Note: Following my exploration of the realities and potential of genetic resistance against CWD with Dr. Nicholas Haley, I found myself still curious regarding other potential aspects of CWD research. Having taken classes taught by the professor who has himself been leading the vaccine-development effort in Canada, I sought him out again to get an update and overview of the process. And so it was that, with a new-found understanding and appreciation for the genetic resistance research, I set out to meet with Dr. Scott Napper of the University of Saskatchewan, to attempt to reach the same level of understanding about a CWD vaccine as I had recently received regarding genetic resistance.
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It was grey and rainy as I left my lab a couple afternoons ago. The light drizzle soaked through my jacket as I trudged across campus in the direction of the Health Sciences building, but I paid it no heed. I was distracted by the many questions circulating through my mind regarding Dr. Napper’s efforts to create a CWD vaccine. Could a vaccine really work? I wondered. How can a vaccine possibly work when a prion is so different from a virus? What would be the environmental impacts of using a vaccine in the wild? What would be the economic impacts of using it?

All these questions and so many more were rolling around in my head as I made my way through the tall oak doors and fought my way upstream through the tumultuous crowd of first-year med students filling the hallways from wall-to-wall. After a few minutes of wandering and checking maps, I found myself standing before Dr. Napper’s office. Despite having had a little trouble finding it, I was glad that he had chosen to meet me in his Health Sciences office, rather than in his office in VIDO-InterVac (the Vaccine and Infectious Disease Organization-International Vaccine Centre) where he normally works; I had heard from others who met him there that the security for such a meeting is insanely rigorous, involving visitor passes, background screening, and potentially biosafety training, depending on where in the building you have to travel. Which makes sense, I suppose, in a building housing a level 3 research facility and containing some really nasty organisms (tuberculosis, Zika virus, and Coronavirus, to name just a few).
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For a guy who works in such an intense environment though, Scott has a surprisingly warm personality. Quick to smile and tell his students that he has his daughters’ names tattooed under his shirt (as chains of amino acids of course, such that spelling out the amino acids with their alphabetical codes reveals the girls’ names), he is one of the most welcoming scientists I have met. His door is open, and before I can knock, he booms out “Dale! Good to see you again, come in and take a seat!”

We chat briefly about CWD in general, the difficulty of securing funding for research, and my progress into grad school before I segue into a few questions about his vaccine development efforts. My first question for him is regarding just how a theorized vaccine would work, since it obviously cannot work the same as a viral vaccine.

“It is definitely different,” he agrees, “but it’s the same basic principle. With a virus, you have a clear situation of ‘here’s you, here’s the virus,’ and as long as the antibodies only attack the virus, you’re good. With a prion vaccine though, it’s almost more like a cancer vaccine, because it’s a part of your own body that has turned against you. A prion protein has one particular shape in the healthy form and another shape in the unhealthy form. So what our research has been doing is targeting regions that are only exposed and available for antibody-binding in the unhealthy form. We call those DSE’s or Disease-Specific Epitopes, and we identified three of those. We developed three potential vaccines, each one targeting a different DSE on the CWD prion. Theoretically, what would happen is that if I vaccinate you with it, and you don’t have the prion disease, the antibodies come along, they see your healthy prion protein, and they don’t even recognize it. But if you DO have it, they recognize it and bind to it. So they only attack the misfolded pathological species.”
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He then goes on to describe how they tested the first of the 3 potential vaccines. “The first one we made was against a YYR target, this Tyrosine-Tyrosine-Arginine site, and that worked when we tried it in sheep. We vaccinated healthy sheep with it and watched them for four years, and there was no sign of the disease—indicating that the vaccine doesn’t cause spontaneous misfolding of healthy prions. Then we moved on to elk and deer and saw the same thing—no sign of any prion. So it was safe. But when we vaccinated elk and put them on infected land,  the vaccinated group actually came down with CWD a bit faster than the unvaccinated control group. Now, it was a small amount—barely statistically significant—but it was significant. The only options for the vaccine were that it 1) worked, 2) did nothing, or 3) made things worse, and in this case, it did seem to make things worse. We don’t know the exact reason, but there are two main possibilities.

