Below the Radar Transcript

Pandemic Conversations: COVID-19 and Selenium — with Dr. Ethan Taylor

Speakers: Paige Smith, Am Johal, Dr. Ethan Taylor

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Paige Smith  0:06 
Hello, everyone, and welcome to the fifth episode of our Below the Radar Conversation Series. Today we talk with Dr. Ethan Taylor, Professor in the Department of Chemistry and Biochemistry at the University of North Carolina with our host Am Johal.

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Am Johal  0:23 
Hi there. Welcome to Below the Radar. We're really excited to have Dr. Ethan Taylor with us this afternoon. Welcome.

Ethan Taylor  0:33 
It's a pleasure to be here and hello to everybody in Vancouver and Canada. I wish I could join you. 

Am Johal  0:39  
You're coming to us from Greensboro, North Carolina?

Ethan Taylor  0:42 
Yeah. Been here for many years after living in Canada a long time ago, 40 years ago. So...

Am Johal  0:52 
Yeah and wondering if you can maybe start by introducing yourself a little bit in your area of study? 

Ethan Taylor  1:00
Sure. Well, I'm a, I guess a biochemist is a more general term. I was actually a pharmacy professor at the University of Georgia for 18 years. So I got a chemistry degree at the University of Winnipeg, back around 1980, roughly, and went to the states got my doctorate at the University of Arizona in pharmacology so and when I started as a faculty member in Georgia, at UGA, I got into AIDS research, which was a new area for me, because my my dissertation was on neuro psychopharmacology, so. But I got into computer assisted drug design, what we call molecular modeling, building, designing molecules with computers and there's a need for that. 

So I got into AIDS research and as time went on, I was working with a pretty high powered team and I made some discoveries that pointed me in the direction of nutritional factors in Selenium in particular. And it was really sort of an accidental discovery, actually, because I was studying the structure of the virus. So when you get into AIDS research, it has a tendency to take over your life and it and it did, and I've been studying HIV for 25 plus years, probably 30 years. And but with this particular focus, I kind of struck out on my own because the more you study drugs, as a pharmacy professor, you understand that most of the time drugs don't really get at the root cause of disease, there are certain ones that can and cure, like perhaps antibiotics, if they help you eliminate the bacterium that's causing the problem. But most drugs just treat symptoms, and I was kind of more interested in what causes this pathology, what is the mechanism of pathogenesis that's going on. And when you get into that, you can't help but get into the whole area of nutritional medicine and the effect of having the right balance of biochemicals in your body. And in fact, there's a guy, a Canadian guy who started, you know, contributed this concept of orthomolecular medicine having the right molecules in your body, and a lot of focus on nutritional factors. So I've been doing Selenium and viruses for a long time. 

Am Johal  3:08 
So when did you first start with Selenium was that in the mid-late 80s? 

Ethan Taylor  3:14
It was mid-90s, actually. I've been doing HIV research for about four or five years and we were studying the structure of the virus, the RNA structure, and we did a fairly seminal paper where we were actually looking at drug resistance, why is it that certain drugs develop or are the mutations that the virus accumulates, that make it resistant to a drug to make the drug not work, most people look at the protein structure. And, you know, if you change an amino acid, then the drug won't fit in the protein and you get resistance. But we were interested at the deeper level of the RNA structure that encodes for that protein and we found that there was a correlation between the second, what we call secondary structure in these RNA molecules, they can fold up in what we call stim loops or hairpin structures. And the hairpin part, the stem part is kind of like a Watson Crick Double Helix, you know, like where you've got two strands that are forming, they pair up with each other and we found that there was more mutations in the unpaired loop regions and that kind of makes sense. But anyway, while I was studying this stuff, I I stumbled across some kind of structure called pseudo knots, which are involved, that are known to trigger a process called frameshifting, where the protein is being made out of a machine we call a rhizome. And the messenger RNA is kind of like a tape going to the tape recorder being decoded. And it reads the triplet letters of the genetic code, but if it gets off one letter, it ends up getting a totally different message. So we call these reading frames. And usually this is called a frameshift mutation when it happens in your genome, your DNA. Like if a base, if a letter is dropped out of the code that that can be a lethal mutation in making this protein. But viruses have figured out how to exploit this mechanism and do it on purpose, slip from one reading frame into another to make a different protein so they can make more stuff, they can get more bang for the buck basically, by making more proteins with the single piece of RNA. So I found these sites and they led me to UGA codons, which is the stop codon, the genetic code which just happens to also be able to program amino acid selenocysteine. So that's where the Selenium link comes in. And that was only discovered in like about 86, or something like that, and it's a very strange process, where a stop code on UGA is reprogrammed to become an actual sense codon for an amino acid selenocysteine. But it requires some very special structures that help make it work. It's a very arcane process.And but what was interesting to me was that we found a high degree of conservation of certain stop of these UGA codons in HIV. For instance, there's a gene of HIV called the Neff gene, which has been widely implicated as one of the most important ones for the pathogenesis of HIV. 

