Pandemic: Coronavirus Edition

What has Epstein-Barr to do with Covid-19?

• Dr. Stephen Kissler and Matt Boettger • Season 1 • Episode 97

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Matt Boettger:

You're listening to the pandemic podcast. We equip you to live the most real life possible. And the face of these crises. My name is Matt Bodecker. I'm joined with a great friend, Dr. Steven Kisler and epidemiologist at the Harvard school of public health. Good day. Do you find

Stephen Kissler:

sir? Good day. Good, good payday day, Matt. It's wait, wait, is it really? Yes, it is 3 1 4. And so this is a, this is a holiday in which mathematicians unite so great. This

Matt Boettger:

is, so this is the exclusive reason why we delayed. That's been damaged.

Stephen Kissler:

That's right. That's great.

Matt Boettger:

So I do apologize for those who were probably looking forward to a podcast two weeks out in that three weeks out, Steven had a lot going on last week and he still is crushing it, but he's still made time to put out a relatively quick episode today because we only have. 30 minutes or less right now, before he has it on the median. So we're kinda really quick. If you want to donate great pandemic, I don't even know how to say, oh, patrion.com/benefit podcast. I'm not trying to go so quickly right now. Like we've got to get Steven

Stephen Kissler:

all these questions here on here.

Matt Boettger:

I know we did that so badly for the intro and outro. So if you want to do that, you can do that in the show notes. One-time gift in the show notes, Venmo, PayPal. Great. It is now two years since we've been going on for the pandemic podcast and the pandemic as well. So this is a big milestone for us. One year seemed normal. Two years seems outrageous for us to be together. Like, I don't know what happened to. Thank you for all those who's left reviews. One quick one, I'll leave on February 25th where there's a couple as we near the two year anniversary of COVID exploring exploding in the U S I want to express my gratitude for the pandemic podcast. You've been and continue to be a steady source of information I can trust. Thanks guys, for all your efforts. So pretty all those.

Stephen Kissler:

Yeah, totally. And real shout out for people who have like been barren with us for this entire time. It's I know, it's yeah, appreciate it. And glad that we've gotten to connect with many of you over the course of the pandemic. So

Matt Boettger:

yeah, it would be great someday in person and the guys are in wherever Boston, Denver feel free to send an email, Matt living in the real.com. We'd love to connect with you guys in one way or another. So thank you for all those reviews. So let's get going. And is there anything else on the show notes I need to talk about for intros? I feel like I'm missing something, but not that important. We have less than 30 minutes. So let's start with the outline right now. Stephen, the first thing I would talk about is policy and guidelines. Things are changing. Things are rapidly changing and things have changed and so much so that like I went to the grocery, no, not the grocery store, but I've been to other places and had been unmasked. Going into restaurants. Now, things are really kind of normal. Hospitalizations are so low now that I feel comfortable that going in and just kind of starting to live a normal life. Now you'd have policies and guidelines trying to keep up. I know Hawaii is going to release. There's finally in in March 26. So no more, you don't need to have quarantine, that kind of stuff. Airlines have continued their mask mandate. Just I think for up until the second week of April, but could change rapidly. I think they're consulting really powerful people like you and other people to figure out what the heck they're they need to

Stephen Kissler:

do. And so that's, yeah, that's a generous description for,

Matt Boettger:

so they're figuring that out. So everything's changing. One thing that changed is the CDC guidance. I want you to inform us in me, particularly because I'm with you, I'm like what's going on with the change of the CC guidelines, because apparently it was one thing. And it was like the cases per a hundred thousand and an article mentioned, I'll put this in the show notes that the new transition to the guidelines or not the guidelines, but the measurements the initial one had like 75 in the country being at high risk or whatever, that, whatever that level was, the new. Guidelines or the new way they measure criteria for COVID infections, but to down along like 15% of the U S at high, high risk. So can you help explain what's going on and how we use this and that going

