Rev Left Radio - The Science of Covid-19: Immunobiology, Virology, and Pandemic Politics

Episode Date: September 7, 2020

Henry Hakamaki joins Breht to discuss the latest science regarding SARS-Cov-2, how it impacts our immune system, how virus' work generally, the politics of it all, and much more.  Support Henry's work HERE Follow Henry on Twitter HERE Please Support Rev Left Radio HERE Outro Music: 'The Devil Wears a Suit and Tie' by Colter Wall LEARN MORE ABOUT REV LEFT RADIO: www.revolutionaryleftradio.com

Hello everybody and welcome back to Revolutionary Left Radio. On today's episode, we have a guest on to talk about really the science of COVID-19 and where it's at right now. One of the big problems with a pandemic like this is because the virus is new, information comes out slowly. And as the pandemic plays out, we start to get better and better understandings of it, which can lead to a lot of misinformation. information, a lot of sort of conspiratorial skepticism, which we see a lot of around the issues of masks and even people on the right calling COVID a hoax overall. So I figured it was a really important thing to cover and really nail down where the science is at this moment. And so today we have on Henry to do just that. Henry, would you like to introduce yourself and tell people

sort of who you are and what your background is? Sure, Brett. Thanks for the introduction. My name is Henry Huckimacki. I'm a graduate researcher of immunobiobiodi. I'm a graduate researcher of immunobiology. My focus is on Ebola virus, but I work in a lab of viral immunology, so I am relatively well-versed in overall viral immunology. In regards to how I've been playing a part in this pandemic so far, this pandemic hit at a really interesting time in my life. I was just finishing up my thesis research and figured I would visit home while I was doing some data analysis. And that was exactly when the pandemic hit. I ended up getting stuck here in the US. I should mention that I do my graduate work in Germany. And I got stuck here in the US and I've been stuck

here ever since. So I'm so sorry. No kidding. But yeah, since I've been unable to get back to the lab and continue with my work, I've been doing appearances on the David Feldman show and writing some articles and whatnot to try to break down the science of COVID for people. Because as you mentioned, there's a lot of misinformation out there and even beyond the misinformation. We sadly don't have as many good science reporters as we should or even as we used to in the country. And so there's just not that kind of information available in a digestible way for the public. And so I've tried to do what I can to at least help people figure out what's going on. Absolutely. Yeah, that's absolutely crucial at this moment.

And, you know, this show will be more science than politics, but it's important and science should always inform our politics. So I knew that this is something that we really, really wanted to do and really had to do. So let's go ahead and dive into the questions. Maybe the way to start is just to talk about what is SARS-CoV-2, what is COVID? Is it different? And what kind of symptoms do people experience when they're infected? Sure. So this is a good way to start the conversation.

you'll see in the news SARS-CoV-2 you'll see COVID-COVID-19 written sometimes it's abbreviated to C-19 and it's helpful to understand what the difference between these things are so SARS-CoV-2 is short for severe acute respiratory syndrome coronavirus 2 which is a fancy way of saying it's a virus it's a coronavirus and it's the second one of this specific type that we're seeing so this is the actual virus itself. It's the thing that's causing the disease, whereas COVID or COVID-19 is the disease that you get from being infected by SARS-CoV-2. So the way that you can think of this is SARS-CoV-2 is to HIV, what COVID is to AIDS. SARS-Cov-2 causes COVID. Okay, so now that we've got that out of the way, if you're infected with COVID, what do you expect to have happen? So somewhere in the vicinity of up to 30 to 40 percent of people who are infected with SARS-Cob 2 are asymptomatic, which is to say they never have any symptoms of COVID. They don't feel like they're sick, they don't have a cough, but these people do have the

virus in their system. That virus is replicating in their system, so they're getting more and more viral particles in their system. And importantly, they're able to spread the virus to other people without ever knowing that they're sick. Okay, so that's up to 30 to 40 percent of the people that get the virus in them. Of the other people, the people who do eventually become symptomatic at some point, about 80 percent of those people have pretty mild symptoms with either pneumonia or really mild pneumonia. Somewhere 14, 15 percent have relatively severe disease where they have a lot of lung involvement, more than 50 percent of their lung is involved within the disease process. They have difficulties breathing. Their oxygen levels and their blood will drop. And then

5% will have really critical disease where we see things like respiratory failure, shock, multi-organ involvement. But if we're looking at just pure symptoms, so if you want to say, hmm, do I have COVID because I'm feeling a little bit sick, it's hard to tell if you have COVID specifically because there's a ton of overlap in the symptomology between COVID and most other respiratory diseases. About 50% of the people that get COVID symptoms have a cough. Okay, well, if you have other respiratory diseases, you also generally have a cough. Just about half of the people get a fever. Again, most respiratory illnesses cause a fever. Muscle weakness, muscle sickness, soreness, headaches, difficulty sleeping, difficulty breathing. These are all things that