​Either a) the antibodies are binding the low-level prions that were always passing through the gut and sort of ‘sopping them up’ into the body accelerating the disease, or b) the antibodies are binding the healthy form of the protein, causing it to misfold. But based on the results from the first experiment—where the sheep, elk, and deer did not show any sign of prions after 4 years—I really think it is the first option. They are binding prions from the gut, promoting their uptake, and increasing the number of prions taken into the body. Now this is fixable, and whether one of the other 2 vaccines might work perfectly as-is is a distinct possibility, but unfortunately, we have not had the funding to test more than the first one. But even if the other two vaccines were tested and ran into the same problem, there are work-arounds for that. We know when antibodies bind, which part is responsible for mediating uptake into the body. We can engineer antibodies to not have that, so they would still be secreted in the gut, still bind to the prion, but not be taken up. It gets a lot more complicated [on the production end], but it can be done.”

​I nodded, still chewing on something he had said in passing. “Now hold on,” I said. “You mentioned that you had tried it in sheep. Does that mean that your CWD vaccine would also work for scrapie?”
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“Absolutely!” he said. “Actually, when I began working on this vaccine, it was intended simply as a prion vaccine, and the primary focus was going to be BSE. But the cattle industry was worried that any talk of a BSE vaccine being developed would lead to panic as people start thinking that it is out of control (when we would simply have been acting pre-emptively to a large-scale break out) and so we were told not to call it a BSE vaccine. Since it would work just as well for CWD, however, we just decided to shift focus to the CWD aspect, and let it be used for BSE once it is completed. It is, in reality though, a prion vaccine that will work for any prion disease. This CWD vaccine, once completed would work equally for BSE, scrapie, Creutzfeldt-Jakob’s in humans, and any other number of prion disease.”  

I was blown away by the implications of such a universal vaccine. The impact it could have on the livestock farming community as a whole is spectacular. However, as I frequently remind people, the farming community is only part of the puzzle. We also have to consider impacts in the wild. A vaccine for CWD would certainly be of use in the wild, but to what extent? I wondered. I briefly highlighted part of my discussion with Dr. Haley regarding CWD resistance and mentioned that such resistance could potentially act as a safety net—in an ‘all-else-fails’ situation, at least some animals should hopefully remain CWD free—and asked Scott how he felt the vaccine would be of use in wild herds. He noted that while he does find it hard to imagine that CWD could wipe out cervids completely from the Earth, species do go extinct all the time, sometimes due to infectious diseases. So while he would expect that natural selection of whatever more-resistant genes exist would lead to some cervids surviving, "we have to consider the fact that this has the potential to be immensely destructive of cervid herds. As a result, to trust solely in genetic resistance seems like too large a gamble.”

How would a vaccine be applied in a wild environment? I wondered.

“Well, we worked on developing the vaccine using an attenuated rabies virus. This vaccine is completely administrable via oral pathway. Now this is in contrast to another study out of New York that claimed to have made some breakthroughs using an attenuated Salmonella vaccine. Besides many other problems with that study, the vaccine had to be applied repeatedly directly to the tonsils. Our vaccine would be a one-time dose, with no follow-ups required. To distribute it, we would simply go to people like yourself, with your outfitting business, and have it distributed in your bait-sites. As the deer congregate to eat the grain, they are also getting their dose of CWD vaccine.”
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“Do you think that vaccinating the wild could potentially create a sort of ‘vaccine dependence,’ where we keep all these susceptible animals alive and contributing their genes to the population when they should have died? Are we setting ourselves up to have to keep applying the vaccine indefinitely, or else face a massive outbreak due to so many susceptible genes in the herd?”

“Hmm… I like that. That’s interesting. You see, with a normal vaccine, the virus can’t survive without a host. We don’t need smallpox vaccines anymore because the vaccine eliminated the virus by preventing it from finding a host to replicate in. But how long will a prion last in the wild? We don’t know. If it will break down in a reasonable amount of time, we could vaccinate until the prions have broken down, while simultaneously preventing distribution of more prions. But we don’t know how long the prion takes to break down in the soil, and there’s always the chance that it arises randomly anyway. But having said that, I don’t know that I would call it vaccine-dependence. There’s still a lot of infectious agents that we routinely vaccinate against, and if we stop, they will come back. We could essentially say the same about polio. I mean, we could stop vaccinating against polio and say “let’s just step back and watch now as natural selection creates a tiny population of polio-resistant people, but I kind of don’t think that’s the best approach to take for some reason,” he laughs.

