of these rabbit viruses and is
Speaker 1: there a possible downside to reducing rabbit populations in Australia.
Speaker 4: I mean, nobody likes killing animals, right like, nobody wants
Speaker 4: to be killing animals if there was a better way,
Speaker 4: you know, one hundred percent. So unfortunately, with the current
Speaker 4: technologies that we have, lethal control invasive species really is
Speaker 4: the only way to manage that. And even you know,
Speaker 4: you can't go around and surgically sterilize every rabbit in
Speaker 4: Australia and things like that, and even if you do,
Speaker 4: then they're still going to have those environmental impacts in
Speaker 4: the meantime. So but of course, yeah, it certainly is controversial.
Speaker 4: There's a few different reasons why it's controversial. I mean,
Speaker 4: I guess obviously animal welfare particularly you know, as we said,
Speaker 4: RHDV is very quick and there are minimal clinical signs.
Speaker 4: You know, although the path of physiology sounds horrific, it's
Speaker 4: really your organs just pretty much go into organ failure
Speaker 4: and you die very quickly.
Speaker 3: So the welfare is way better than something like mixo.
Speaker 4: People have raised concerns about releasing viruses viruses of alve
Speaker 4: you know, will it spread to native species or other
Speaker 4: species or could it cross species? And certainly I guess
Speaker 4: with the many decades at least with RHDV one. These
Speaker 4: viruses appear to be incredibly species specific and we haven't
Speaker 4: seen any evidence of infection in non lagomorph species. Obviously,
Speaker 4: the impact on domestic rabbits is controversial, and for that,
Speaker 4: as we said, we need a vaccine, but the vaccines
Speaker 4: are very effective when they're available. Possible downsides to reduce
Speaker 4: rabbit populations. I think one thing that's frequently raised is
Speaker 4: that if you reduce rabbit populations, that would lead to
Speaker 4: predators turning to native species. And again there's been quite
Speaker 4: a lot of research actually done investigating that, and there's
Speaker 4: been no direct evidence to actually support this prey switching
Speaker 4: by either feral or native predators in Australia, and so
Speaker 4: actually it was the opposite. Reduced rabbit abundance was shown
Speaker 4: to actually reduce feral cat and fox abundance and reduce
Speaker 4: the predation of native fauna because you know, a large
Speaker 4: population of rabbits supports a large population of these predators,
Speaker 4: and so just by reducing the number of predators by
Speaker 4: reducing their food source was actually beneficial. But it is
Speaker 4: something that's quite frequently raised. And then just briefly, I
Speaker 4: think the other thing that perhaps is not so frequently
Speaker 4: raised by opponents of bio control, but for users of
Speaker 4: the buyer control, I guess the efficacy of the agent
Speaker 4: can be quite variable. So it depends on you know,
Speaker 4: the virus dose that the animal receives, the level of
Speaker 4: pre existing immunity, the maternal antibody status, and it really
Speaker 4: needs to be used at the right times, and so
Speaker 4: they're require a little bit more finesse than something like
Speaker 4: putting out a poison.
Speaker 1: So one last question about r HGV two biology and
Speaker 1: so on before I get to ask a bunch of
Speaker 1: questions about you, and that is the impact of climate change.
Speaker 1: So what do we know or what is thought to
Speaker 1: be the potential impact of climate change on rabbit populations
Speaker 1: or on the distribution of these rabbit viruses in Australia.
Speaker 4: You know, rabbits are known to be really adaptable their
Speaker 4: native range of that Mediterranean ecosystem, but they've really managed
Speaker 4: to adapt to a lot of Europe. There's feral rabbit
Speaker 4: populations in British Columbia and Canada. You know, they colonized
Speaker 4: Australia within a seventy year period or so. They are
Speaker 4: really adaptable and so if the rabbit populations thrive and
Speaker 4: particularly in adverse environmental conditions, then this is going to
Speaker 4: really have more impacts on our native plant and animal species.
Speaker 3: And so for the.
Speaker 4: Viruses themselves, as we said, they're pretty environmentally resistant. But again,
Speaker 4: if we start to see these really prolonged periods of drought,
Speaker 4: then that's going to probably reduce the environmental burden of
Speaker 4: these viruses. And I think we're probably already seeing some
Speaker 4: of these impacts in terms of the variability that we've seen.
Speaker 3: Over the last few years.
Speaker 4: So last over the last couple of years, we've had
Speaker 4: a La Nina event in Australia, so a lot of warm,
Speaker 4: wet weather, and certainly the last two years we've seen
Speaker 4: really massive outbreaks of callicivirus in spring when those fly
Speaker 4: vectors start to increase. But I would assume that drought
Speaker 4: may then reduce environmental survival. So there's probably arguments both
Speaker 4: ways on how that would affect the actual virus, But
Speaker 4: certainly I think rabbits will survive or adapt to climate
Speaker 4: change a lot more readily than our native species, which
Speaker 4: is a concern.