a fair amount of people see, but not everybody that has COVID has these symptoms. sore throat. Some people get diarrhea from it, which is interesting, considering that we typically think of COVID as a respiratory disease. Some people vomit because of it. But one of the more interesting symptoms, and it's the thing that really sets COVID apart in terms of knowing whether you have COVID or just the flu, is that loss of smell that you may have heard of in the media. You know, people that have COVID are losing their sense of smell or are losing their sense of taste. This is, is something that we rarely, rarely see in other respiratory viruses. And the reason for this is because the virus that causes COVID can actually enter our olfactory bulb of our brain. And that's something that is not very common. So it's something that definitely sets it apart. But other than that, the symptoms are pretty standard for a respiratory illness. Yeah. I hear a lot of talk about the viral load, you know, how much of the virus that you're exposed to. Is it right to think about the connection between the viral load and the intensity of symptoms that one

gets, a bigger viral load, more intense symptoms, or is it just a certain threshold that once crossed really depends on the individual person, their underlying conditions, et cetera? That's an excellent question, and it's something that it's still not 100% nailed down with COVID because it is such a new disease. Usually it takes years to figure this kind of thing out. But what I can tell you is it looks as if the increased viral load, the person is exposed to does increase their likelihood for developing severe or critical disease. So if you're trapped inside an enclosed space for a long period of time, let's say you're sharing a hospital room with somebody who's sick and you weren't sick with COVID.

You had some other problem. You're trapped in there for a long time. You're going to be exposed to a lot of viral particles. And to the best of our knowledge that is contributing to the increased likelihood of having severe disease. But we're not 100% sure on that yet because there are a lot of diseases where you're right, there's a threshold where once you get to a certain number of infectious particles into your system, then you're just sick. And the severity of the sickness is just based on what disease you're exposed to. Some diseases have a minimal infectious dosage of one

particle. So Q fever jumps to mind. If you get one Q fever particle in your body, that's enough to cause disease. Yeah, COVID is not quite as low. It's low. We're looking in the ballpark of, again, it's not 100% nailed down, but between 10 and 100 viral particles is likely enough to cause disease. But to the best of our knowledge, the larger the amount of viral particles that enters your system to infect you initially, the higher your likelihood for developing diseases. But of course, there's a lot of other factors that play in regards to whether or not you're going to suffer severely or not. Absolutely.

Yeah, interesting, interesting. Okay, so how do our immune systems respond to COVID infections and pathogens more generally? I just think, you know, a lot of people understand the basics of, you know, you get this particle or you get this viral load and you get sick, but what is actually happening at the level of the immune system when this happens? Yeah, great question. And to explain what our body is doing when we're fighting COVID, I'm going to take a step back and explain how the immune system responds.

in general when we have something foreign come into our system. That is to say something that shouldn't be in our body comes into our body. The first thing that that pathogen, which just means anything that can cause a disease, any small organism that can cause a disease, when that pathogen enters your system, the first thing that it's going to come across are cells that are associated with what we call the innate immune system. So we've got two branches of our immune system, the innate and the adaptive. The innate immune system responds really quickly. Almost immediately after the pathogen comes into your body, it's getting responded against by different cells. Now, what separates the innate from the adaptive beyond just the fact that it's happening

very quickly is that it's not a very specific response. So these pathogens that enter our body have patterns on them that distinguish them from things that are inside of our body. And these cells, will recognize these broad patterns. We call them pathogen-associated molecular patterns. So these pathogens will come into our system and we'll have a cell, let's say, a macrophage or a neutrophil, which are cells of the innate immune system. And they'll say, you know, I don't know exactly what that is. You know, I know it's a bacteria. I think it's a bacteria because it's got some markers that are consistent with it being a bacteria and none of our cells have those markers on their surface. So it's not supposed to be here. So I'm going to do my

function. And depending on what kind of cell it is, they have different functions. Macrophages eat the invader. Nutrophils have several different things that they do, but one of the things they do is dump a bunch of chemicals into the system to try to destroy what that is or destroy cells that have been infected by that pathogen. So that's the innate immune system. So that'll happen for a few days, maybe a week, maybe a little bit more than a week. So those are the only cells that are responding are these things that don't actually know what has infected you, but they know that it's something that's not supposed to be there. After about a week or so, what happens is we get cells from the innate immune system, specifically dendritic cells, we call them DCs, and more broadly the category

of these cells are antigen presenting cells. And what they do is they pick up little bits of the pathogen. So the pathogen will get destroyed by the innate immune system. at least one particle of the pathogen. And these antigen presenting cells will pick up these little bits, the fragments, of the dead pathogen, and they'll stick it onto the outside of themselves, the outside of the antigen presenting cells. And then they go trolling around through our body, looking for B cells and T cells, which are the cells of the adaptive immune system.

And those cells have a very, very specific antigen that they recognize. So we can think of it this way. A T-cell, we have a bunch of T-cells in our body, million T-cells, more than a million T-cells. Every T-cell will only recognize one antigen, and that is already pre-programmed before we've ever been infected with that pathogen. It's a really interesting way that this happens. But it's a bit in the weeds, so I'm not going to get too into it. But the thing that you have to remember is, let's say we have a T-cell that will respond against plague. just picking something out of the hat here.