And it ends in a UGA codon and that UGA codon is very, very highly conserved throughout the main group of HIV subtypes and variants. And it's kind of hard to explain that because if there's two other stop codons that it could mutate into and since these viruses are notorious for mutating very fast, why is it conserving this one particular stop codon and so we've been interested in that one for years. So in 1994, I actually predicted I think the stop codon can be occasionally translated as selenocysteine, which would make an extended form of this protein it would no longer stop there, it would, it would add on about another 30 plus amino acids. And that could explain a link between that virus and Selenium. So that was kind of the start and I found, you know, similar kinds of things going on in different viruses.

The problem was, where it became controversial and why it was not accepted very much by especially the Seleno Biology Community is that we can, there's some special hardware to make this magic happen to reprogram this stop codon, you have to have a special kind of structure, one of these stem loops, usually down at the far end of the RNA, the messenger RNA, and it helps trigger a process,it  binds some proteins, it sticks onto this machine, the ribosome that translates the RNA into protein and it prevents the termination for happening and enables the selenocysteine transfer RNA to get in there and be put in that place. And the problem was, we could never find one of these little RNA hairpins, they're called SECIS elements. We can never identify, we found some things that look like them, we had them tested, we could never find one that worked.  When you put it in, say a human selenoprotein gene, so that was why people that they, you know, but at the same time, we could express that protein, we could clone that viral protein, that hypothetical viral selenoprotein. And we could put it, put one of the mammalian elements there to help do that magic, and express the protein and we could prove the protein had the function we predicted.And, but still at that, I don't know if people just thought we were just making this up or didn't believe it. So where it all kind of finally came together, it took years for me to like, finally realized this. It was during, it was during the Ebola epidemic in 2014. Because we'd shown some similar kinds of things could happen in Ebola. And we were trying to persuade people that you know, you should really consider, you know, Selenium for Ebola infection. And I realized that, you know, viruses, they don't really encode much of their own stuff, right? They're notorious for taking over cells and using the cell’s machinery, I mean, they have the minimal stuff, they have a few genes that enable them to get in and out of cells, and to copy their RNA or DNA. And then the rest of its, just, you know, tricking the cell into making stuff for them. So I realized that, you know, the virus doesn't need its own SECIS element, because it can hijack one from the cell just like it hijacks all this other machinery from the cell, that's the virus modus operandi, right. And the way I realized it's doing it for something called antisense where we have two complementary sequences from a, you know, in this case, one from the virus and one from a cellular gene. So here you have a cellular mRNA that makes a cellular selenoprotein something called thioredoxin reductase. That's one of the Selenium containing proteins in the body and it's got this little magical SECIS element that enables it to reprogram the UGA stop codon. And guess what happens? Well, we just found complementary sites where the virus comes along and it's got an anti sense that is the inverse complement sequence that can pair up, bind to the cellular one and now that element can do the same magic on the viral UGA stop codon. So that was a mechanism and then we started finding this all over, we found and we showed—so we published the paper in 2016. Where we showed HIV could do it in this site in the Neff gene that I predicted in 1994. And there's a gene of Ebola, the nucleoprotein, which is a protein that coats the viral RNA, you know, deep inside the snakey virus particle and there's many, many copies of this gene. And it also ends in a UGA codon, which is also extremely highly conserved. In the very, varielant Ebola Zaire strain. Whereas you look at Ebola Reston, which is non-pathogenic. Guess what, there's, it isn't the UGA and that one, it ends in a different codon. And for both of those we've shown, there's a technique called reporter genes where you can put something like green fluorescent protein, which will, if synthesized in the cell, will fluoresce green when you hit, you know, with the right wavelength of light. And so you put that gene downstream past that stop codon in a construct that you've cloned. And, and it's a way of testing because if this is just stopping at the stop codon, you won't see any green fluorescence. But if it reads through the stop codon putting an amino acid there or somehow bypassing it. That's the only way you're going to get green fluorescence. So, some of those results are in a poster that I presented at the Ebola meeting in Paris in 2015. That's actually on my researchgate site. So if you want to put that out, people can go and actually look at that poster and see the green fluorescence both from HIV Neff gene, and from the Ebola nucleoprotein gene. And we're actually just resubmitting a paper today on the Neff story with all of that. So trying to get this stuff out there and of course, in the meantime, COVID came along, and there's a whole similar story, some similar phenomena in COVID. So this is why all of that I've been talking about is basically the backstory or the precedent. 

