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Things Discussed in Episode:
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Things Discussed in Episode:
You're listening to the pandemic podcast. We equip you to live the most real life possible. And the host today's crises. My name is Matt Boettger. I'm joined once again every two weeks. I'm a good, good, good friend, Dr. Stephen Kissler and epidemiologist, the Harvard school of public health. How are you doing in this wonderful wintry weather? You got blasted by storms or did you do.
Stephen Kissler:We did. Yeah, we got buried. It was it was pretty well there was, it was about two, two and a half feet of snow almost. So, gosh. Yeah, it was it's pretty well melted by now, amazingly, which doesn't usually happen here. Usually it kind of lingers and just turns, you know, ugly colors from all the cars going by. But yeah, it's so, so we're doing better. But it just, it's proper winter up here in, by.
Matt Boettger:Oh, my gosh, I do not NVU or do not want to be there. I just want to be someplace for warms. So yeah, it's cold here. We've had like negative 14 waking up in the morning kind of stuff, and it's just brutal. And of course the boys, like let's go outside and play and we get them all jazzed up and get them all clothed. And I'm taking, they're going to last like two minutes, but somehow their resiliency and the negative weather outside. It's so inspiring. So yeah, it's winter for most of us here in the U S a lot of storms going on, and it's been a couple of weeks and like usual, there's a bunch of things on my mind. So this episode might be a little bit different now it's probably the same, but just like, I have a random questions that I want to throw a pass. So. The he'll have brilliant, great answers to somebody which I might catch him off guard because I don't know what to do with some of this stuff, but before we get going the same stuff. So if you can't leave a review, we love it. Now. I can't believe we're almost in two years of having this podcast. It's like mind boggling. It's like, I like one year felt normal two years for like, wait a minute. That's that went way too fast. Second year went way, way, way too fast. But nonetheless, the reason why I mentioned. It's because I think we have hope, gosh, I don't know how many reviews. We have a bunch of reviews, I think 180 some or something. And I thought, man, if you guys would all hop on and we could cross the 200 threshold by our two year anniversary would be phenomenal. So I was looking Stephen, I was looking all all the random, like, have you looked around at the other random COVID coronavirus podcasts. I'm like, I didn't know. We're kind of like a we're a hit, I didn't know this. I was looking at the ratings and I'm like, oh, we've got like 4.8, most like 4.3 and a lot them like 50 to a hundred reviews. And I was, I'm like, it's really, I was really surprised, I think partly because you guys are incredible and we have like a little family. We're just not, so we don't get into the politics. We don't get into all this stuff. We're just here to help. You know, do the best we can to serve. And Stephen, you guys have taught me so much about just embracing complications and I think a lot of people love that and so they dig it and want to listen more. So
Stephen Kissler:thank you. Appreciate it. It's yeah, this has been a lot of fun and yeah, excited to keep. Yeah,
Matt Boettger:absolutely. So we've got another one from January on January 30th, just a few days ago. Five stars listener 1, 2 0, 2, 1 9 says this is the best of all the COVID podcasts. It sets the problem in context so well, and I actually learned something new and significant each time, keep up the good work. So that's great. Keeping appreciate that. Love it. So if you can't leave a review, do it apple podcasts as well. If you wanna support us financially, we'd love that at patrion.com/pandemic podcast, as little as$5 a month can help or just a one-time gift. Do you want to all in the show notes, that'd be Venmo or PayPal there's links there. So let's get going. I want to start with this because I think let's just start with experience. It's been a wacky few weeks for me, Stephen, because outside of you, which I kind of feel like you're kind of in some sense of anchor of reality for me, I'm my circles might not necessarily reflect that. And you know, what was it two weeks ago? We talked about my pediatrician and the thing that he talked about for those of you who haven't listened to the episodes. Basically, I love him. We trust him dearly, but just, it was interesting how he was really not really for the COVID vaccine for our little ones. But was for the flu shot. And just, I was confused by that. We talked about this, I think that was two weeks ago. And just seeing how it's not as simple as things just consult your primary care physician for the rock solid answers seems then my wife went to my primary care physician and got a similar answer of like, oh, you know, don't do it to the kids. And I, you know, I'm just following the data and all this stuff. Right. And so the kids too, for two, it's just really weird. And then last Friday, Stephen. My mother-in-law goes to see her oncology. And she's like, oh, see, you know, she's like, oh, sorry for waiting. I just wanted to get my booster. And the oncologists made this very quick, small response, like, oh, you know, vaccines don't work anyway. So forget about it. Right. So here I am, Stephen three for three, an oncologist, a pediatrician, and a family practice person, all kind of same, roughly the same thing. And I'm just so I don't take infused. Blown away by the, even in the medical field of just what's going out there. And maybe you will speak back to it. We were talking about a little bit about this off. I know you mentioned the best person right now, be mark to have on, because he's the one on the ground doing this stuff, but you've been helpful to kind of give the distinction of, you know, possibly what two kind of sides are looking at and how it can get a little blurred at times.