Speaker 1: So we're going to take a quick break here and
Speaker 1: then when we get back. I want to ask you
Speaker 1: what it's like to work in the rabbit biocontrol program
Speaker 1: and what a veterinary virologist does.
Speaker 2: I'm so excited.
Speaker 1: Thanks, Welcome back everyone. Okay, So, I want to know,
Speaker 1: as the team leader on the rabbit biocontrol program, what
Speaker 1: do you end up doing on a day to day basis,
Speaker 1: or maybe it's more accurate to ask you how much
Speaker 1: does what you do change from d to day?
Speaker 4: Yes, So, I think you know what's really exciting about
Speaker 4: our team or the research that we do is it
Speaker 4: spreads quite a few broad areas. So you know, we
Speaker 4: do animal experimental work, so infection trials, and then we
Speaker 4: do a lot of in vitro work policy viruses notoriously
Speaker 4: don't grow in cell culture, and so we're trying to
Speaker 4: establish an organoid system for these viruses. So there's some
Speaker 4: you know, molecular biology, there's cell culture, there's animal experiments,
Speaker 4: and then there's field work as well, so we get
Speaker 4: to go out and sample rabbits in the field, which
Speaker 4: is lovely, and then there's a lot of molecular surveillance
Speaker 4: and diagnostic testing as well. So we really have broad
Speaker 4: techniques and are able to do a lot of variable
Speaker 4: things that that keeps life interesting for.
Speaker 3: Me as team leader. I'm not really in the lab
Speaker 3: so much.
Speaker 4: These days, which is quite sad, but you know, like
Speaker 4: many sort of pis, I guess, I'm working across several projects,
Speaker 4: you know, working on the next grant, working on the
Speaker 4: next publication. I'm also a facility veterinarian here, so I
Speaker 4: respond to animal emergencies and yeah, you know, life's never
Speaker 4: dull in science.
Speaker 3: I think, Yeah, that's that's right.
Speaker 1: You practiced as a veterinarian for a bit, it's and
Speaker 1: you are still practicing as a veterinarian, which is amazing.
Speaker 1: So can you take me through how you got from
Speaker 1: veterinarian to veterinarian and veterinary virologists.
Speaker 2: Lots of views in that sentence, lots of made it through.
Speaker 4: Yeah. So you know, I was one of those kids
Speaker 4: who was I always curious, you know, I was why
Speaker 4: but why?
Speaker 3: But why? But why?
Speaker 4: And you know, I love nature, I loved animals, and
Speaker 4: so I from a very young age, I said I'm
Speaker 4: going to be a vet and so that's what I did.
Speaker 3: And I actually thought I was going to be in.
Speaker 4: Small animal practice for the rest of my life, and
Speaker 4: I got into small animal practice, and you know, I
Speaker 4: think I found that I wasn't really asking why so
Speaker 4: much on a day to day basis. There was a
Speaker 4: lot of routine and you know, there's a lot of
Speaker 4: other considerations, and so that sort of that curiosity wasn't
Speaker 4: satisfied the way I had expected it to be, I guess,
Speaker 4: and so to me that lent itself to going back
Speaker 4: to do a PhD. And when I was applying for
Speaker 4: PhD programs, you know, looking back, everything I applied for
Speaker 4: was an infectious disease of some sort, and so I'm
Speaker 4: guessing that infectious diseases piqued my interest somewhere along the line.
Speaker 4: And yeah, ended up doing a virology project working on
Speaker 4: recombinant vaccines for the poultry industry. And yet from there
Speaker 4: I just fell in love with viruses, like they're just
Speaker 4: they're so cool and they're so diverse, and heaps of
Speaker 4: different opportunities have stemmed from that. So after my PhD,
Speaker 4: I worked for a period of time as a diagnostic
Speaker 4: virologist in one of the state labs, and then went
Speaker 4: to do a postdoc in rabbit callisi viruses, and you know,
Speaker 4: like we've just talked about.
Speaker 3: They're so cool. How you know, there's so much to do,
Speaker 3: so I've stayed stayed. Since do you.
Speaker 1: Have a favorite virus or bacterium, I'll allow that too,
Speaker 1: or parasite.
Speaker 3: Well, I mean I probably have to say O HDV,
Speaker 3: don't I you.
Speaker 1: Don't have to, but I would. I would think that
Speaker 1: that's a very strong contender.