Am Johal  12:28
Yeah. So it's been, it's been kind of shown that Selenium is an anti pathogenic factor in emerging zoonotic infections and so as COVID erupts, and this research has been done, historically, you've also published quite recently, at least a preliminary paper with colleagues and so this relationship between Selenium and how it interacts with COVID. What are some of your initial findings at this date? 

Ethan Taylor  13:05 
Well, yeah, as you say, there is, you know, meanwhile, I was doing all of this sort of theoretical stuff, you know, very arcane molecular biology, you know, theoretical genomics stuff that that is kind of out of the regular sphere of typical virologists and so on who are focused on the experimental side, but meanwhile, there was a lot of data accumulating Well, with HIV, it was became overwhelming, just dozens of studies published showing a decline of, progressive decline in Selenium status correlating with outcome and mortality. And then they did some clinical trials, at least about three or four of them that have proven that there was a clinical benefit from that. But in China, where they have some really, really low Selenium regions, and also some really high Selenium regions, because of the low Selenium regions  being so large, and back in the mid 20th century, there was a lot of subsistence farming, so people were much more susceptible to the influence of how much was in their soil, because you got to remember, this is an element, a trace element that, you know, can't be created or destroyed except by a nuclear reaction. So if it's not in your soil, it's not going to be in your diet. And if there's an essential requirement for it in your diet, you're in trouble if you're in a really low Selenium region and you, you know, grow your own food or eat animals that are eating the same foraged plants of that soil. So they had some problems with heart disease way back in the early mid 20th century.

It was called a non obstructive cardiomyopathy or dilated cardiomyopathy, the heart would swell up, the muscle would get really weak and swell up and people would die, especially women and babies, but it would happen in outbreaks. That was where they couldn't figure out, it didn't seem to just happen to everybody in that region, it would come in seasonal outbreaks breaks and they suspected there must be maybe there's a virus or some infectious agent, and they ultimately show that yeah, there's an enterovirus called Coxsackievirus that they could isolate from hearts and some people, scientists, Dr. Melinda Beck at UNC Chapel Hill used a, made a mouse model of this and showed and got even more interesting because they showed that if you got a benign strain of Coxsackievirus, put it in mice that were Selenium deficient, it would cause this heart pathology but then it would mutate into a more virulent form, which would even cause problems in mice that were not Selenium deficient. So that has some pretty profound implications. But then there's been others in China, they also have problems with liver disease and liver cancer associated with hepatitis viruses. And then there's something called hantaviruses, which are pretty common in Asia, they cause various syndromes called epidemic hemorrhagic fevers, which can have a respiratory syndrome or renal syndrome. But just in 2015, an international team, kind of like the team that I just worked on doing COVID. They showed us kind of a similar thing that in the low Selenium regions in China, you have a six times higher chance of getting this hantavirus infection.