Stephen Kissler:

forward? Yeah, totally. I mean, I think this really folds in nicely to a lot of conversations. Previously about just the complexity of making decisions and changing guidelines around the pandemic. It is, it is, it is not an easy job. And I, I can't say that I am excited about every, all of the updates to the CDC has made, but I also kind of understand. Where a lot of it is coming from and what it's been motivated by. So, the, the, I think the, the the biggest thing that has caught people's attention is this big shift in the U S map, right? Where it's like places turn from red to green where it's like high risk versus low risk. And it's like, what the heck? Like, somebody just decided to change the rules and then, and that, and that again, plays into this notion of like that. And I think there's this false notion that that good faith and honest communication implies consistent unchanging communication, right? Because the context is constantly changing too. And it's changed hugely in the in the context of increasing vaccination rates and a lot of underlying immunity from previous infections. So now the same number of cases that we saw a year ago does not mean the same thing as the same number of cases that we're seeing today because due to that underlying immunity and due to our improvements in our ability to treat COVID, we have, we have drugs now that are effective at each stage of infection. Like it's, it's just a different ball game. And so it's not that, eh, Just that, someone decided that the pandemic was over and we need to, change, but it's like this, this also reflects to a large degree, the reality of the situation, which is that the risk of severe outcomes given infection is, is hugely reduced. Now, thankfully in this country due to all of the, everything that we've been through and everything that we've done to try to make it that way. And so that's really what the guidelines reflect. The, I think there is still room for criticism in that. They're they've really scaled back a lot on surveillance and have made the triggers for changing these guidelines tight to mainly tied to hospitalizations. Nope. On the one hand, that makes sense because the that's by far the sort of the most stable indicator of how much. COVID is, is circulating at a given time because there are so many idiosyncrasies with testing. Like it's really hard to know what case counts mean in one place versus another. I think those people get tested for all sorts of different reasons, but of course the difficulty is that hospitalizations are hugely delayed. And so by the time you see a big rise in hospitalizations there's a good chance. There's already a lot of COVID spreading Too late to really turn around a major event. So something we're gonna have to watch this closely. I do think this is sort of a, a work in progress, defining what these guidelines should be. But yeah, hopefully that, that gives a little bit of nuance to what's going on.

Matt Boettger:

So w guess would probably be to be expected then if it's still an, a kind of an evolving situation that we could probably see a series of changes within the CDC, as it grows and understands and reflects and, and kind of finds its stable ground for this new endemic it's. This is not the final say of how we're going to measure going forward. Cases and

Stephen Kissler:

how to respond to it. Exactly. Yeah. I mean, this is, this is the scientific and political process and I, and I don't mean political here as a dirty word. It's like, it's, the CDC has made their guidelines and then there's been a lot of response from other government institutions, from other academics, from other, just even lay people who are responding to these guidelines and maybe even pointing out things that the CDC hadn't considered, despite their good faith efforts to consider all possibilities. And then Nope. Factor that in. And then if it is, changes need to be made, then I am confident that they'll be.

Matt Boettger:

Okay, sounds good. All right. We're going to, we're going to do a lot of speed rounds here. So next being around variant let's touch base on this. I was really not thinking much of B2 still don't but there was one article that kind of raised my eyebrows a little bit about how maybe New York has seen a little bit of a sub variant spread. Not sure how accurate that is. I haven't got a chance to kind of chase this down to see, but a particular line in this article. I'll put in the show notes. And that is that a, this B2 variant is up to 30% more infectious. Last I heard this was, it was like three to 6% more infectious. And I was like, oh, well, that's, that seems about right. 30% of an already outlandish, like crazy variant. What are you hearing? Whereas B2 on your radar right now. And are these, are these kind of Well, is the

Stephen Kissler:

accurate, yeah, so there's, I mean, there's a huge amount of uncertainty around these statistics and a big part of that is because, again, the context is changing hugely. And so, as, as we've talked about, and I think there's been a lot of discussion about this sort of in the media as well, that that an increase in infectiousness can be due to a whole bunch of different things. Maybe that's increased intrinsic infectiousness, but a lot of times it's actually an interplay with previous immune exposure which vaccines you've gotten, how recent they've been, which various strains have infected your community, how recent those outbreaks have been. And that can create a huge amount of variation in the infectiousness of a given various. In a given population. So I think part of the reason we're seeing these like vastly different estimates of the infectiousness of BA two relative to BI one is, is just due to that because it's spreading in different populations. I mean, I think it's worth noting that we've, we've had BA two circulating at low levels in the U S for months now, and it hasn't really taken off in most places. So that's kind of confusing too. So there's, there's a lot going on here besides just sort of a baseline difference in infectiousness. It seems like it really needs to get to get lucky in a way in a given population before it can really take hold. And it just hasn't been able to do that. So, so at least in the U S it seems to me like that 30% is probably, as, as just a baseline figure. I think that that's a little high, because I think if that were the case as. Every every BA two is 30% more infectious than BI one. We would have seen huge outbreaks of BA two already at this point, but in some communities, I'm sure that's the case that that 30% is, is, is accurate. And so it's just a matter of finding the right communities. And then once it gains a foothold, it can spread. Okay,