Speaker 4: Yeah, yes, I just you know, I think, yeah, viruses
Speaker 4: are also perfectly adapted to their niche, right, and so
Speaker 4: every single one of them has such a cool story
Speaker 4: to tell. So I mean, I think perhaps one of
Speaker 4: the coolest ones is, you know, since sittin. So since
Speaker 4: sittin gene, which is the gene that allows the development
Speaker 4: of placenta, right, it allows the cells to fuse, which
Speaker 4: is the basis for the you know, for placental development.
Speaker 4: Since sittin is a captured retroviral gene from a human retrovirus, right,
Speaker 4: and that that allows the evolution of all placental mammals.
Speaker 4: So I guess I kind of have to say sincitan
Speaker 4: otherwise I wouldn't be here, you know, or whatever virus
Speaker 4: gave rise to sincitin. And also, you know, I would
Speaker 4: hate to live in a world without my dog, and
Speaker 4: so you know, but yeah, you know, viruses have just
Speaker 4: shaped evolutions so strongly, and so every single one of
Speaker 4: them is just amazing. And that you know, there's those
Speaker 4: POLYDNA viruses in parasitoid wasps that they inject the virus
Speaker 4: along with their eggs that suppresses the caterpillar immune response
Speaker 4: so that the caterpillar immune system doesn't kill the egg
Speaker 4: and things like that. And then there's a microvirus that
Speaker 4: infects a fungus that infects rape seed, which turns the
Speaker 4: fungus from virulent to actually beneficial for the plant and
Speaker 4: things like that, and so they're just I mean, I
Speaker 4: can't pick one. There are just there's so many cool examples.
Speaker 1: You just give some of the most fascinating examples that
Speaker 1: I don't think I've heard of any of those. And
Speaker 1: so that is like I am about to go after
Speaker 1: this is over, I'm going to go like on a
Speaker 1: Wikipedia rabbit hole about every single one of those.
Speaker 2: And I'm very excited.
Speaker 3: Worth it, totally worth it.
Speaker 1: So you work at CSIRO, which is a government institution,
Speaker 1: and what do you think are some of the pros
Speaker 1: and cons of working at a place like CSIRO versus
Speaker 1: like a university for instance.
Speaker 4: Yeah, so I think, you know, one of the things
Speaker 4: about working for Sarah that I really enjoy and that
Speaker 4: really vibes with my values, I guess, is the really
Speaker 4: applied focus. You're doing research because someone or an industry
Speaker 4: body has said this is important to us, can you
Speaker 4: look into this? And so they're really applied outcomes that
Speaker 4: end users really care about. It's really output driven and
Speaker 4: you really do get to work closely with stakeholders, so
Speaker 4: you know, setting the next research agenda, it's like, okay, well,
Speaker 4: how do you feel about what we've done so far?
Speaker 4: What like where we go from here? And so it's
Speaker 4: it's a real, really collaborateive approach with the end users,
Speaker 4: which is great.
Speaker 3: You know.
Speaker 4: The flip side of that is that there are really
Speaker 4: strict milestones and deadlines and there's not so much of
Speaker 4: the opportunity to sort of just follow the science for
Speaker 4: the science's sake that perhaps you may get in an
Speaker 4: academic institution. Similarly, it's a lot harder to I guess, pivot. So,
Speaker 4: for example, with the whole coronavirus situation, I know so
Speaker 4: many virology labs, you know just completely pivoted to SARS
Speaker 4: Kobe two and obviously like that was never going to
Speaker 4: be an option because you know, the agriculture industry isn't
Speaker 4: going to they have a rabbit problem. They still have
Speaker 4: a rabbit problem. So, yeah, the pros and cons, you know,
Speaker 4: they're both the same side of the coin. It's really
Speaker 4: achievement focused. But then it's a little less curiosity driven.
Speaker 3: I suppose on.
Speaker 1: The podcast we're always talking about one health and how
Speaker 1: much we love it and how important it is for
Speaker 1: different fields to work together to consider the whole picture.
Speaker 1: And so do you feel as though so your experience
Speaker 1: as a veterinarian has given you more of an insight
Speaker 1: into the one health approach?
Speaker 3: Yeah, I really do.
Speaker 4: I think you know, at VET school well and in
Speaker 4: practice you have to have your head both around the
Speaker 4: individual level treating the individual animal, but also how that
Speaker 4: impacts the herd and the population and interspecies level as well.
Speaker 4: And so I think it's just drilled into us and
Speaker 4: we've never considered otherwise that you know, how does what
Speaker 4: I do here, how is that going to impact the
Speaker 4: rest of the ecosystem? And you know, and again from
Speaker 4: the vetnory perspective, it incorporates nutrition, and in terms of
Speaker 4: large animals, that incorporates pasture, and so that involves drought
Speaker 4: because then different weeds will pop up with different climactic
Speaker 4: conditions and things like that.