We've got a T-cell that'll respond against plague. The T-cell is not going to immediately be where the plague is coming into our body. What it needs to have happen is an antigen-presenting cell, like a dendritic cell, pick up a bit of a plague, bacterium that had been destroyed, and go looking around and trying to match this antigen to all of the T-cells that it's coming across. You can think of this like a lock and a key. The antigen is the key. the T-cell receptor is the lock.

And it goes around and it tries to stick this key into all of the locks and the T-cells as it goes around the body. And eventually, it'll find the one T-cell that has the lock that its key fits. Once that happens, that T-cell will expand and expand and expand. It'll make a bunch of clones of itself. So now we have a bunch of T-cells that recognize that. The same thing happens with B cells. Once we have that expansion, we call it clonal expansion,

then we have B cells and T-cells that can respond. and go around and respond very, very specifically to that pathogen. And just to briefly explain what B cells and T cells do, B cells are the ones that produce antibodies, which everybody has heard of antibodies, and we'll probably talk later about what antibodies do and why they're useful to have when we're responding to a disease. But B cells are the cells that produce antibodies, specifically plasma cells, which is a subset of B cells. T cells, on the other hand, there's two broad categories of them. There's helper T cells and cytotoxic slash killer T cells. And the helper T cells will help

the function of other cells to respond. So they'll help B cells produce more antibodies. And they'll also tell innate immune cells like macrophages, neutrophils, eocinophils, et cetera, all of these innate cells that don't recognize specific pathogens. They'll say, hey, here, I recognize pathogen here, come here and do your thing because you know how to kill stuff. You're just not very good at recognizing exactly what it is. And the killer T cells, on the other hand, they do exactly what their name says. They just kill either the pathogen itself directly or they'll find cells that are infected with, let's say a virus. The virus is on the inside of the cell. They'll recognize that that cell is infected and they'll just kill the whole cell. The complexity of the human

body is absolutely mind-boggling and getting into a field of science that you know you might not have any training in really highlights just how deep and profound every sort of section of science can be when it when it really zooms in on its sort of object of investigation in the most layman terms to re sort of gurgitate which you just said there's basically two waves the immune system has when it when it detects some foreign body the first wave is sort of general immune response whatever it is, we're sort of going to attack it at first, and then the second wave is a hyper or much more specific response to the specificity of the pathogen entering the body itself. Is that sort of a super simplified way of thinking about it, or am I off?

No, that's exactly right. And the thing that you want to keep in mind here is that there is a time delay between these two things, and that's why we can see that there's different stages within these infections between being infected and with it being cleared. One of the first things that we see when we're infected with a pathogen is generally inflammation. And that's because these innate immune cells, the first immune cells that respond, a lot of the things that they dump out of their cells to respond to a pathogen are pro-inflammatory cytokines, which just means that they're chemicals that cause inflammation.

And that doesn't necessarily mean inflammation of the skin, where we would typically think, but it's inflammation locally to where that pathogen is. So that's early phase. We don't get antibodies until generally at least a week. into the infection because that's associated with the adaptive immune system. And if I just want to add one more thing quick. So when we're saying that the innate immune system is not acting specifically, that's not necessarily a bad thing. We can completely clear pathogens using only the innate immune system if our innate immune system is functioning well and the pathogen isn't doing

too many sneaky tricks to try to evade it because a bunch of different pathogens have a bunch of ways evading our immune system. But if the pathogen's kind of a dumb pathogen and our immune system, let's say we live a healthy life, we take all of our supplements, we don't have any sort of immune complications, it's entirely possible to clear the infection with just the innate immune system before the adaptive immune system actually kicks in. But because there's not a lot of specificity, what ends up happening is a lot of the damage that's being done in our body and COVID, a lot of it is in our lung cells, specifically our type 2 alveolar cells. A lot of the damage being done is done by our own innate immune cells, specifically neutrophils, because as I said,

neutrophils, one of the things that they do, and they do a bunch of different things, but one of the things that they do is they dump a bunch of really, really toxic chemicals into the system to kill the pathogen. But what happens is they'll find an area where there's a lot of pathogen. They'll dump it out, and it'll kill the pathogen, but it'll also kill all of the bystander. cells in the area. So if we have a virus in our lungs, let's say, like SARS-2 coronavirus, the causative agent for COVID, we've got this virus in our lungs, and our neutrophils recognize, hey, there's something here that we don't like, we're going to respond to it. Sure, we need to respond to it, but the problem is, is they're dumping so much of these neutrophilic chemicals, they just dump

them out of the inside of their cells. They're dumping so much of it into the system that the lung damage that's actually occurring is largely due to our own immune systems. Wow. That's incredibly fascinating and a really important thing to understand. I do want to talk about inflammation specifically when it comes to children and the inflammation, sort of rare inflammation disorder that has been appearing or at least was a few months ago. But I think we'll get to that when we talk about kids specifically. I'm a parent of two young children.