Matt Boettger:

great. Anything else that we should be concerned about or on our radar? Because I've been kind of out of the loop. I've been snipping articles here and there, but I haven't seen anything about variants of concern besides B this B2, is that a proper kind of reflection right now? Nothing bigger

Stephen Kissler:

than that. It's pretty much all that right now. We we've seen some upticks in cases, for example, in the UK where they've already had a large BA one wave and, and some of that seems to be driven by BA too, but there's so far in all of the increases in cases that we've seen around the world there aren't any new variants that have been implicated in that. And it also doesn't seem like from what we've seen, there's really any difference in clinical severity between BI one and BA too. So I think that's a big reason why, that's, that's pretty much all we've heard about and that seems to reflect what I'm seeing too.

Matt Boettger:

Okay, great. So let's hit now the vaccine booster situation, there's a few articles here and there. Talking about the second booster is, is this something that's going to be coming down the pipeline for us relatively soon? Maybe not. Where did you guys thinking about. This booster in some articles will say that, ah, it's been tested. It's a very marginal boost compared to the original booster for the Omicron, particularly. So maybe it's not something is going to be on our, the forefront of our radar. Come this fall. What are you guys talking about?

Stephen Kissler:

Yeah. So, at this point it that's, that reflects my understanding too, that there especially for people who are who have. Normally functioning immune systems and I've gotten a booster, it seems like getting a booster booster. Doesn't really it doesn't give you a huge improvement in protection against severe disease. We're still gathering that information because again, one of the, probably the biggest element of this. Rate at which protection from the vaccine declines. And we just haven't had people who have been vaccinated and boosted for long enough to really know what that rate is and, and what the floor might be in that reduction in immunity. No, that said, one of the big promises and boosting was that it would give you much longer term immunity. And so my hope is that it's holding up better over time. We'll have to wait and see, but that's so far I haven't seen any data that suggests that another booster is, is. Makes sense at this point. Great.

Matt Boettger:

And that, it's good to hear. That's probably mostly speculation cause their number articles are saying that, oh, it looks like the booster could last for months and months and months, if not years and years and years. And that's really, at this point in time, people just probably speculating on what little data we have right now, but this doesn't take time before. Okay, so this one, you said you don't know too much about, but I want to put it on the radar for people who might be interested because this article was fascinated me and I haven't heard anything about this until this one article. And this is about this from AstraZeneca and I'm probably going to blow the name, but it's like Abu shelled or something like that. And for those of you who are immune compromised and have received your vaccine and your booster, and then maybe got tested and realized, man, I had no antibodies surface from this. This is a promising reality. I do know it seems incredibly scarce and that people who actually desperately need it are on huge waitlist. So, I'm hoping, I'm hoping that by just even putting this out here and making it more people can be aware of it, then it might push for more readily available, but this has ever shelled AstraZeneca. I think it's a. And then, or maybe a vaccine, I couldn't quite gather that, but whatever it is, you take it beforehand and it's kind of vaccine specifically for immune compromised and it should prompt promising results of those who had zero antibody. From two vaccines and a booster that people received antibodies and felt a lot more confidence in going out and even doing basic stuff in life. So huge check to up in the show notes, read about it. Okay. Last few things when we'll talk about it. Yeah. That are that are kind of pressing for me. COVID side effects. So I've been reading about this now. I know you you've, you've punted a couple of the, one of these things to mark needs a chime in, on some of this clinical stuff. But we have long covet. We've been seeing this for years. We talked about from the very beginning. And now for me, a new thing on my radar, clearly probably not for the scientific community is this Epstein-Barr thing has been really, I've been seeing this a lot lately in the news and now seeing connections towards maybe long covet and Epstein BARR. And I'm out of live on this. So maybe you can start with this. What is this EBV thing that 95, apparently 95% of us carry. And a few of us, it can raise its ugly head and do something. Terrible things like Ms. Which my cousin has even cancer and other times it just doesn't do anything kind of sounds like COVID itself. Right. Where sometimes you're just escaped completely and otherwise you're in the hospital and near death. So in fill this in and where we're at might be in its relationship to long COVID and other things.