“That’s very true,” I agreed. “On a farm, routine vaccination is no problem. In the wild though, to commit to 100 years of vaccinations is pretty intense. But then again, if it is that or potentially watch cervids face extinction, that’s clearly something that should be done.”
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“That’s right,” he nodded. “But it may be more of a cyclical 10-year strategy where the vaccine needs to be redistributed every 10 years. It would be a big undertaking, but maybe not as bad as it seems looking at it from this side.”

Another thought had occurred to me as we were talking. “You have repeatedly said that CWD is not like a virus,” I said. “Are you familiar with Dr. Bastian’s work [who, interestingly, received two of his degrees from the University of Saskatchewan], regarding the spiroplasma always found in CWD positive animals? He believes this means that the bacteria, not a prion, causes the CWD.”
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He nods, and states “Personally, I think it’s [ridiculous]. Quite often what you get with any infection is a secondary infection. Likely, this is correlation, not causation. Prion diseases ravage your immune system, so becoming infected with a prion disease could make you more susceptible and hospitable to a certain type of bacteria. It’s similar to Johne’s disease in cattle. The agent that causes Johne’s disease, when we look into people with Krohn’s disease, we find the same bacteria there. But what it may be is that when you have chronic inflammation of the gut (a common symptom between both diseases) the bacteria are able to colonize the host and make a home there. The bacteria are a result of the disease, not vice-versa. So while those questions need to be asked and avenues explored, no, we are past that point in the science now. I can’t even remember the last time I was at a prion conference and someone presented that with a straight face.”

*Note: Dr. Bastion is the scientist who is currently being touted in hunting communities as 'having found a cure' for CWD. Watch for a blog update on that, however, these claims are extremely exaggerated and misleading at best. He has not found a cure and, as Dr. Napper points out, is likely pursuing a deeply-flawed line of research that will lead to nothing.*

 “Now, I’ve heard that there are potentially many different strains of the prion, and that they are all slightly different. Could that be a problem, where you create a vaccine that works on CWD in Saskatchewan, but not elsewhere?” I asked.

“Oh absolutely,” he agreed. “That’s why we are being careful to account for that. That's  why targeting all 3 DSE’s would be ideal. Think of it like if I took a swing at you. You might be able to avoid one swing, but if I try two punches and a kick, chances are at least one is going to connect.” I wondered if this example indicated that he was getting tired of having me in his office but his laugh indicated otherwise. “So that’s why we were pushing for a multi-valent vaccine—a vaccine developed in Saskatchewan would work equally well for reindeer in Norway.”

“And what is the current state of this research now?” I asked. “Is it still being tested?” Scott shook his head, a wry smile crossing his face. “No. Sadly, after getting so close and having two more vaccines already developed and awaiting testing, they have cut us off, and it is sitting on a shelf now, waiting for new funding.”

I shook my head in disbelief. “But this sounds so huge! And the cure might be literally already in hand, sitting on a shelf! Why would they do that?”
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“Well, getting funding has a lot to do with politics. Funding goes where the politicians think it will get them the most votes. And reality is that a lot of people have no idea what CWD is, [and BSE is not as large an issue as it once was, and Creutzfeldt-Jacobs disease, while severe, only infects a very small percentage of the population].If you ask someone in Toronto when the last time they saw a deer was, the reply might be ‘never.’ And so for the areas with the most votes, the loss of deer would be unfortunate, but hardly an impact on their lives [or so they think]. So funding opportunities shift to different diseases. And unfortunately, running a lab is also like running a business, and we need to be kind of opportunistic. I have employees whose paycheques depend on my ability to secure funding. So sadly, when the funding for CWD just isn’t there, as disappointing as it is with two potential vaccines sitting on a shelf, I have to focus on where the funding is. And to me it’s so short-sighted. I mean, this has the potential to be an absolute disaster—it already is in the cervid industry—and it could become so much worse. And they spent ten years funding it to the point where we were right on the edge of this breaking point, and then they went ‘you know what? That just doesn’t seem to be what we want to send funding towards anymore.’ It’s the nature of the game I guess, but it’s so frustrating.”