Meanwhile, back about 40 years ago, an old Chinese guy... There was an outbreak of epidemic hemorrhagic fever in Mongolia, I believe. And he decided to treat it with sodium selenite, a simple Selenium compound. And he got really stunning results. Overall, his overall reduction in mortality was about 80%. Now, if that was a drug, they would be screaming from the rooftops about how great this drug is right? But everybody just ignored that paper and it's obviously it's a hemorrhagic fever. It's not as lethal as Ebola, but that could be a precedent for Ebola, so we've always kept pointing that out. And then of course, there's influenza, Melinda Beck showed similar results for influenza. There's a lot of papers about Selenium and influenza.

So now we have COVID. So you asked about our new paper. Well, basically, we suspected something similar with this Coronavirus and we were able to get because they've had all these big problems in the past in China in these low Selenium regions. The data is very well documented. They basically get hair samples from people that live in these regions and they can say, well, the average hair level of Selenium in Beijing is approximately this and in these other towns it’s this. And of course, we're collecting COVID case data town by town. And so we just really put that together and we showed what's really striking is there's a town called Enshi City, it's in Hubei Province, which is where Wuhan is, which is where the outbreak started. And Enshi is famous, it's probably got some of the highest Selenium intakes in the entire world. Some people are taking probably 10 times what the Americans—or eight times what they say is the quarter the minimum daily requirement here. But it turned out that compared to the rest of the cities in Hubei Province, the survival rate of COVID in China at the time we took our snapshot of the epidemic, was three times higher than the survival rate in all these other cities in the Hubei Province. And similarly in this low selenium province called Heilongjiang, where Keshan is where they've had this heart disease I've mentioned earlier. There, we compare that to all the other cities outside of Hubei and there the death rate was about five times higher than in these other cities that were, you know, not in this really low selenium province. So that seemed pretty striking. So ultimately, we were able to make the correlation. We got a bunch of cities outside of Hubei and showed that there was quite a significant linear correlation that the higher the selenium intake, as measured in hair levels in these cities, the higher the cure rate for COVID-19. 

So that was the paper that we just published in the American Journal of Clinical Nutrition with Dr. Margaret Rayman of University of Surrey in the UK as the team leader and my collaborator, Dr. Jin-San Zhang and I were the two lead authors on the paper. So now that was, there was no coincidence that we looked at that because Dr. Zhang and I had looked at the SARS virus 17 years ago, when the 2003 SARS epidemic happened, I did my genomic analysis when they first sequenced, I think out of Toronto, they got the sequence of the SARS virus, they published that and sure enough, I found a couple of these frameshifts sites, which have very, very specific requirements in this in this sequence to function associated with a UGA codon in the overlapping reading frame.

Just like what I'd seen in HIV in the past. And furthermore, one of them had significant sequence similarity to a selenoprotein called glutathione peroxidase, which is the prototypical selenoprotein. That was the first one discovered. And in fact, that was one of the sites in HIV we showed had, the one we cloned and showed it was functional, had glutathione peroxidase activity. And other they, they actually discovered a couple of other teams have found these, this kind of selenoprotein gene in some DNA viruses much larger viruses. So the idea that a virus can encode this is no longer quite so crazy. But there's actually sequences with glutathione peroxidase, and an overlapping reading frame of both the original SARS virus and now the SARS COV-2 virus, the cause of COVID-19. So I don't think that this Selenium correlation that we've seen, just has to do with, oh, it's important for the immune system. And if you don't have enough, your immunity is weaker, and therefore you're more susceptible.