Stephen Kissler:

Yeah. So this is, this is great. It's, it's an area that I'm personally and scientifically really interested in as well. And I think it, it folds into this broader discussion of like, w w how is it that we have so many infectious diseases and yet we know so little about the sort of long-term outcomes from them. So for a bit of background, you're right. This Epstein-Barr virus is extremely common. As you said, most of us have been infected by it, or will be infected by it at some point in our lives. And, and in the vast majority of cases, it seems like it doesn't really do much. But in some it's, it's been implicated by an, different cancers. There's a recent really paper in science that really did convincingly link the Epstein-Barr virus to Ms. And so, but again, I think the really important thing from that is that getting infected with Epstein-Barr does not mean you will get Ms. It just means that it's one of those. Important conditions amidst an entire backdrop of genetic and environmental conditions as well, that could lead to the development of Ms. And so the difficulty in understanding these things is really related to another phenomenon in medicine and science that I hear people talk about a lot, which is like, about nutrition. So like, why do we know so little about how, what we eat on a day-to-day basis? Affects our health and the long-term. We do know a fair amount, but, but like, what's, what's the deal there? Like how is it that something as common as eating is something that we have so little information about, and that's really because the of two things coming together, which is that the results, the health outcomes of different diets are subtle. And delayed. So usually, the difference between, taking in, a certain number of grams of red meat versus half as many grams of red meat. The impact of that is probably there. But it's relatively small and it only accrues over a long period of time. And so that's, that's, that's the sort of question it's really difficult to study scientifically. And so with infections, it's very similar because usually you have, you have very high rates of infection that might lead to a slight difference in risk for a given infectious disease or for a given health outcome. And oftentimes they're delayed hugely. I mean, the development of cancer, the development of Ms is going to be vastly delayed from the point of infection. And so it's really difficult to go back in that causal chain and say this thing. Is what caused this downstream serious effect. And so that's part of why we're still learning about this, but there are ways that we're beginning to get a lot more information about this. So I do think that there are there's probably a lot of links that we don't yet know that we're just beginning to understand between infectious diseases and more long-term chronic and outcomes. Things that we understand to be chronic. And one of those is this link between Epstein-Barr and various other health conditions. I think it's certainly the case with COVID. We don't really know what the longterm effects of COVID infection are, but it does seem like certainly, long COVID certainly exists is debilitating. And we don't really know how long. Certain cases of long COVID might last that's related to other things, we had mentioned mano, which Epstein-Barr can, cause there are some similarities between mono and long COVID. There's some similarities between lung COVID and other types of inflammatory disease that can be triggered by other sorts of viruses that lasts for long periods of time. And I think really what a lot of this comes down to is that we don't have a really clear understanding of how viruses interact with our with our immune system. Because really what a lot of these things are is that an infection has perturbed the way that our immune system responds. And usually, at best the immune system has a short. Intense response that clears the virus and then returns to normal, but sometimes an infection can prompt the immune system to have a longer lasting response and it doesn't ever really return to that normal state. So, so that, that seems to be part of what's happening here with with these different viruses. So genetically, Epstein-Barr and COVID are very distantly related. SARS cov two is a RNA virus, meaning that it uses RNA to encode its genome Epstein-Barr is a DNA virus. So it actually uses a genome that. More similar in some sense, at least molecularly to ours. That may also be part of the reason why Epstein-Barr can cause some of these downs long long-term outcomes is because it's it is just a little bit more close to our actual genome and so can integrate into our genome in in ways that is a lot harder for something like SARS, cov two to do. So there are a lot of important micro biological differences, certainly at the clinical level. And, and thinking about. The outcomes of these things. I do think there are some similarities that we have a lot to learn from.

Matt Boettger:

Great. A couple of things before you had the last thing before we get going in about 10 minutes, this reminds me, I read an article about how I think some countries like Sweden and stuff, how they did their first wave, it didn't get much of any kind of impact. And there are Tracy and some of the things I, I don't know if Epstein-Barr was part of this equation that this might be kind of a tangent reminded me of like a series of reasons why. And you were saying that I think the reason why I was triggered by this, cause he would say there might be a distant relationship between Escobar and COVID. I mean, there was some, but not really, but they mentioned that how, when they were trying to trade. Like maybe why some people didn't get infected in Sweden. They saw a relationship between each one and N one and the Corona virus. There was like some similarities in its, in its like molecular just enough similarity that maybe somehow that H one N one outbreak, blah, blah, blah, helped the protect them just enough, a serious of people. Have, did you see much about that, of this connection between. You