Speaker 3: So I think training as a veterinarian really gives.
Speaker 4: You that broader perspective of the animal, but also the
Speaker 4: environmental and then the human and zenotic disease picture as well.
Speaker 1: So can you tell me about a cool project that
Speaker 1: you're currently working on?
Speaker 4: So perhaps I may have given away a bit earlier,
Speaker 4: but the whole recombination story has just over the last
Speaker 4: couple of years has really peaked my interest. So, as
Speaker 4: I mentioned, ERHDV two first arrived in Australia probably in
Speaker 4: twenty fourteen, and we've been tracking the genomic epidemiology of
Speaker 4: these viruses since it arrived. And what we've seen through
Speaker 4: the genomic surveillance is at least six independent recombination events
Speaker 4: since the arrival of RHDV two in Australia. And that's
Speaker 4: just the recombination events that have generated epidemiologically fit viruses, right,
Speaker 4: not all the viruses that died out. So that's unprecedented
Speaker 4: or at least I didn't appreciate it prior to that
Speaker 4: how important recombination was, and then seeing these successive waves
Speaker 4: of epidemiological replacement by these variants, and sadly, I think
Speaker 4: it's been superseded now by the coronavirus variance.
Speaker 3: And everybody's like, well, yeah, what did you expect? But
Speaker 3: for me, it was really striking when I saw this
Speaker 3: with Kaleci viruses.
Speaker 4: And I think what's been really intriguing. So among those
Speaker 4: six recomninant variants that have arisen, they all contain almost
Speaker 4: identical capsid proteins or you know, effectively the spike protein
Speaker 4: to each other. So it's not immune escape that's driving
Speaker 4: this epidemiological replacement of these viruses. And so if it's
Speaker 4: not immune escape, like what is it? Because again there's
Speaker 4: all this focus on immune escape. And so we recently
Speaker 4: had a got funding support for a postdoctoral position to
Speaker 4: start to try to look into what is driving the
Speaker 4: epidemiological fitness of these recombinant variants. So which of these
Speaker 4: non structural proteins and why if it's not immune escape,
Speaker 4: what is going on? And so I think that's really
Speaker 4: got my interest at the moment.
Speaker 1: All Right, So I've got one last question for you,
Speaker 1: and that is an.
Speaker 2: Advice seeking question.
Speaker 1: What advice would you give to someone who is interested
Speaker 1: in pursuing this career or maybe you know, what type
Speaker 1: of advice do you wish you had received when you
Speaker 1: were just starting out?
Speaker 4: You know, in hindsight looking back, you know, I think
Speaker 4: there's a lot of talk now about this fixed mindset
Speaker 4: versus growth mindset type thing. And I think, as I said,
Speaker 4: I decided from a really early age that I was
Speaker 4: going to be a vet, and so I guess my
Speaker 4: whole identity, as you know, through my school years and
Speaker 4: then going through vet school and everything was like I'm
Speaker 4: going to be a vet.
Speaker 3: I'm going to be a vet. And that really fixed mindset.
Speaker 4: I mean it was good obviously, like you need to
Speaker 4: have that the drive, but it also you know, it
Speaker 4: probably made me pass up or bypass other opportunities that
Speaker 4: may have popped up in the way along the way.
Speaker 4: So I think, in hindsight, you know, if I could
Speaker 4: have adopted more of a growth mindset instead of this
Speaker 4: focus on being a small animal practicing veterinarian, it could
Speaker 4: have looked really different. So I would just say my
Speaker 4: advice based on that would be be open to opportunities,
Speaker 4: like you know, have a plan, but be prepared to
Speaker 4: adapt it.
Speaker 3: Be curious.
Speaker 4: And I think for me it was really important finding
Speaker 4: out what my values were and you know, as I
Speaker 4: sort of briefly mentioned, reconciling that practice wasn't satisfying that
Speaker 4: core curiosity value that is so strong for me, and
Speaker 4: knowing that there's other things out there where you will
Speaker 4: be a good fit sort of thing, and so yeah,
Speaker 4: be open to different directions and yeah, just be curious.
Speaker 2: That was so fascinating.
Speaker 1: Oh my goodness, Thank you so so much doctor Hall
Speaker 1: for chatting about rabbits and viruses and evolution. I had
Speaker 1: such a great time. If you want to learn more
Speaker 1: about the work that doctor Hall is doing, I'll link
Speaker 1: to the project's website, as well as a bunch of
Speaker 1: cool articles related to doctor Hall's work on the post
Speaker 1: for this episode on our website, This podcast will Kill
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Speaker 2: We've got another
Speaker 1: Regular season episode coming out next week covering a whole
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