Because that's kind of the party line that oh, you know, and there's no point in taking any Selenium supplements beyond that. Whereas I think if you look at some of the precedents like Dr. Ho treating Hantavirus in Mongolia epidemic hemorrhagic fever he used quite a high dose. It was equivalent to about 900 micrograms a day but he only did it he only gave it for nine days. So this is what we call a pharmacological use not a nutritional use of a Selenium compound. And so we’re you know, I'm thinking I'm hoping that somebody will try this. Now there's there's actually something going on in Liberia, there's a guy there who actually was using, did a trial of selenium versus Ebola back in 2014 and it never really got much publicity outside of Liberia itself but they,

It must have done something because you can find a news item. The guy's name is Dr. Jerry Brown, he was on the cover of Time magazine in 2014 December as you know, one of the persons of the year, the Ebola fighters and they didn't, of course didn't mention Selenium in the Time magazine article even though that was part of why he was, he'd become famous in Liberia because you could find news items in Liberian press talking about you know, people walking out of that Ebola treatment unit and having been treated there with Selenium by Dr. Jerry Brown. And now he's come out, you can find some quotes online where he's saying, Oh, well, it wasn't rocket science, we just used multivitamins and Selenium you can buy across the counter, but we really but someone truly should investigate and see why this works. But anyway, he's now doing the same thing for COVID we just found a news report how someone had donated a few hundred bottles of Selenium supplements and he's using the 14th military hospital where they're sending their COVID patients in Liberia. So maybe we'll get some kind of interesting reports.

Am Johal  23:21 
Now Selenium can be found in everyday foods. I have you know one Brazil nut here depending on where it was harvested would give me you know, a daily recommended amount even more than necessary, perhaps, but what other kinds of foods can it be found in if you weren't taking supplements?

Ethan Taylor  23:41 
Yeah, yeah, well, you know, it's unlike, it's not like a vitamin like you know, vitamin C or whatever that a plant can synthesize so if you eat your citrus fruits you'll get it because the plant makes it because it's an element there's absolutely there's no guarantee if the soil at any point even your Brazil nuts you know there you could possibly grow Brazil nuts in Heilongjiang Province in China, it's really not a climate but if you could, they might not have this level of Selenium it's because there's high Selenium in soils in Brazil. So typically, whole grains, especially ones that are grown in North America, we tend to have pretty good Selenium in our soils, whereas there's less in British soils and if you're a carnivore, supposedly organ meats like kidney and liver have, you know, higher levels. This can be somewhat problematic, like you probably have it but the problem is there's more mercury pollution and Mercury can completely antagonize and neutralize the benefits of selenium and vice, and Selenium can also have an anti detoxification effect on mercury and arsenic. So it's a little bit risky if you are trying to get your, even your Brazil net there's a lot of mercury in Brazil from gold mining and also because of deforestation all the mercury that's in the biosphere normally they they burn it all up and it comes down as ash and increases the mercury content in the soil. So, you know, there could even be, you know, some other contaminants that are neutralizing it. So the only way to really be sure you're getting it, it's one of the, most things, I'm a total whole foods advocate, you know, eat your fruits and vegetables and, and whole grains and nuts, and you should be fine. But, and that's true of almost everything. But Selenium is one thing where it probably doesn't hurt and especially for having this potential kind of anti pathogenic role against viruses. So I'm, you know, I'm taking a little more if I suspect I have COVID or if I think I have a cold because this mechanism applies to many RNA viruses. Maybe we can get to that shortly before we run out of time. If I think I'm getting a cold or flu first sign of symptoms I'll take, I'll usually take 200 micrograms of sodium selenite and a few other things. That's just my personal thing. I'm not prescribing anything for anybody. I'm not a medical doctor.

Am Johal  26:17 
Now there is a phenomenon of Selenium toxicity if you take way more of course as well.