Stephen Kissler:Yeah. I mean, I think that, you know, the most important thing to remember is that, you know, Dr. Epidemiologist, whatever that we're, you know, we're people who are bringing all our own stuff to all our things. And I think that it's easy to sort of see a person as the as the role that they fill. Especially when it's somebody with some kind of expertise or authority especially thinking about somebody like a doctor and then just, you know, remembering that, like to some extent A doctor will has the same probability of falling along any one of the lines of opinion and conviction as anyone else. And that's, you know, it, but I understand how, you know, especially with something like vaccination, you would expect maybe a practicing doctor to have a different opinion than the ones that you that you heard from them. And so to try to sort of break some of that open, I mean, I think that Maybe it's easiest to separate out the advice given to your kids versus the comment about vaccines not working. I think that it's relatively easy to dismiss the idea that that the vaccines are ineffective for people who are older. I think that that's, you know, there, the evidence of. Overwhelming that they are safe, effective, hugely valuable in making sure that people who are adults and elderly are staying out of the hospital and not dying from COVID-19. And again they're not perfect, but they, boy, they are extremely good at what they do. And I think, you know, that is a pretty solid scientific consensus. And so I'm not really sure where that information would have been coming from, but that, that just isn't doesn't make sense to me. Now we can think about kids. So, there's been a lot of conversation about Authorization of vaccines for kids recommending vaccines for kids and sort of what we should do in this next stage. And I think that there's a little bit more latitude because COVID-19 seems to be a lot less severe, generally on a case by case basis for young kids than it is for older people. And there's Also seems like, vaccinating kids may not be a super effective way at controlling spread because there are so many breakthrough infections happening. Right? So, so those are generally the two reasons you would want to vaccinate somebody is to protect them from severe disease or from infection and to prevent the spread of disease. So, you know, while I still, you know, from all the evidence, I've seen it, vaccinating kids does seem to. Reduce their risk of severe disease and illness as well. Just bearing in mind that their absolute risk the baseline probability that they end up with severe disease is already very low and lower than a lot of other things, other risks that they probably face in their lives from day to day. And so, you know, I think that there is a little bit more space for complexity there. You know, the thing is that I've been thinking a lot about sort of what I would recommend to people who have young kids in terms of getting vaccinated. I'm a strong, strong supporter for making sure that the vaccines you know, assuming they come back with Acceptable safety and efficacy that they be approved for use in kids. And I think that's especially important for the many kids who who have respiratory conditions or who have other conditions that put them at higher risk of severe disease. I think, you know, and there are a lot of. Out there who are immunocompromised or who have asthma or who have down syndrome, who are at higher risk of certain respiratory illnesses. And for those kids, I think that it makes an awful lot of sense to get vaccinated. Now, I am less certain as to whether it makes sense to have a blanket vaccine recommendation for all.'cause there, I think the cost and benefit I'm not really sure yet how that's going to fall out and it's a lot less clear cut to me than it is for older people and even kids over the age of 12. And so there's, I do understand some of the complexity there, and while I would probably recommend. People get their kids vaccinated, you know, once, once the vaccines are approved, I, I, I have a lot more understanding for both physicians and parents and guardians who may be less onboard with that.
Matt Boettger:That's great. And we're going to talk about this later, but Monza, bring it up now in this, adding to the complexity. So, you know, I just read about how the Pfizer vaccine is getting FDA approved for the little ones, I think from two to five or two to fours. For at the data, but you know, adding to this thing is I saw this, I don't know who this doctor is. Zeke Emanuel person is, but you know, mentioned vaccine children five and above. It seems like it's a no brainer according to this doctor. And it was a very short article up in the show notes, but the, the, the quote that kind of caught my attention was this with the Omicron variant kids are either going to get the vaccine or they're likely to get a serious condition of. It just seems like this is where just adds more confusion too. I think the flames, because I don't think is an accurate reflection of what you're seeing and what globally we're seeing with
Stephen Kissler:kids and Alma. Yeah, no, that's right. It's and, and I was actually just just as we were doing our little minute long countdown, I was looking up this guy and it sounds like he's recently just said that he misspoke that, that I think what he was referring to with a severe case of COVID, it was just a case of COVID that like, as opposed to a vaccine where there's, you know, you're, you get the vaccine and you might have side effects from the vaccine, you would get a case of COVID and potentially show symptoms of some variety. But but, but I think, you know, all of what we just said stands, but you're right. I mean, I think what's, what's more important here potentially is just that there's what is said. Can't be unsaid in a way. And so this does contribute to a fair amount of confusion as well. And to a lack of trust, you know, this this person is also a doctor, I think an oncologist. And and so it's like, you know, it sort of continues to sort of build this kind of a sense of. I don't know, just a caution and maybe I'm lack of trust in the medical establishment from all angles. And I think that that's, that's really difficult. That's sort of an even deeper problem that we've we've got a lot of work to figure out how to sort out in the coming years. Absolutely.