Stephen Kissler:

know, I didn't see much about the connection between certainly, different types of viruses. I've heard some, some conversation about previous, previous coronavirus outbreaks that might've given some amount of protection, but it is true that know, one of the other examples that comes to mind is. We do know that flu and RSV give you some amount of immunity against one another. So if you have a really big flu outbreak that can push the spread of RSV, which is usually a childhood respiratory illness and it can move it around and it, and it's, they seem to interact with each other through this sort of broad spectrum immune response. And so it wouldn't be surprising to me that a, the, an outbreak of a virus that does ramp up the immune system's response could actually provide some short-term protection against infection from another virus. Yeah, it's I, I haven't seen a lot of data on it, but it's totally plausible.

Matt Boettger:

Okay, great. For those of you just, I'm going to keep a close eye. We'll keep a close eye on this whole kind of EBV thing. It's been passing to me and where am I go in the future? The questions I had also, I was like Pimms and em, and Missy, which I w that Stephen's defaulted to mark. I'm curious about this. So, it will have mark I know mark, if you're listening, get back on or submit your resignation. Okay. Last part before you get going, the endemic, what does the future hold for us now? This is we only about 10 minutes or less. I'm really curious of what does it look like going forward for us handling one great article came out from the Atlantic. Why America became numb to cupboard. You have to read this, if you haven't. So please open the show notes for those of you. One of the things they talked about is this kind of like bifurcation of direction, where are we going to go now? Is it, we do, do we desire going back to normal? Is that what we're trying to do? Or do we want to build back better? Right. And so it was a great article about how most people actually truly do want to build back better, but they perceive as if the rest of the world just wants to go back to normal, probably because we're just so desperate, right. To just go back into our habitual lives. But we do. On a large sense, want to build back a better. So I want to kind of throw it back to you and you had some insights with potentially with Ukraine, this kind of stuff that I haven't heard yet. So I'm fascinated about how, what the future holds for us as we move forward to this, living with this and what, what direction we ought and should, and shouldn't be going.

Stephen Kissler:

Yeah. So I mean, one of the things that I'm thinking about a lot with us is how there's The the COVID pandemic has really I think in, in many ways highlighted our collective relationship with mortality because it's been a long time since we've had such a new profoundly impactful. Event that globally has caused an increase in mortality on the scale that COVID-19 has. And so, I think it's interesting because prior to the pandemic we had become numb to all sorts of different types of death. And so now there's this question, we're starting to see this phenomenon with COVID-19 where it's like, okay. So at some level we're going to have to start to accept a certain amount of death, but now there's there's. There's this there's this sort of recognition and intentionality about it, where it's like, well, Hey, wait a minute. Like what w what other things have we been doing this with? But we didn't even realize it. And I think that that's really, one of the big motivations for like, how do we build back better? Like, we've been using flu as a baseline. We accept X number of flu fatalities per year. But then that raises the question like, that's, that's a choice too, to a large extent, there w we can never, we can never eliminate all, I, I don't think that will ever be immortal in the, on this world, but like, we won't be able to remove all of our risks of death. I, I think that in many ways that's a fool's errand, but a lot of these things are, are when. Get right down to it, their choices, right? We're in many ways, they're like choices about who lives, who dies and how many, and and. It's you know, that, that is, that does simplify it to some extent, but that, I think that thinking about it in those terms is really useful because we do have a fair amount of agency in some of these things. And we do have to ask, w what, what is acceptable and what does it mean to build back better? And so folding this into sort of another area is that, we're, we're thinking a lot about building back better returning to normal. But I think it's also easy to forget that this idea of normalcy is a little bit of an illusion to that our lives both individually and collectively as a society operate as a as, as this movement from crisis to crisis in a way, right? Like we're all dealing with one, I don't think that. Any of us can probably honestly say that when the COVID-19 pandemic hit, that everything in our life was perfect, everything was good. We were at a tournament, totally normal state. We were in like this perfect equilibrium, Zen, whatever. And then the COVID pandemic came through and messed everything up. Right. We were all dealing with all sorts of stuff before it hit. And our experience of the pandemic has been a layering of this new crisis over the top of all of the other crises that we had been dealing with on a personal and community and social level. And so I think a big part of what we need to think about as we're thinking about this endemic relationship with COVID-19 is this recognition that it's not, we can't just think about it in isolation, but we need to think about it in the context of the messiness of life. And so that's where you're my thinking about the conflict in Ukraine was also coming in, which is that we're, we've, we've been talking all about the pandemic and shifts and variants and And, and what it looks like to return to endemicity, but, but the return to endemicity looks very different when you're in a country, who's at peace versus when you're in a country at war similarly the sorts of concerns that we have. And, and again, so I'm an epidemiologist. So I'm dealing with, with a lot of the infectious disease outcomes here, but of course, the biggest issue right now is, is in, in Ukraine is not really coming from pathogens. It's coming from bullets. And and that's, that's, that's a difficult reality too, but that's, what I want to note here is that there is also a lot of issues with. Here to where people are unable to get care for their chronic illnesses. Women are having to deliver babies and bomb shelters, and that's not good for anyone's health. And infectious diseases are spreading as well. So thankfully we're at a place with COVID-19 where if this conflict were to have happened two years ago, COVID-19 would have been. An absolutely awful layer over the top of this, it's still not good. But certainly, as people are crowding, as people are displaced, there's going to be a lot more spread of COVID-19. Actually one of my biggest concerns is actually with other infectious diseases as well. It turns out that the rates of tuberculosis and Ukraine as some of the highest of anywhere across Europe. And so again, crowding people indoors and close proximity and the sort of mass migration out of Ukraine could also create a really big issue there. So there are a lot of infectious disease outcomes that we need to think about. And I think that the biggest upshot from all of this is that there, there really is no normal. It really is just this sense of how do we manage this? Crisis and issue that that is becoming more familiar and more predictable in the midst of lives that are unfamiliar and unpredictable at every single turn. And, and I think that that's, that's the much bigger question that I don't know how to answer. I mean, I'm just raising all of these points that all of, and like, you know, we all know that like that's our tagline, right. Life is complicated and it will continue to be. But I think that it's important to think about how we. Develop our relationship with COVID-19 and other infectious diseases against this backdrop of realizing that everything else is also going to be difficult and complicated at the same time.