 We were running out of time, but I had one last, broad question. “If you had one thing you could explain regarding a vaccine, what would it be?”

“It would be that the vaccine is essentially an extra layer of defense. If we created this vaccine, fair warning: there is a chance that it still might not be the perfect answer [especially in the wild]. But it’s equally plausible that genetic resistance is not the complete answer either. What it might be is that genetic resistance, coupled with a vaccine, together can force Dr. Haley’s ‘ladder’ high enough that deer no longer get CWD, regardless of the level of environmental contamination with prions. Adding live diagnostic tools to the tool kit as well, then between these three, we should really be able to get it under control in the cervid industry at least.”
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And that was a good place to end it, I thought. Once again, I was seeing how important it is that we work together as an industry, recognizing the value in other research, even if it is not the ‘answer’ that we ourselves subscribe to. Just as deer farmers and hunters need to work together as a cohesive group to maintain a positive public image and to prevent the spread of CWD, we also need to work together in exploring the options that exist to combat, and potentially cure, the disease. So let’s not denounce valid research simply because we think there is a better option, or (heaven forbid) we want to downplay the severity of the disease. Let’s celebrate the successes of each research branch as they come, and support them as they encounter obstacles. Just as we need to celebrate and support each other in the hunting community. Remember, we’re all in this together. 

If you haven't read the prequel to this blog, where I interview Dr. Nicholas Haley about genetic resistance to CWD, make sure to check it out! 

This blog is adapted from an article I recently wrote in Deer Tracking Magazine. The information here is applicable and important when considering the potential implications that CWD may have for wild populations, despite this being geared heavily towards the deer farming industry (the primary funders and original audience of this research). This is just one aspect of the current science regarding CWD, but may prove to be the most realistic route for our wild populations to overcome CWD in the future.

“Resistance is futile.” These words are part of the common greeting frequently employed by an invading alien race called The Borg, from the tv show Star Trek. I’ll bet you never expected to see a Backwoods Boys blog open with a Star Trek quote, now did you?

I realize this seems like an odd quote to begin with, but it is a phrase that has been rolling around in my mind for the last while. Once stored in some dusty, near-forgotten corner of my mind, it was dredged up during one of my frequent visits to a popular Facebook group, where the topic of CWD is regularly discussed. Most recently, the CWD discussions have revolved around the exciting realm of “CWD resistance,” where deer breeders have begun to advertise deer as genetically resistant to the CWD prion. No longer are ads comprised simply of impressively antlered bucks with a score attached and perhaps a pedigree—many now include phrases such as “carrier of double alleles for CWD resistance”. Posts advertising sires as carriers of the highly sought-after 226K gene have become more and more common, with the resulting comment threads generally containing a great number of questions regarding the validity of any claim of resistance, as well as wondering about the science behind this new aspect of the deer-breeding market. Consequently, I have spent the past several months mulling over the potential that genetic resistance may hold for deer farming (and even wild deer herds). Is resistance really as good as it sounds? I wondered, or is resistance futile, simply one more grasp at straws to combat the ever-growing threat of CWD?

A quick search of the most recent literature failed to turn up many results about this topic, so I was left pondering my question for a few days. Eventually, I decided to do what any curious soul would do; contact the lead researcher directly and ask him for a crash-course in CWD genetic resistance.

Dr. Nicholas Haley is very open and friendly, and responded to my request for an interview “sometime in the future” with “Sure! How about tomorrow?” Less than 24 hours after approaching him, I was receiving the crash-course to end all crash-courses and by the end of the phone call (which went significantly over my allowed minutes of Canada-US calling on my cellphone plan) I had a good grasp on the science behind the hunt for resistant genes.

The Markers

There are actually five different variations of markers in the whitetail’s genome which can affect an individual’s susceptibility to the CWD prion. These markers began to become of interest during Dr. Haley’s large-scale studies regarding the efficiency of live-tests, where it was observed that several markers were under-represented in the positive results (in other words, they comprised a lesser percentage of the CWD positive animals than would have been statistically expected based on a null hypothesis that the markers do not influence resistance). In most cases, these animals that had the more-resistant markers, even when positive, were only in the early stages of the disease. Clearly this warranted further investigation.