Matt Boettger:And we're not even needed. We do a bookmark that as well. Cause we're gonna talk about that in a second, but just. How science is under the microscope by the public in so many ways, because of just either, you know, from a lot of different reasons that we're a, because of our ignorance are not understanding the field, the beam, you know, and also just the way it's communicated and how it gets confused and those kinds of things. But before we get into that, one more thing about this. Maybe you can touch on this because. Pfizer striving to approve through the FDA. The vaccine for the little kiddos, you know, was weeks ago. We were talking about how, oh, it looks like the two dose didn't work. It's going to go to a three dose. I would imagine this is going to be the talk of the town for a number of months, because number one, just, just at the baseline of exposing your little kids to a vaccine is already going to have a lot of questions behind it because you were in the protective as much as. Then when you get a narrative saying, quote, you know, I'm using my narrative, it didn't work, whatever that means. Right. So we're gonna do a third shot and then we're ready to go. And we're going to do two shots. Wait a minute. Now I'm confused. You just told me it didn't work. In other words. And now, and part of this I read here was this idea of looking through two different, like a micro lens and a macro lens. And initially it was the micro lens. Now it's the macro lens. Now of course, now we're adding more complications. Of course can cause more hesitancy. So I thought I knew. Maybe you can at least help start the ball rolling on this discussion of what's really going on. And as you were saying before we even got on the podcast, this is maybe a reflection of maybe even the development of vaccines in general of how they're looked upon and those kinds of things in light of what we've experienced with other vaccines with COVID.
Stephen Kissler:Yeah. So let's, that's great. I think we can get into some of the nuts and bolts of the, the vaccine approval for young kids. So, as a, you know, as, as we talk about. A long time ago. I mean, I think that we've, we've been anticipating it taking a long time to get the vaccines approved for kids in large part, you know, both because as we were saying, they, they face a lower, absolute risk of severe disease from COVID-19 and because it's just trickier all of, all of the ethics, all of the approvals, everything is just a lot harder, especially when you start getting into the youngest age groups. So I think we're seeing some of that. So, so, so I think a couple of things to just Review an outline. I'm most familiar with with the Pfizer trials. And and the first thing to note is that the vaccine doses that they've been testing in young kids are quite a bit smaller than the doses that they've been giving to adults. I think they're like on the order of a 30th of the size so much, much smaller doses that they're giving. Which, you know, might, it might already lead you to suspect that, you know, maybe they're not going to have as strong of a response because you're just getting a lot less vaccine. And so, and, and that seems to be in part what they've seen. So, these vaccine trials have been ongoing and. Administered vaccines to young kids. And they've been trying to measure the effectiveness of the vaccine through a couple of different ways. You know, normally the gold standard for measuring vaccine efficacy is by. Giving a control group, a placebo and giving the experimental group, the vaccine, and then comparing their risk of clinical disease as you go forward in time. And so early on in the pandemic, when we were recruiting the vaccine efficacy numbers for Madrona and Pfizer and the different vaccines, that's where those were coming from. So when you see an 80% and 90%, 95% vaccine efficacy, that means that the, the, the experimental group has a. 95% reduced risk relative to the control group of something. And in that case, it was usually showing symptomatic disease or symptomatic illness. Now with kids, there's been a bit of a different approach taken. And it's in large part again, because kids. Don't show symptomatic disease as often. And so to do these vaccine trials in the traditional way where you're measuring differences in the rate of symptomatic disease you have to follow a lot of kids and you may have to follow them for a long period of time, simply because the absolute risk of showing symptoms is so low. So to get any sort of statistical. Accuracy around the effectiveness of the vaccine. You need a massive trial for a long period of time and that's difficult to do so they look for other proxies. And one of those proxies is looking at immune response. So the easiest immune response to measure is your B cell immune response. And so, that does seem to be a pretty good proxy for protection, even though we know that other types of immune response, especially our T cell response is the one that's most effective at keeping us out of the hospital and from severe disease illness. But that's also much harder to be. And so my understanding is that in these trials from the micro perspective, what Pfizer has been doing is looking at the B cell response and they've been finding, well, actually it doesn't seem like we have much of a response from two doses of the vaccine. Maybe we'll try three and see if we get to get a better B cell response. But as that's been going, they've also been following the kids in this macro trial. And over time they've been collecting more and more data. And it actually seems like even the kids who have been dosed twice, They do seem to be less likely to show up in the hospital and have a severe outcomes, even though the baseline probability is so low, they've been able to distinguish now finally, because enough time has passed and enough kids have been through this trial that there does seem to be a reduced risk of severe disease for kids who are doubly vaccinated. And so I think that's part of what's going on here is that it's just taking some time to wrap up. Evidence. And because, you know, because kids face such a lower risk, absolute risk of, you know, acute, severe illness it was just a lot, they had to look for other ways to measure. That