Ethan Taylor  26:25 
Yeah, yeah and it should not be high doses should not be taken for a long time, like the dose that Dr. Ho gave, versus epidemic hemorrhagic fever was two milligrams of sodium selenite a day for nine days and if you took that long term, you would definitely start getting you know, some signs of Selenium toxicity that level would probably wouldn't really be lethal but you might see finding your your weird things happening with your your, your nails and your hair falling out or things. But usually I think the sort of no adverse effects level is about 500 micrograms a day, total intake. And so you could be taking a couple 100 micrograms as a supplement and not really having a problem but you don't need there's no benefit in taking mega dosing. It's definitely something that people shouldn't just run out and gobble handfuls of Selenium pills, it's not going to help. You know more is not necessarily better. So it has to be done...

Am Johal  27:27 
In a context like this, where we do have the novel Coronavirus out there and just as from a health point of view rather than medical advice point of view what levels of Selenium should people be looking to get in terms of having some positive benefits from it?

Ethan Taylor  27:50
Yeah, well I mean for long term if you're taking it as, you can get a multivitamin that might have anywhere from 50 to 200 micrograms depending on whether it's touting itself as a real antioxidant formulation or something and you know, and any of those are probably fine. And probably for long term supplementation something with Selenium yeast in it is a standard thing, is good. There's a lot of evidence that suggests that the inorganic form sodium selenite, which has been used in certain, you know, short term treatment things might have some pharmacological activities that are unique, that are superior. So that's why when I, you know, I might be taking a multivitamin with Selenium and it might have Selenium yeast or selenomethionine, but when I think I have an acute infection, I will switch to sodium selenite because of evidence that I'm aware of, of different mechanisms, that it might be more quicker acting, and have a few other properties which are too complex biochemically to try to explain. So that's the story there. But I think again, you've got to realize that nothing works in isolation. You can't just take that and have a terrible, terrible diet and expect to get you know, the full benefit. You should really really… Because, you know, one nutrient depends on others. So for instance, for Selenium to be incorporated into selenocysteine requires vitamin B6, that's a cofactor in the enzyme that does that synthesis. So you need to have your B vitamins, you need to have, you know, vitamin A, you need to have, you know, a complete spectrum of nutrition. And there's some things that have been shown to be possibly… If you're talking about COVID, There's some evidence that vitamin D3 is particularly important. There is a malt in your body called glutathione which is also important. And so there's some people advocating glutathione precursors like N-acetylcysteine, or NAC, which was also used by AIDS patients, and maybe still is.

Am Johal  30:03
So what would be the next piece of research that you would be doing in terms of the preliminary work that you've already done related to Selenium and COVID-19 specifically?

Ethan Taylor  30:19 
Okay, well, we're working towards trying to validate that some of these sites that I've talked about are functional, when in fact, these frames have sites in the original SARS virus. We use these invitro assays and so they actually were functional but it's just very, very first level. But let me… before I get into any of that, let me tell you, the simple, kind of the elevator speech of why I think Selenium is important for RNA viruses in general, okay? Because this is something that we only really figured out after I figured out this antisense mechanism where these viruses are doing this antisense pairing up with a selenoprotein RNA for something called thioredoxin reductase. Well, thioredoxin reductase it's an important antioxidant to your body, and it does a lot of things keeping thiols in a reduced state. But one of the things it does, it's also involved in DNA synthesis, okay, so there's two types of viruses. There's viruses that have RNA genomes and viruses that have DNA genomes. So some DNA viruses are things like smallpox, you know herpes viruses, papilloma viruses, number one, not typically ones that are involved in pandemic type of stuff, or zoonotic transmission is almost all of those ones, you make the list, you know, HIV, Ebola, Zika virus, Dengue virus, the whole list goes on, the coronaviruses, they all have RNA genomes.