One of who has gone back to school. So I do want to touch on that in a bit. But before we move on to the next question, to thinking about the immune system and there's so much with this pandemic that individuals have no control over what are some ways that individual people can you know meaningfully perhaps boost their immune systems to just sort of do everything they can on an individual level to sort of create a bulwark within themselves against this against possible infection is there anything that we can do that that noticeably and quickly boosts our immune system or makes it

healthier? Yes and no. So there's things that are just generally good for our immune system, but that doesn't necessarily mean that it's going to be good for responding to COVID-19, because one of the things that I just said was if our immune system is overacting, that's actually going to cause more damage. So one of the things that they're using is a treatment right now, at least the results of it coming out are positive right now, is immune system suppressants because the less keyed up your immune system is, the less damage you're going to caused by the immune system. But yeah, the point is well taken. There are things that we can do that might help us in terms of biomolecular things that we can take. But the bigger thing is

going to be public help. But in terms of things that you can take, vitamin D is likely to be at least not detrimental, but vitamin D just in general is quite good for your immune system to make sure that you have enough of it. Something like 25% of Americans are deficient in vitamin D at any given time. And yeah, I mean, that's a big problem. So zinc might also help somewhat, but that's completely unclear. It's just another thing that in general is decent for your immune system. But the bigger things that you can do to keep yourself safe, because vitamin D, it might have some slight benefit, but it's not going to be the thing that really makes the difference for you. The thing that's going to make the difference for you is not being infected to begin with. And the things

that are going to prevent that are the things that we've known about for a long, long time. Wearing masks, wearing gloves, perhaps, if you don't have very good, let's say, you're not particularly good at remembering not to touch your face with your hands when you're out in public, which most of us struggle with, keeping your social distancing, washing your hands properly, we know that these things work. And in regards to masks, they work whether or not you're infected. They work better if a person that's infected is wearing it, but they also work to protect you if you're not infected. There's studies that have been done via meta-analysis, which is to say they just collect data from a bunch of other smaller studies from hospitals specifically and

other small publications. They compile the data and then they release this huge data set. And these meta-analyses have found that just wearing a mask if you're not infected can decrease your risk of being infected by the virus by up to 65. percent compared to if you were not wearing it. And if people that are infected wear it, it can decrease the risk by up to 85%. Now, that's a huge drop. So now couple that with social distancing. We're talking about keeping distance from other people in public. There was another study that was done. And again, a meta-analysis study. This is an experimental where they're just infecting a few people or taking a few infected people and standing people different distances apart. This is based off of like computer-generated analytical models based on other results, but they found that keeping a distance of at least one meter away, which is just over three feet for those of us that use the imperial system, can reduce the amount of spread by up to about 82 percent, is the number that stands out from one of the studies that I've seen, and that for every increasing meter, you're 2.2 times

less likely to be infected than you were if you were one meter closer to them. So you can think of it this way, if you're standing right on the person that's infected and you take your chances of being infected as, let's say 50% if the person was infected, you're standing right on them, you have a 50-50 chance of being infected. If you go one meter away from them for that same duration of time, that 50% would be reduced by 82%. And for every meter beyond that, so two meters away versus one meter away, you'd take whatever risk of that is and divide that by 2.2. So it's a swift drop-off in terms of your risk, the farther away you get from infected people. Hand washing, just to wrap up a few other quick things that are just generally good health tips, but particularly in a time of a pandemic are

useful, hand washing is highly effective against viruses. The outside of a virus is basically like a little fat capsule that protects the genetic information and the soap degrades that and helps wash it away off the skin. So hand washing diligently doesn't have to be antibacterial soap that that doesn't have any additional benefit, just regular soap is fine. And if you can, if you have to meet with people, or let's say you're feeling very depressed because you haven't been around your aunt in a long time or your grandma, for example, and you just, you know, you need to be around them. So in addition to wearing masks and keeping at least a few meters away, one thing that can help

is being outside, particularly on sunny days, because beta coronavirus, which is the family of viruses that SARS-CoV-2, it belongs to, they don't handle UV light very well. So being out in the sun is going to help reduce the amount of virus that's being able to be maintained in the air. So staying outside also would be a good way to reduce the risk of being infected. And of course, being out in the sun is the natural way in which a lot of people get their vitamin D, right? So it's like a double, a double whammy. Right, right. There's, yeah, there's a lot of different things that we've been seeing where there's multiple positive effects from the exact same action or the exact same drug. So looking at these things that have these multiple effects

is certainly a good idea. You know, you can look at using the sun to get vitamin D and reducing the viral load in the air. There's certain drugs that have multiple effects, but we might get into that later. I don't want to drone on too long about that. Okay. Yeah, so let's go ahead and move on to the next question then and um this is a question about uh how the virus sort of enters ourselves so can you talk about how that happens and is there anything that can be done to prevent this from happening beyond what we've already discussed sure so the virus if comes into our body typically through our nose and sometimes their mouth but typically through our nose and also through our eyes frankly uh we we have the potential to be infected through our eyes and our

mucous membranes there. Once that virus is in your body circulating in your system, the virus is just kind of floating around and it can't actually do anything without being in your cell. Viruses, we don't typically consider them as living things because without being in another cell, they can't do anything. They just float around. But once they're in our cells, what they do is they hijack our machinery and make our own cells a little virus factory. We pump out a, a ton. I was going to use a different word, but we'll say a ton of viruses from our own cells. It's like a little factory for viruses. So that's what viruses do once they get into the cells. How this specific virus gets into our cell, let's think for a second about what SARS-Co2, the virus that causes

COVID, looks like. And you've probably seen pictures of it, but let's just think anyway. Imagine that you've got a tennis ball with a bunch of little toothpicks sticking out of it. You know, you've seen pictures of it. It's a little ball with little spikes sticking out the outside. Those spikes sticking out the outside are aptly named the spike protein. There's a bunch of these spike proteins that stick out from the outside of the cell. And what this spike protein does is when it's going through our system, that spike protein is looking for a receptor that it matches.