Matt Boettger:makes sense. That's really helpful. And just shows a little, you know, you just, I think unfolded beautifully because it's so multilayered in its complexity, because you just said that part at the end, which was like the grand finale, but then you touched on the other huge piece at the beginning, which is just getting these groups in general is exceedingly difficult. So you have to obtain the groups incredibly difficult. And then the measurement incredibly difficult that you have a lot of creative creativity is needed here. And it just goes back to. The first thing we talked about of pediatricians and physicians having different responses and saying, well, I look at the data it's not working. And I know we we've eaten this to death in some regard of always asking the question, what is it like, what is the it they're talking about? Yep. You're absolutely right. When if you're really trying to control the spread of the virus and then that we're on the same page, it's not even, it's not that effective, but it is like, you don't want your kid or your grandma. Going to the hospital and that it is very different, right?
Stephen Kissler:Yeah. Yep.
Matt Boettger:Great. Helpful in that let's, let's switch gears for a second and let's come back to this variant of Omicron, just chat about the updates. It seems like nothing to be concerned about. I don't know if you could speak in as we didn't talk about this before we started, but I found it a little weird how, when the first version of yeoman Cron, which apparently best these, these both. I guess sisters they've kind of came at the same time. They're not really that, but just one kind of dominated ones. I don't know. But anyway, nonetheless, I was amazed how, when Omicron raised its first ugly head, there was a series of the case. You know, we need to take some time evaluate where, you know, maybe week two, we'll kind of have this week four, we'll have this week eight, we might have this information. It seemed as though. As soon as Susan, it came into the media outlets. There's already information like right away. That was so much faster than the first Alma Cron variant, where like I was hearing right away, like two weeks ago I saw an article. Like it looks like it's maybe one to 3% more infectious, like that's a very quick conclusion after the first article. So maybe a couple of things. I what's the status of this, this ugly. And to how on earth did we get data so quickly compare to the first summit?
Stephen Kissler:Yeah. So, these are, these are great. So, right. So, so the, the Omicron that we normally think of is also one of the other ways that we've been referring to it as B a one. And I think, you know, we can talk, I think we've talked about nomenclature on previous episodes, so I won't, I won't get into all of that. But this, as you said, is a closely related lineage that we've been referring to as And and yeah, so it's, it's not totally clear where this thing emerged from. There's been a lot of And conversation going on to try to sort of clarify this and try to understand sort of like how these two related lineages emerged that were actually, you know, very distantly related to what we had seen before. So that's still a bit of a puzzle, but we do know that they're closely related to one another. Part of the reason we know so much about it is because it's actually been circulating for as long as BA one has been circulating too. And so we've, we've had cases of BA two in the U S since December. But they've been sort of bubbling along at relatively low. It's a bit of a mystery right now. Why hasn't taken off and why it didn't take. Before BA one did. Because it does seem to be maybe a little bit more infectious. We're starting to see a BA or sorry, a BA to wave in South Africa, you know, which was the first place to see a major documented BA one wave. And so that's interesting because it suggests that BA two can spread in places where BI one has just had a huge impact. So that's a little bit puzzling, but why is it taking off there? Here. So there's a lot, we're not totally sure about, but one of the reasons we've gotten information relatively early is because again, within we've been actually tracking it for a long period of time, but it's only started now to emerge as something that is starting to cause an increasing number of cases. And also because it's growth rate is. Relatively slow compared to BA one, even though both are very fast that also gives us a little bit more time to sort of track it because of its growth or it was explosive than relative to epidemiological time. Then we wouldn't be getting information very quickly at all. But since its growth is relatively slow compared to BA one, that also gives us a little bit more time in terms of the spread of the pandemic itself to get information about BA too. So. The couple of things about BA too. They some of you may