So the important point is that the way life evolved on Earth, DNA synthesis, DNA chemistry came later, life probably started as RNA. And so DNA chemistry is an add on to the RNA system. So a cell can only make DNA by using some of the stuff it uses to make RNA. So the, in other words, deoxyribonucleotides are made from ribonucleotides, by reproducing this, OH group to hydrogen, a bit of chemistry there, but it turns out to sustain that reaction thioredoxin reductase is what keeps the cycle going and that's where Selenium comes in because thyroxin reductase is a selenoprotein in mammals. So one way that a virus could make more RNA is by blocking thioredoxin reductase and with this antisense mechanism that I've been talking about in terms of hijacking the SECIS element, another thing that it would cause is it gums up the work for this RNA, to go through the ribosome and make thioredoxin reductase. So thioredoxin reductase levels could be declined, because of this mechanism. And that would then potentially cause these different problems that could contribute to the pathogenic effects of the virus, such as oxidative stress, or risk of cell death, apoptosis, all of these things. And so essentially, the take home message is, any RNA virus is going to be inherently somewhat sensitive to fluctuations in Selenium levels in the post, because of this important role. That selenium is involved in DNA synthesis. And so if you are Selenium deficient, you're going to be more susceptible to this, because if the virus actually causes a decrease in thioredoxin reductase, RNA translation, and there's not much Selenium to go around, it's going to aggravate the process or exacerbate the process. And that could lead to enhanced pathogenesis and mortality and so on in people with low Selenium status, which is what the what we've reported for COVID in China, that the low Selenium people seem to be much more at risk of mortality, and the people, but the interesting thing is the people in Enshi city who have unusually high intake of Selenium, their survival rate was three times higher than the people in other comparable cities in Hubei Province, who had lower Selenium levels or normal Selenium levels and that to me says that actually having higher than the recommended amount might be helpful in this acute viral infection. It doesn't mean you should take that forever, it doesn't mean that you want to go and take, you know, hundreds of micrograms of Selenium every day of your life but maybe for a week or two where you're exposed, maybe it might be helpful. Now, I'm saying maybe I'm not a clinician, I'm not prescribing anything. I'm just saying this is what the data says to me.

Am Johal  35:17 
Anything you'd like to add?

Ethan Taylor  35:19 
Yeah, well, I guess you know you asked, you know, before I got into that thing about the R, the, I call this RNA viruses versus DNA synthesis. And it's a, it's a new explanation of why so many of these RNA viruses, like the list I gave you earlier, appear to be sensitive, or have increased pathogenic effects in low selenium populations. And you asked about what research we are doing, and we're essentially trying to prove that these frameshift sites are active, and we're gonna try to clone a couple of these genes that are frameshift variants of known genes and prove that they're functional and hope that that will persuade. I'm also working with my Chinese collaborators, the fellow Dr. Jin-San Zhang who joined with me on this new paper, and he is working with some scientists in China, and they're looking at expression of cellular selenoproteins in infected cells, and I'm saying, based on these antisense interactions, we can see, we predict certain of these humans selenoproteins will probably be suppressed in terms of their level and so we're kind of collaborating with those, those folks. And also trying to write a big review about all the different mechanisms involved, hoping that people in the medical field will pay attention and maybe do something. So I'd encourage people to go to my Research Gate site, it's going to Facebook for scientists, it's just And if they just search ResearchGate and then Ethan Taylor, they will find me and they go to the Taylor Lab. I've got different projects and so we're putting updates there. So I'm trying to write some, you know, educational materials, and also as new research comes out we will be posting those research articles on that site. 

Am Johal  37:22 
We'll link to those in the site. Thank you so much for joining us, Ethan Taylor on Below the Radar. 

Ethan Taylor  37:31
Okay, my pleasure. Let's hope it gets above the radar eventually.

[both laugh]

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Paige Smith  37:38 
Thanks again to Dr. Ethan Taylor for joining us on this episode of our Below the Radar Conversation Series. Below The Radar is created by SFU's Vancity Office of Community Engagement and is recorded on the territories of the Musqueam, Squamish and Tsleil-Waututh peoples. As always, thanks to the team that puts this podcast together, including myself, Paige Smith, Rachel Wong, Fiorella Pinillos, Kathy Feng, and Jackie Obungah. David Steele is the composer of our theme music and thank you for listening. Tune in next time for a brand new episode of Below the Radar.

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Transcript auto-generated by and edited by the Below the Radar team.
June 05, 2020

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