​Each of these markers (96G, 96S, 116G, 95H, 226K) comprise a different percentage of the wild population, with the more-resistant alleles generally contributing to a much lower percentage of the population (often 3-5% at the most). While it has been argued by some that this indicates that the alleles, while providing a higher level of resistance towards CWD, also produce fitness disadvantages in the animals, this is not necessarily the case. In biology, the term “fitness” refers to an individual’s ability to survive and reproduce (not to physical condition and body fat). Consequently, it has been proposed by some naysayers that the under-representation of the more-resistant alleles in wild populations indicates that while these animals may be better able to survive the onslaught of CWD, they are less capable of surviving other stresses in life (perhaps they are less intelligent, or unable to avoid predators as easily, or less productive when breeding, etc).

Dr. Haley, however, is quick to refute this claim, basing his argument on observations of the alleles’ geographical distribution. He notes that, as far as he has seen so far, Canadian populations do not have the 226K allele within their genepool. This allele is generally concentrated in the New England area. Conversely, the 116G allele is absent in United States, but present in Canada. The 96S allele, however, is most common in the southern states. To him, this uneven distribution indicates that the various alleles are relatively recent mutations in the genepool, and simply have not had time to be dispersed throughout the population as a whole. Given time, he suspects that these alleles would become more common as interbreeding occurs between populations and as individuals emigrate from one geographical area (and its local populations), immigrating into new areas and populations where their novel genes would be introduced. His argument is further supported by the fact that some animals who are homozygous for the resistant markers, when compared to their twins who are homozygous for the susceptible markers, are identical and unable to be told apart. This indicates that there is no phenotypic (phenotypic: physical expression of a gene) difference resulting from the markers that would influence fitness. He states however, that this is certainly something that will be monitored as time goes on.
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The Resistance

It has been stated by many that genetic resistance in deer is the safest bet, because genetic resistance to scrapie was successfully integrated into sheep herds years ago. Consequently, sheep from these resistant lines can no longer contract scrapie. Or so it is commonly believed. Dr. Haley points out, however, that the average lifespan of a sheep is 8-10 years, and so what may appear as bulletproof resistance may actually be a delay in scrapie infection, such that the sheep do not generally live long enough to contract it. It is certainly possible, he says, that given a lifespan of 20 years, these so-called “resistant” sheep may eventually come down with the disease. Thus, the scrapie resistance that has been implemented into sheep populations may be more of a “functional resistance” in that for most practical purposes, the animals are resistant. Given the longer lifespan of farmed deer, however (especially does and breeder bucks), it is possible that the same issue could arise even among the most resistant lines. On the other hand, as the average wild deer only lives to 3 or 4, resistant lines (such as a homozygous 226KK) are much more likely to maintain resistance throughout their lives. 

All this talk about markers and resistance had me wondering how they all compare to each other, so I asked Dr. Haley for clarification on this point. He says that the best illustration he has come up with so far is to imagine a ladder in a room that is slowly filling with lava. Each rung on the ladder is a different allele, and the lava is the CWD prion. As the room fills with lava and it reaches each rung, the animals with that allele will come down with CWD. The rung lowest on the ladder (ie. the allele with the least resistance and highest susceptibility) is 96GG, followed by 96SS, 116GG, 95HH, and finally, 226KK. As CWD prevalence grows and prions accumulate in the environment (ie. the lava rises), individuals with each of these markers will contract CWD in turn. The first to go will be those with the 96GG allele, and the last to get it will be those with the 226KK allele. It is important to note, however, that even those with the highest resistance will likely contract CWD if the lava rises too high. As a result, Dr. Haley warns that using terminology such as “immune to CWD” is misleading and may lead to misconceptions and unrealistic expectations. As of this moment, he states, there is no evidence that any allele will make a deer immune to CWD. Rather, the alleles that confer the highest resistance will prevent the individual from contracting it as quickly as the others, potentially allowing the animal  to die before contracting the disease. Consequently, it is important that the term “resistant” be used in place of “immune” and that people recognize that “resistant” does not mean 100% resistant—simply more resistant than other markers. Think of it like “water resistant” boots versus “waterproof” boots. If you jump in a puddle with water resistant boots, you are still going to get wet feet (albeit not as rapidly as jumping in with sandals). “Waterproof boots” however will keep your feet dry. As of today, there is no such thing as “CWD-proof” genetics, only “CWD resistant”. Applying this to the speculation that testing a deer and finding that it has the K allele should be as good as a live-test for guaranteeing that the animal does not have CWD, Dr. Haley says that this is not the case. Since the K allele does not guarantee immunity, but rather the highest known level of resistance, finding the K marker in an individual’s genotype would not be comparable to finding it negative (either through a reliable live test or post-mortem test).