remember hearing I think the guardian had an article about stealth Omicron awhile ago. And so I think this is what they were referring to. It it's this it's this other lineage of Omicron. And the reason they called it stealth Omicron is because boy. Alright, so, so Omicron. Like alpha had this strange thing that caused one of the three PCR primers to drop out. So that means that when you got tested with PCR with both alpha or Omicron, you would light up as positive on two of the, sort of two of the, the redundant tags, but negative on the third. And that's actually really useful for surveillance because that, you know, that that helps, you know, if it's something that's likely to be Omicron versus Delta, where just Delta had all three adults to lit up all three. Omicron BA one only lit up too, but now BA two lights up all three again. And so the reason it was called stealth Omicron in that sense is because it on a PCR test, it might look like Delta, but was actually related to Omicron. And so it was a little bit harder to keep track of. And so, so that's one of the characteristics of BA two is that it's. It it's lacking this S gene target failure which is what that dropout is called. So that's one thing that that differentiates it. There are a couple of other things, too. It seems like there's maybe heightened resistance to some of the monoclonal antibody therapies. Maybe one in particular that still worked against BI one, but it seems to have reduced efficacy against BA two. So there's maybe a higher degree of immune evasion for BA two than there was for BA one. But in terms of, as far as we can tell clinical severity risk of reinfection early data suggests that it's really actually pretty similar to what we've seen with Omicron so far. Which I don't know if that's, I don't know if that's good news or bad news or what kind of news, but it's news. And so, yeah, so there's there's, there's roughly what we know. I think, you know, once again, South Africa is probably the place where we're going to get. The most new information about VA two from, because again, they had such a strong wave of and now they're seeing a lot of BA too, and more than many other places in the world, actually, Denmark has a pretty big BA two wave right now. And one of the things that we've seen there actually is that it seems to be actually tracking the relative severity of Omicron pretty closely where it doesn't seem to be any more severe to people who are vaccinated. Then overcrowd was so, so that's all, that's all I, that I think is generally good. Okay.
Matt Boettger:Good. Good. Well, you know, I don't know if you can predict this, this early, but you know, having the South Africa, maybe starting to have its own way with BA too, what do you think about, is this something you think is going to happen to the U S or because of the inundation of Omicron here that the first one may not compete? Or what do you see the next two months?
Stephen Kissler:Yeah. You know, I don't know this is, this is really puzzling it's. You know, I I've been joining these weekly calls with colleagues about the variants and then this one has had us puzzled for a little while. We're, we're starting to see BA to picking up in the Northeastern us and in a lot of places that have just seen the spread of BA one. And. So, you know, that that might lead you to think that you almost need a BA one wave before you see a BA too, but that also doesn't seem to be the case because Denmark is seeing a big BA two wave and they really didn't get much original Loma Cron at all. So that's a long way of saying we really have no idea what's what's going to happen. And to what extent this is going to cause continued infections. I think, you know, it's important to note that in South Africa, the BA two has sort of lengthened the tail of their own McCrone wave, but it actually hasn't really caused much of an increase yet. So hopefully Omicron crown still provides good protection against BA too. That would be my hunch because they're so closely related. But we'll see.
Matt Boettger:Okay, let's keep it. I just saw a comment here from Catherine. She's watching live. Thanks for watching. She's one of our long time listeners. And so, let's continue on. Cause I want to put a bookmark on you have no clue because I think this is because it's really going to be an important piece of our conversation in about maybe seven minutes or so. Two more big things I want to chat about. Related to maybe I have no clue, but this, you do have a clue about because you actually helped publish this article. So Harvard medical professors says it's time to move on from the pandemic. Now that's not
Stephen Kissler:what we published.
Matt Boettger:Yeah, sorry. Yeah, that was totally two connected. Right? A Harvard professor. I just said that. Yeah. So that's not what you publish, but this is a medical professor saying this what caught my attention? Not so much the article, I guess it did. Cause I read it. But this quote that came from this, that this is from Dr. Stephanos kales. If I said the name, right? He says once a macaron peaks, subsequent variants are likely to be even more mild than. Totally threw me off because daddy have likely to see, oh, wow. Okay. This is pretty confident that coming from Harvard, that we're, this is all downhill from here, so we can kind of be in the coast and you kind of gave an excellent explanation off the podcast now. And to bring it back on the podcast, explain it. Cause then we can bring in Dr. Fowchee as well, and kind of juxtapose these two and show that where these nuances come from.