This also is like a lock and a key. like we were talking about antigen and receptor. This is similar. But in this case, the spike would be the key. And the key is going around looking for a lock that it fits. That lock that it fits is a receptor that's on the surface of our cells called ACE2. Now, ACE2 is a really important thing in our cells. It helps reduce blood pressure.

We have ACE which raises blood pressure. Ace 2 reduces blood pressure. And they have to be in a very, very tight regulated range between each other because otherwise our blood pressure goes to crap and we die. So ACE2 is important for our cells, but the spike protein finds ACE2 and it matches up with ACE2 and then it allows the virus to fuse with our cell membrane and enter our cell in order to make our cells little viral factories. Most of our cells have ACE2 on them. There's different cells that have more amounts of ACE2 on them, which would increase the likelihood that that cell would be infected. So cells

have a lot of ACE2 are type 2 alveolar cells, which are in our lung, the epithelial cells of our nasal tract, gut epithelial cells, the GI tract, as well as cardiac cells, so heart. And we have seen heart complications associated with COVID infections, and we might talk about that later. So these cells have this receptor on them. The spike protein recognizes the receptor, and that's what allows it to enter our cells. There's not really good ways that we can block the ACE2 receptor from doing its job because then, like I said, we die of blood pressure dysregulation. But what's being looked at being done is these vaccine candidates that are being developed are trying to produce antibodies that are targeted to the

spike proteins that that spike protein can't fuse with the ACE2 receptor and therefore can't enter our cells, right? They're also looking potentially at using something that's called nanobodies. I'm not going to get too much into it because it's way too much science, frankly, for the amount of time that we have. But they're little synthetic antibodies that we can dump into the system. And the idea is that we would have those engineered to also target the spike protein to block them. But this actually ties in really well to the last question, where we mentioned that there's some things that have multiple beneficial effects. One of the other things that's required for viral entry.

There was a paper that came out about a month ago, I want to say, that showed this. We always knew that the ACE2 receptor is how it entered our cells. It's how most coronaviruses work. But there's another thing that's on the surface of our cells that basically acts as a co-receptor. It's also required for the virus to enter, and it's called Heparin sulfate. And I'm not going to get into what's Heperan sulfate usually does. It has a bunch of different things, blood pressure related a lot.

as well as coagulation. So heparan sulfate generally is relatively near to ACE2 on the surface of our cells, and it turns out that the spike protein actually needs to match up with both of them, heparan sulfate and ACE2 in order to fuse. Well, that's not a problem for the virus typically, but there was a study that was done that showed that using heparin, which is basically a synthetic heparan sulfate that we can use by injecting people with it, and right now they're looking at making an aerosol

version of it, like an inhaler. Heparin is used as an anticoagulant all the time. If you have blood clots and you're in the emergency room, it's pretty likely that they're going to be using heparin in you. It's a really, really common drug. And what happens is the heparin is incredibly similar to the heparan sulfate. And so let's think of it this way. The spike protein is like us. Imagine that you're the spike protein. You've got your two hands, right? And you want to go to a party and you're supposed to bring a fruit salad. Now you go to your kitchen and you're looking for fruit. You find an apple and that's the ACE 2 receptor. You've got to have that. But you can't just have a fruit salad of only one fruit. You've got to find an orange too. So your other hands looking

for an orange. Now if you find the orange and this would be Heparin sulfate, there you go. You're pretty much good to go. I mean, you have to cut it, and there's another thing on the surface of ourselves called TMPRS2 that does the cutting, but we'll skip that for now. You've got enough fruit to come to the party and get into the party. But let's say that we have a, we're looking for, we've got the apple, we're looking for an orange. Let's say we've got a tennis ball painted orange in the kitchen, a hundred tennis balls painted orange in the kitchen and only one actual orange. The likelihood of us accidentally picking up one of the tennis balls is pretty high because there's a lot of them in there. And if we pick up that, well, we only have two hands. We can no longer

pick up the orange and therefore we can no longer make the fruit salad. And if we try to go to the party, we're not going to get to go to the party. So this is what the idea with heparin is we're putting so much in there that it's going to confuse the virus into not being able to fuse with heparan sulfate not being able to enter our cells. So that's something that in cell culture, so this hasn't been tried in people yet, but in cells on a plate, this looked like it worked really well.

And the thing that I want to mention here is that heparin is something that we could potentially look at using for treatment of severe patients anyway because one of the more severe complications of COVID is blood clotting. I don't know if you've heard of that or not. It's been reported a little bit in the news, but not particularly focused on.