Another important consideration when planning a breeding strategy is to remember that these resistant alleles only naturally make up 3-5% of the population. As a result, there is potential for creating a genetic bottleneck, where the majority of future deer can be traced back to the same few sires. Such a situation would greatly decrease the genetic diversity of the domesticated deer population as a whole. If we think it’s difficult to find a unique lines now to avoid inbreeding, then we need to be cautious and far-sighted when creating breeding strategies for resistance as well. Consequently, it is imperative to keep the genepool as broad as possible by identifying as many of these sires as we can, and not breeding everything to the first few sires to show these alleles.

​The Genetics

Now all this talk of genes and alleles has had me wondering how a breeding program could make use of this strategy, and what sort of crosses would be most useful. Since each parent donates a single allele for the gene, it is very important to know which alleles each parent has the potential to supply to their offspring. Although much of the fine-tuning of the genetics is not 100% proven, it is believed that the genetics follows traditional Mendelian genetics, meaning if the parental alleles are known, the potential outcomes of these crosses can be fairly easily determined assuming 50/50 chance of either allele being passed down from the parent to the offspring. If, for example, the sire is known to be homozygous KK, he can only provide a K to the offspring. Similarly, if the mother is homozygous HH, she can only provide an H to the offspring. Testing this with a simple Punnett square (although it is simple enough that the diagram doesn’t need to be used) shows us that the all offspring will be heterozygous KH. While it is not known for certain how the different alleles interact, it is believed that they have a “codominant” effect (codominance means each allele expresses somewhat; codominant red flowers and white flowers combine to create pink offspring). In this case then, the offspring would be expected to have resistance somewhere between KK and HH. Dr. Haley speculates that the resistance in such a cross might still be high enough that the offspring would likely die before becoming infected (and so be indifferentiable from KK and HH), but admits that little is known for certain and that high prevalence in the herd could potentially lead to infection of these heterozygous animals. Similarly, a cross between a KK and a GG would result in KG offspring—almost certainly reducing the resistance of the animal to somewhere lower than an HH individual. As a result, it would be important for anyone who decides to pursue the route of genetic resistance to maintain a strong stance against breeding even the most attractive “G” genetics into the herd in an effort to maintain maximal resistance. Consequently, the most ideal crosses would be between a sire and dam both homozygous for the K allele (KK), although such animals are likely few and far between.

As mentioned earlier, it is believed that each allele has a 50% likelihood of being passed down, however, like many of the aspects of genetics in this study, this is not known for 100% certain. Dr. Haley admits that there is some slight anecdotal evidence indicating that the 226K gene may be favourable passed down over the 96G, and that the 95H might be unfavourably passed down compared to the 96G, however, insists that this is likely due simply to a small sample size. It is not, he states, statistically significant at all at this point in time, and is expected to be proven to be 50/50 passdown in the future with a larger sample size.

Vaccines Vs. Resistance

At the moment, the two most popular routes of research are development of resistant lines and development of a vaccine. Each has their pros and their cons, and ironically, the cons for one often are the same for the other. Although some argue that resistance is futile because the deer can still potentially contract CWD and shed the prion, the same applies for any potential vaccine. A flu vaccine, for example, does not guarantee that you won’t get the flu. It reduces the likelihood of contracting the flue and decreases the severity of the sickness. So, arguing that one is better than the other based on the animals shedding prions is a double edged-sword.

Similarly, any argument that the prion could mutate and overcome the resistance runs into the same problem. Dr. Haley states that it would be foolish to ignore the potential for the prion to mutate, however, he points out that the same could easily happen with a vaccine. In fact, one of the reasons why flu vaccines may not be as effective year to year is due to the virus evolving to combat the vaccine.