Stephen Kissler:Yeah. Yeah. So this idea that, that future. Variance of SARS, cov two will be less severe is is a common one and it's not entirely incorrect. But I think it's important to know where it's coming from so we can put it in the proper context. Right. So, part of the reason why this doctor and many other people, I think rightly believe that it's likely that future SARS COVID two variants will be less severe is simply because our immune systems. Good at doing what they do that with repeated exposures to a pathogen either through infection or through vaccination our immune systems learn and they learn better and better. The more they're exposed, generally speaking, that's often the case. And it seems to be the case with SARS COVID. Were repeated exposures. You know, that's why the three dose vaccine series is helping keep people out of the hospital. That's why people who have been previously infected and vaccinated are better than people who've just been previously infected in terms of their protection from being, you know, going to the hospital. And that's likely to continue that that as we move forward, Higher and higher proportions of the population will be vaccinated or previously exposed. So that will reduce, you know, people going to the hospital, which will help reduce burden on the healthcare system. And, and, and I think that's, that is likely to be the case for sure. The place where I've also seen arguments for this, that I don't think are accurate is with respect to the inherent severity of the virus itself. There is some belief that pathogens naturally evolve to be less severe and from sort of a pop site from a pop evolutionary perspective. That kind of makes sense because you know, the idea is that if a pathogen kills its host, that's not beneficial to the pathogens. So a pathogen will evolve to be less severe. So it doesn't kill its host. So it has opportunities to train. It's true, but only true for a pathogen that can only transmit after it's caused a severe disease, but that's not true for SARS. COVID two, most of SARS COVID two transmission happens before you even realized you've been infected. So there's no selection pressure for it to become less severe because it's already done it's transmitting by the time it causes any sort of severe disease. So, so the severity, the inherent severity of SARS, cov two is just totally decoupled from its transmissibility. Maybe not totally, you know, nothing in biology is totally disconnected, but you know, for our purposes here, we can say that. So, so, so is that statement right? Well, yes and no. I, I think that, you know, generally speaking where our experienced impact with COVID-19 is likely to be less severe with future variants because our immune systems are good. But you know, one of the areas where this really matters is for people who can't mountain mean a good immune response, right. For people who are immunocompromised for you know, that for them future variants of SARS, COVID two are likely to be. Just as severe, maybe not justice severe, but much more so than the population level data suggests. And I think that's really worth bearing in mind that there are going to be a lot of people still living around us that when, for whom, you know, this, this isn't just another, you know, Mine are cold. And, and won't be for a very long time if ever. And so I think, you know, I think that that is worth bearing in mind. Now the other thing that we were talking about at the beginning that relates to this is that while I agree that the most likely scenario that our average lived experience with COVID-19 is going to become less severe with future variants as our immune systems get their. Exposure. That's not to say that we can rule out the less likely, but still possible scenario that we will end up with a variant that is more severe. And so while I don't think that's something that like we, as a. Nation and world need to be necessarily concerned about all the time. That is something that we as epidemiologists, if we, as doctors are going to be concerned about thinking about all the time, because there's this trade-off between likelihood and hazard that we constantly need to be bearing in mind where we, even, if something is a rare scenario, If it's a really bad scenario, we still want to be prepared for it. And so that's one of the things that we'll be thinking about a lot. And so, you know, all of that is to say that I don't, I don't anticipate that we're going to have a variant that totally escapes our immunity and brings us all the way back to square one with COVID-19. Is it a real remote possibility? Yes. I mean, it's also a remote possibility that we end up with a flu pandemic next year. And we, you know, we have an entirely different pandemic to deal with as well. I'm sorry. I know I have probably half of our listeners shifts hearts just dropped out of their chests, but, you know, and, and again, I want to emphasize the rare, you know, this is, this is not likely, but it is a possibility and something that we're thinking about as well. So yes, I think with this pandemic, as in my own life and our own lives, we're always sort of seeking after this certainty and reassurance and believe me, I know this as well as anyone I'm constantly trying to find. Comfort and reassurance and, you know, certainty that things are going to be okay, whether it's with this pandemic or with anything else in life. And so I think it's a really natural thing to really gravitate towards these kinds of things that like, oh yeah, future variants are going to be less severe. We can sort of be done with this. And I think that that is probably operationally a reasonable way to live one's life going forward. But I think the most accurate statement is that yes, that's probably true, but we're also. Keep bearing in mind that there there still remains some risk and and, and that risk is going to be why I keep doing what I do.