Some of the severe complications are blood clotting, thromboembolisms that go through our system and clot up our arteries and veins, and particularly they go to our lungs, and heart problems. So heparin is what breaks up those clots to begin with. So if we're putting heparin into our system and it's both blocking the ability of the virus to enter our cell

and it's preventing blood clots from happening in the severe cases of COVID, that's a double benefit right there. And that would be something that would be really great to use. But they have to test it in humans before that's something that we would be looking at doing. Right. And for the development of vaccines, I mean, it's common knowledge at this point that the Mumps vaccine was the fastest one ever made, and that took four years. That's right.

On the same hand, though, we have so many different governments and corporations and academic institutions working on a solution with better technology today. So, you know, it stands the reason that we could. get a vaccine in under, well under perhaps even four years. What are your sort of feelings on the likelihood of that coming by, say, the end of this year, or is a more likely route of the development of treatments that can effectively treat but not be a vaccine? And those will come out quicker. Like, what is your sort of thinking on that from where we stand today? From where we stand today, I would say that we're looking at it being a little bit more likely that we're going to

have effective treatments, at least in severe cases, as opposed to. to a vaccine. So just to briefly run through how a vaccine goes goes through its development process. And if people are interested in a more in-depth look at it, I have a post on my Patreon page describing the vaccine process. But the vaccine process goes like this. First, you have some scientists in a lab that try to figure out what would be a good way to develop a vaccine, what the vaccine should look like, what kind of things you're going to target. They come up with a plan. then they make it. Then you have three phases of trials of increasing size. So you start with just a handful of people, then maybe a few hundred people, and then right now our phase three trials

for this specific virus are about 30,000 people per vaccine candidate. And these early trials look at first safety and efficacy, and then they want to see on a bigger scale, whether it's both safe. Are we seeing side effects due to the vaccine? And is it efficacious? Is it actually preventing people from getting the disease. I mean, this is fairly obvious that that would be what you would want to look for in a vaccine candidate. The thing is that this usually takes years to run through these trials. But with the amount of money that's being put into this project, we're developing candidates

incredibly quickly. I mean, we have hundreds of candidates that are out there. And we have between three and six, depending on how you would count them, candidates that are in phase three trials right now. which is the final phase of trials. These trials typically last more than a year on their own, just the phase three trials, but again, they're trying to fast track this as much as possible. Then after the trials are done, the FDA reviews the literature, or each individual government

has their own regulatory agency, but in the U.S. it's the FDA. The FDA will review the literature and determine if it's safe and if it's effective, And if it's effective enough that it's worth any potential risks, then they approve it and then it's put out and they do monitoring to see if there's any negative effects. You're right. The fastest that this whole process has been done before was four years. The amount of money that's being put out there right now and the amount of kind of corner cutting that's going on in terms of how long each of the trials are going on for is definitely going to end up with a bunch of vaccine candidates that are on track for being. approved within a year as long as the regulatory agencies are willing to side with the governments in trying to get a vaccine out there. So by the end of the year, I'm a bit skeptical that we would

have something that would have been rigorously tested enough to be put out there. But sometime early next year, it's possible that if we get positive results from the vaccines that are in phase three trials now, that they would be approved and be out there. But in terms of treatments, we're already seeing treatments that might have effects. Like I said, we have some glucocorticoids, which are basically immune suppressants, steroids, that at least in severe cases appear to be beneficial from preventing people from dying. And those are the people that, of course, need it the most are the people that are suffering severely, and those are the people that are getting the benefits from it. These drugs have already been approved. They've already been manufactured. They've been

develop, they've been approved, and we know how safe they are, and we know what dosages are acceptable. At that point, it's just a matter of finding out what dosage is required of that drug to be effective against COVID. And there's a bunch of other drugs that are being used for other diseases already that we're trying to repurpose for being used against COVID. And if these work, we could have them out really quickly. It's just a matter of testing them in Burferson's cell culture and then in humans. And if they're effective, well, we've already got them. So that would be really good. It's unlikely that we would make a treatment from scratch by that before the vaccine is out. But, and if you'll allow me to spend just a second on public health,

there's three arms to responding against a pandemic disease. One is a vaccine. Two is biomolecular therapeutic treatments. And the third, which is the cheapest and also probably the most effective and the quickest the institute by far is public health measures. And this is where, as you said, politics plays a big role in this. Public health is the interface between science and policy. The scientists in the lab and the scientists doing computer modeling will come up with what the science says. And then it's up to the government to institute policies that keep people safe, whether that's mandating mask wearing, whether that's mandating people stay at home, et cetera, etc. You know what these public health policies are. And that also includes things like financial

support for people. Some countries have been doing an excellent job of making sure that people can stay at home because they can afford to stay at home. Canada did a great job of this. On the other hand, the U.S., people got their one-time $1,200 stimulus, which frankly I wasn't eligible for, so I didn't even get that. There was an unemployment stimulus bump, which again, I was not eligible for, so somebody like me didn't benefit from that either. But those were relatively meager protections when people were being forced to choose between staying home and going to work. If we had really strict public health policies, we could have completely nipped it in the bud. And it doesn't require a lot of money. Let's look at the case of Vietnam, for example.