And while some will insist that developing resistant lines in the wild will take too long unless the higher-ups in Wildlife allow the introduction of resistant lines into the wild (which we all know is never going to happen), Dr. Haley questions whether attempting to vaccinate every deer in the countryside for 50 or so years (until the prions that have accumulated in the soil have a chance to degrade) is really that much more realistic.

In the Wild

Now, you might be thinking “resistance is all well and good on a farm, but how is this going to help with wild populations?” And that’s a great question. Dr. Haley believes nature will eventually select for the resistant lines on its own. While this may sound like good news to us, however, this would likely involve significant declines in the wild population along the way, until the 3-5% of resistant deer become the more prevalent gene-donors. Such a process could take as long as 150-200 years he speculates. Clearly, this would be a long term strategy, best paired with other, more immediately effective short-term management strategies. The existence of resistant genes does not negate the responsibility of deer hunters, farmers, and government to seek out management strategies to mitigate the impacts of CWD along the way.

One Other Potential Strategy

One new line of research that Dr. Haley is exploring, while promising, is also likely to be the most controversial. He is currently working on creating a genome in which the gene susceptible to the prion is completely “knocked out.” In simple terms, a biological “tool” called CRISPR is used to cut the DNA strand on either side of the gene responsible for creating the proteins (that when misfolded become the prion), completely removing it from the genome of the animal. If this process were completed in both a potential sire and mother, the resulting crosses would not be able to pass the susceptible gene on (because they would no longer have the gene themselves to contribute to the cross). While this is an exciting use of cutting-edge biotech (pun intended), it opens a whole slough of issues regarding the morality of creating genetically modified deer (beyond simple selective breeding).

I suspect many deer farmers have heard the accusations leveled at us whenever a member of the public happens across a video of a farmed behemoth on Facebook, when we are subsequently called out (wrongly) for using steroids or “genetically modifying” our deer. Despite the fact that these accusations are unfounded and based on a total misunderstanding of deer farming and genetics, should this route be employed in the battle against CWD, we would no longer be able to truthfully say “nope; it’s all in the breeding.” The truth would be that, while the antlers that are being attributed to genetic modification are still only attained through careful breeding, the animal itself would be a genetically modified animal. And that is a can of worms that Dr. Haley and myself agree we need to be careful about opening. At the moment, a line of cells has been developed with the knocked-out gene, and the next step would be to grow these cells in a petri dish in the lab, followed by development and birth of a fully CWD resistant deer. Obviously, Wildlife would never allow such “monstrosities” to be released into the wild to combat CWD, however, it may be worth considering the fact that, should deer farmers make the jump to these GMO deer somewhere in the future, they could safely and truthfully insist  that deer farmers no longer play any role whatsoever in transmitting CWD. Not only would our deer not get sick with CWD, they could not even get it in the first place. Again though, we are forced to debate the morality of genetically modifying animals or potentially contributing to the spread of CWD. Luckily, such a decision is a few years off at the nearest, so we have some time to consider, discuss, and fight over whether such a risk is worth taking.

Finally, with enough new information rattling around in my head that I figured it was time for me to start writing it down before it got lost in whatever corner that Star Trek quote came from, I bid Dr. Haley farewell (and promptly sent him an email full of questions regarding the genetic relationship of the alleles that I had forgotten to ask). Once again, he was quick to offer his insight to these questions, while admitting that nothing is known for certain. How refreshing to hear someone able to both boast about the successes of his research and admit when knowledge is lacking as well as the potential limitations of the research!

No one knows what the future holds for CWD, deer hunting, and deer farming. All we know is that the battle is still raging on and shows no sign of coming to an end any time soon. As a result, it is important that farmers and hunters alike be proactive in both preventing the disease and supporting research that seeks to combat it. Remember that we are all in this together, and we all (deer hunters, deer farmers, wildlife conservationists, and the general public) stand to benefit from any science that may help us overcome this disease. And remember that science works by exploring many routes simultaneously. So every time you see research that seems to conflict (resistance, vaccine, GMO), keep in mind that we are all searching for an answer, and multiple tactics simply increase the likelihood of finding it quickly. Don’t view opposing research as competing, but rather each pushing onward toward a common goal—the eradication of CWD and the growth and continuation of the North American deer hunting tradition.