Matt Boettger:That's perfect. I love it. Cause you know what number one full, I need to make a, an apology. This is not the article that you're talking about. This. I, my eyes went to a different whole different article. So when I mentioned about Stephen publishing article, it has nothing to do with this one. It's the next one we'll talk about, but I think this is a great. Like place of discussion note, because here's where I am at. Like, I have a, tends to be a little too optimistic. Ah, it'll be fine. Right. That's my thing. It'll be fine. It'll be fine. So I would make an, a terrible epidemiologist. Like it would be literally would not want to put the world's fate in my hands because you would hear, oh, plague. Ah, I think would be fine, you know, and we just, we just stopped there. Right. So, so this is where the. Yeah, like the eternal optimists, whatever. And they knew where you internal testaments, whatever those are kind of pigeonholed people, but like, it takes both to really be able to cope with life because we need people who, and this is where I say you have like the Stefanos kales. Well, I'm not gonna, I'm not gonna put him in a box, but like, Maybe I'm going to put them in a box just for a second, but just for the caricature, not, not for any, just to try to make this kind of this dichotomy of like, okay, I'm optimistic, it'll be fine. No big deal. It should be less. And then you have someone like Fowchee, he was being criticized nonstop, like a fearmonger. And I think this is, I think Stephen, you just really helped to show the nuance. It's not being a fearmonger it's doing his job. Like, I mean, he's, you know, this quote, it was in the same article. He says. Though he were talking about Fowchee. He's cautiously optimistic about the pandemic. Dr. Anthony Fowchee said another variant could arise. That alludes current immunity. I hope that's not the case. He said, I don't think it will be, but we, but we have to be prepared. Right. So I think you just, you hit that were Fowchee is not a fearmonger he's doing his job. He's not going to overlook the data that there's a possibility of. Ah, you know what? I'm a really good scientist, but let's just forget about, let's just focus on the optimism. Right. You know? The we who's the, we, I think I want to take myself out of that week and be like, that's you Stephen? That's you Dr. Fowchee. You guys think about that. You guys make sure we're okay. I'm going to focus on the optimism, but be also cautious as well. So I like that. Thanks Stephen, for bringing that to the attention. Now, let's go to the last article here, and this is when we're at. An article that was grounded in your research and somebody took it and did again, not the, probably the best articles, very short from nature, nature, magazine, or nature, the nature article and the, the, the, the title of this one is how does Omicron spread so fast, a high viral load? Isn't the answer? And so I wanted you to talk about, because I read it, it was very short. Three minutes long to read. And I got no conclusion about it. It basically just said, Hey, look, there's the viral loads the same, in fact Delta, maybe a little bit higher, but then it's landed the plane somewhere. I'm like, okay. So then how does on God's green earth does this thing spread way faster than Delta? If it, if the viral loads the same.
Stephen Kissler:Yeah. Yeah. So this is, I mean, in a way, this is interesting, cause it's like a message that we've sort of been repeatedly sort of putting out. But I think that it bears repeating, you know, with each new variant because there's this really sort of strongly entrenched and actually well founded idea. In epidemiology. And I think even more broadly that that if something is more transmissible, that means that there's, it's, it's generating more virus because. You know, that's is more virus means more likely to spread in that kind of thing. And, and that's true for many viruses. I mean, we know that a lot of our understanding of the relationship between transmission and viral production comes from HIV where the two are very tightly. And the, to the point where, you know, there's, there's a very common phrase in the HIV positive community. That undetectable means untranslatable right. So like, if you can't detect the virus, that means that you can't spread it. And, and to detect the virus, they're using things like PCR, right? Like the same things that we're using to detect stars. And so, so yeah, from, from our previous experience with viruses, we really expected there to be a tight relationship between the amount of virus that a person produced and how infectious the virus was. Based off of what we've found both for Delta and for Omicron, that really doesn't seem to be very much the case. Definitely I've had a slightly peak a slightly higher peak viral load relative to previous variants. But as you said, I'm a chronic. A lower peak. And so that doesn't seem to be able to explain why it's more infectious. No, some of this has confounded, right? Because not only were we comparing Delta against Omicron, but also more people were vaccinated and. Between the Delta and the underground waves. And so there's a little bit of confounding there too, where we're vaccinated. People may be less likely to show peak viral loads, but, but the conclusion is still the same, right? Like, even so Omicron is able to spread explosively. Why? So I think there are a couple of likely reasons for this. And the most obvious thing is, is, is that there's an increased infectiousness on a per viral per, per viral particle basis. And that can happen for a number of reasons. One of them is that maybe there's a differences in Omicron that allow it to be more stable and aerosols. And that's