Vietnam is a pretty poor country overall. But their response to COVID was incredible because their government was willing to step in and do really drastic measures to prevent people from getting sick without having a treatment or a vaccine for the virus just by doing these actions. So, for example, they had gone the longest time without having any deaths due to COVID, a really long time. And then there was no cases for a while. Then all of a sudden, there was a city in Vietnam where there was, I believe, a family of, I think, three, where the three people all tested positive for COVID. So what happened? In the U.S., those people, well, under the current guidelines, those people would be quarantined and they wouldn't even test people that had contact with them

unless they had symptoms at that point. That's the new guidelines from the CDC, which are absolutely insane. Vietnam, on the other hand, what they did is they evacuated the entire 60,000 person city so that the quarantine was the entire city around these three people. That's a drastic measure but that explains why Vietnam has done such an unbelievably well job at preventing people from dying and it's it's cheap and it just requires a government that's willing to act and that's why we're seeing you know even regional governments like in carola and india um where it's governed by the communist party their response has been unbelievably better than the rest of the country but i digress yeah no i think that that that's incredibly important i think to point out this intersection between

science and politics, the non-response by the U.S. government qualifies it for just complete criminal negligence. I mean, just a disgusting display of a lack of leadership, a lack of focus, a lack of that public outreach and education. The three countries that have done among the worst are all big capitalist countries run by far right-wing, almost neo-fascist characters, Trump in the U.S., Modi and India, and Bolsonaro. in Brazil. So I think the political outlook and the political structure of these societies goes a long way in dictating how this pandemic plays out. And then, of course, in the U.S., you have the added problem of even if the science can effectively produce a vaccine and

the manufacturing capacity is there, and we get the vaccine out to people, there is a huge segment of Americans who are just, they have their brains rotted out from conspiracy theories, And in recent polling, you're seeing as much as a quarter, if not much more, of Americans saying that even if a vaccine is available, they won't take it on grounds that it's Bill Gates, whatever, conspiracy, la, la land, story, fever dream. And that is ideally where public health policy would come in with, you know, targeted messaging from the very beginning and the necessary education to inform the populace of not only what's happening, but also, I think, think an important thing would be to inform them that this is how science works and things will change as we learn more about the virus because the moment the CDC or any sort of institution shifts their policies or shifts recommendations, the, you know, certain segment of our society at least immediately points to that and says, see, it's all a hoax. They're lying to us,

etc. So that just inbaked American ignorance, I think, is also throwing fuel on an already criminally negligent response. You're right. And I just want to to point out the irony of one thing that you pointed out. As you said, there's a few countries that have done significantly worse than everywhere else, basically, and three of them are the United States, Brazil, and India. Right now, we're the three biggest contributors to global cases. And the ironic part about it is that all three countries are run by authoritarian strongmen who, in a different world, if they cared more about people than about the capitalist class, they would be undertaking these measures because they have that grip on power that's so strong

and they'd be able to do it effectively whereas if we look at vietnam a socialist country they don't have any money but they have again a strong control on political power within the country and they do care more about the populace than the capitalist class and therefore they're willing to take the actions that are going to prevent people from becoming ill and dying but we have we have the leaders in these three countries that you mentioned that should have that kind of strong man you know political power the political might to actually do it but they've just been unwilling to do it yeah and in the case of i don't know much about modi but in the case of balsanaro and trump the first crucial months of the pandemic they spent the entire time calling it a hoax saying it would go away blaming their political opponents for creating a big fuss out of nothing and so those even like it's in the early days of the quarantine here in the U.S., you know, people are supposed to quarantine and social distance and stay home from work if they can, precisely so that things can be marshaled by the government to help people when they come out of quarantine, get a grip

on the spread, do contact tracing, all of the stuff. But instead, in America, nothing happened. So that first wave of everybody going in and staying in their house was completely botched. Nothing was produced. Nothing was done to control the spread, no contact tracing whatsoever. And so then a few months later, Americans just said, I'm bored, I'm done with this quarantining, and we had made no progress on the virus. And now we're looking down the barrel of almost 200,000 dead Americans. And a recent poll showed that 57% of Republicans have said that that's an acceptable loss of life.

And it's just absolutely mind-boggling on every level. Yeah, I agree entirely. And there was somebody had this out there. I believe it might have been in the American prospect or something like that where they said, yeah, we could have nuked our economy but kept people safe or we could have tried to keep the economy running and nuke our people, but instead we ended up doing both. We nuked our economy by having this ineffective shutdown and then not doing anything to control the spread of the virus so that once we reopened, it would be safe.

So people ended up dying anyway. We nuked the economy and nuked the people. But, yeah, that's been pretty accurate for how the U.S. response has been. And the last thing I'll say is a good economic response. The best case scenario for our economy during this pandemic was always, always hinged on a competent pandemic health response. So, you know, the people from day one are saying, well, what about the economy? Well, what about the economy? The economy's health is dictated by how good and competent and overwhelming our reaction to the pandemic is.