Matt Boettger:

That's great. I mean, yeah, I mean so much in my mind, I only have like a few minutes left. I think this has been a big learning lesson for me. And I think for the whole girl, I think in some sense, we're in our infancy in dealing with like global connection. We're not, we haven't really reached maturation in this reality because I think hundreds of years ago, we lived in, we lived in a small village or a community, and that became our world. And then because of technology, our world expanded and became large, so much larger than my mind and my heart and my soul can grasp. Right. I can easily get overwhelmed right now. My problems exist beyond my community. I see them, I read them on the news. They're bigger. And so then chances for greater anxiety. And I feel like the gift here is the pandemic is expedited expedite in our maturation, right? Of like, okay. The fact of the matter is we live in a global community. We learn very much that we can not be siloed. Even if we try, we Americans try to be a silent in our small little bit. It's. The COVID taught us that there's no way we can actually fully eradicate the outside world and live in our bubble of utopia, which doesn't really exist anyway. And so just now trying to regroup together, understand how do we actually live in a world that can be joyful, can be peaceful in some level, but also without, without becoming siloed and realizing that there's a world out there that's in constant crisis and we're in constant crisis in one way or another. And how do we incorporate all the. And still live a fulfilled life. And I think that's, that's the complication right? Where it never was utopia. And this is, this is the next step of us, of our, of our growing of how do we still live life, move forward, be hopeful without ignoring the things around us and keeping our eyes open. And I ended up for me. That's probably it for those of you who are like living the real, that's my whole concept of like, that's kind of what it is like, how do we actually like live in a complicated. And respond simply without having to, silo the rest of the world from us. That's a hard task. I don't have an easy solution, but that's the awakening. Right. So, thanks for that. That's really, that's really awesome. Okay. We've got to go. He has a meeting in eight minutes and he probably needs at least two and a half minutes to prep. So. Thank you all for listening on this episode, you can reach out to me mad@livingthereal.com. Please email me, let us know what's going on at four. It to mark and Steven always. If you want to support us patrion.com/pandemic podcast Elizabeth$5 a month or one-time gift PayPal, Venmo all in the show notes. If you want to reach out to Steve. S T E P T N K I S S L E R in Twitter. It's an awesome place to follow him and get a lot information, a lot of information epidemiology, and what's going on in virus, the virus studies and all that kind of stuff, which is beyond my pay grade, but I li I read it anyway. Okay. I have a wonderful two weeks. We'll see you for sure. Well, hopefully God willing in two weeks. Take care and have a wonderful couple of weeks. All right, bye. Bye.