something that has been studied by a lot of Aerosol engineers and experts, you know, people who study fluid dynamics and such. And, and that, that's a really interesting thing because it actually does seem like, Sometimes the more transmissible variants on their viral surfaces actually have different sort of electrical charges in a way. Like they have different proteins that have different electrical charges that attract different kinds of molecules to them when they're suspended and aerosols. Could potentially protect them as they move around from being sort of denatured and dehydrated in the air. So that's one possibility. The other that I think is also very likely is that it's better at binding to ourselves. It's just better able to A third possibility is that it actually binds slightly different types of cells or cells in different parts of the body. And that may actually be part of the difference in severity as well. That it seems like Omicron is maybe less detectable in the nose, but more detectable in the throat. At different stages of infection. And so maybe that's just the way that it's getting into our bodies is a little bit different and that sort of gives it an edge for transmission too, but we don't observe any of that in the raw amount of virus that's being produced. So, so I think that's, you know, that that's one of the key takeaways from the study. The second thing you know, is that we, we found that people remain positive at potentially infectious levels of virus for. Generally well over five days. And so w w when we posted this pre-print and we're working on sort of the full submission now for a peer reviewed article, but this pre-print, we were, we were sort of reviewing that in light of the CDC has updated guidance that after five days you could essentially end isolation. I, yes, but you should also be aware that like, if you end up isolation after five days, there is a good chance that you're still infectious. So you still, you know, try to distance and mask and all of those things. And I think the best strategy is to use a rapid test to detect. That you're negative before you leave. So that would be my recommendation, but that's sort of the other thing that we were trying to evaluate with this study is just how long are you positive with Omicron? And it seems like you can be positive with Alma crown for just as long as you were positive with the other viruses, the other variants as well.
Matt Boettger:Okay, great. Super helpful. It seems like Kate measuring viral loads because you, one of the easiest things to do as a scientist. Right? So these other things I'm guessing are these kind of like more like just Intuit, like intuitive theories, because I would imagine. How would you study a viral product called a virus, a virus particle to see whether it's qualitatively more infectious than a non I'm? Sure. That's a whole other level of like, I don't even know if it's even, you can even do that. If this is just like theories of, well, it's not this, and it's probably this, this, this, or this. How do we actually define. We have no clue or maybe you do have glues. I have no idea.
Stephen Kissler:Yeah. So, so there are, there are studies you can run to, to sort of get closer and closer to that information. I think probably the next step and something that we're thinking about doing is what are called viral culture studies. So then what you can do is for a given viral load, you can isolate that virus and spirit on a plate and see if it grows. And so, so one way. Of of measuring infectiousness is to just to see if the virus is viable on a plate that is seated with the types of human cells that we have in our nose and whatever. And so, so that's one way you can also measure with much larger epidemiological studies. You can actually see, you know, you can try to compare very into variant how many new infections are caused. If you're tracking people very closely, then you can maybe reconstruct. How infectious, they were at different points in their viral load trajectory, but that that's really difficult and haven't seen many studies of that type at all. But those are really, probably the two best ways to go about it. The other way potentially is using animal models. But that's also not very good because. Our animals, one animal to another differs, a ton in immune response and the cells that we use and such, so that that's a very rough proxy, but it's something people have tried. Okay,
Matt Boettger:great. Thanks buddy. I appreciate the answering all my questions. I hope this was helpful to all the listeners here to get a little information about. Totally keep you on your game. Little newbie mat, trying to get their simple questions answered. All right, well that wraps up this episode. Thank you all for listening. Again, you want to support us. You can do that at patrion.com/pandemic podcast or one-time gift to PayPal Venmo in the show notes, please leave a review and leave some comments. I'd love to get over 200 by. I think the first week of March would be our two year anniversary. It'd be an awesome little gift to us. And I think that wraps it up. Of course follow Stephen S T E P H E N K I S S L E R on Twitter. I did that more and more every week now, as my main focus of updates. If you want to get ahold of us, matt@livingthereal.com, just an email, and I will forward it directly to Stephen and mark. Those of you who are new listeners in the past few months, you probably thinking who in the heck is mark. I've never heard of this dude. He used to be a part of our show. He still is, but he's been very busy at home with a lot of stuff, but I would imagine he'll report back sometime soon. I have a wonderful two weeks. We'll see you in two weeks. Take care. And bye-bye.