And so when you refuse to do anything about the pandemic on the terms of I don't want the economy to crash, as you said, you end up creating two tragedies, the health one and the economic one, because in order for our economy to really get back to normal, the pandemic itself would have to be brought under control. And so I just, yeah, I mean, we could sit here all day and talk about the utter deficiencies in American political and cultural life. But let's go ahead and move on. Now, we did talk earlier about how to protect ourselves. Did you want to say anything else about that before we moved on because you covered masks and hand washing and whatnot? You know, I think that what we covered is pretty effective between the hand washing, social distancing masks, gloves, if you're, again, not very good at keeping your hands off of your face because if you have a contaminated hand and you touch your eye, well, you just contaminated your eye and that's where the virus is able to spread. So those are going to be the main things for keeping yourself safe. everything else is going to be trying to keep yourself alive after you've been infected,

but it's definitely more beneficial to look at how to prevent yourself from being infected in the first place. Yeah, absolutely. Okay, so let's go ahead and move on to kids, and this is particularly interesting to me, because as I said, I have two young children. I have a sixth grader who is very mature for her age and, you know, given the sort of spread in our community or the lack of huge spread in our community, and given the rigorous response by our public school system,

we felt that, you know, our sixth grade kid can go back to school, and we'd pull her, obviously, if there was any spread. But, you know, we trusted that the system was doing okay, and we trusted her maturity to do the necessary things while she's in school to stay safe. And, obviously, we monitor closely. But we also have a kindergartner who, because he's a kindergartner, just too young, doesn't fully understand it,

and cannot keep his hands out of his mouth or any of that. So we kept him home. But this is obviously a huge debate, a point of contention, and something that especially working parents all over this country are really tying themselves in knots over. The poorer you are, the less likely you are to be able to take off work or work from home, the more forced you'll be to make your kids have to go to school so that you can go to work so you don't lose your house.

I mean, it's just a tragic situation all around. So having placed all that on the table, what do we know about kids and their ability to spread the virus and how badly the children suffer, particularly with that rare inflammatory disease that we were hearing quite a bit about a month or two ago? You can take that question in any direction you want. Sure. So you're right. The economic setup of our country requires a lot of parents to use school as essentially a daycare for their kids while they go to work because we don't have any sort of. of social safety net for people to do anything other than use school as a daycare for their kids. And that's, that in itself is a tragedy and a farce. But if we want to look at the terms of

the science of what is happening with kids, kids don't suffer particularly badly from a COVID infection. It's incredibly rare for kids to die from COVID. And it's pretty darn rare for kids to even have severe illness. Typically, it's mild or asymptomatic entirely. But there's a few things to keep in mind here. The key point is not are the kids themselves dying in droves? It's are the kids able to spread the virus to other kids and other adults? And for a long time, we didn't really know because the schools last year closed just about

the time that the virus was coming here. So we didn't have much data on whether or not schools could be drivers. of infection. But we have some data on kids specifically. So first I'm going to start with a very sciencey point before we go into anecdotes. There was a study that was done where they took nasopharyngeal swab. So that's the swab where they put the swab up your nose and it feels like they're poking your brain, but they're not really poking your brain unless they're doing it horrifically

badly. Yeah, it just goes into the cavity behind your nose. But what they do is they took these sworembergly. swabs of people at different ages, people over 18, people between the ages of 5 and 17, and people under the age of 5. And what they did with these swabs is something that's called QRT-PCR, which is quantitative, reverse transcriptase, polymerase chain reaction. And that's just to make me sound smart. But here's what it is. Okay, so PCR is a method that's used for amplifying genetic information. We can do it from anything. You get a few bits of DNA or RNA, and then we make a bunch of

DNA or RNA that's all exactly the same so that we can detect it. RT, the reverse transcriptase, just means that it's changing it from RNA to DNA, because something that we didn't mention earlier, SARS-2 coronavirus is a RNA virus. It doesn't have any DNA. It requires different things than the DNA viruses, and there are DNA viruses. But this, this virus specifically is an RNA virus. And so the RTP part of QRTPCR just means that the test converts the RNA into DNA because that's how the PCR part works. And the Q standing for quantitative, that's the most obvious part of it,

it allows us to find out how much of that RNA or the DNA at the end of the process there was. So what they did is they took these swaps from these different aged people, people that were infected, I should mention. These people had already tested positive. And they amplified the RNA and converted it into DNA until they were able to see how much there was of this RNA within the person's nasopharyngeal tract, which is generally where the virus is coming out of when it infects other people. And what they found was really interesting. So a lot of people assumed, and for no real reason, they just kind of thought it, that adults would have, a lot more virus in their system because they were generally suffering worse.

But what they found is that kids between the ages of 5 and 17 had just as much viral RNA in their nasal-ferengal tracts as people over the ages of 18. And kids that are under the age of 5, and this is the scary part, because kids under the age of 5 are not particularly disciplined. Kids under the age of 5 have more viral RNA, a lot more in their nasal-ferential tract. When they're infected, they have somewhere between 10 and 100 times more viral RNA in their nasal-ferengal tract. And just one disclaimer before I move on to the anecdotes, viral RNA is not necessarily directly, you can't directly say that that's the exact amount of viral particles

that are in that person's nasal-ferengal tract. Just because there's more viral RNA doesn't necessarily mean that there was more viral particles. But studies on other viruses have shown that it is a very, very strong indicator and that they are directly linked in these other viruses, that having more viral RNA means that there was more viral particles to begin with. And it makes sense. It's just we don't have that data on SARS-CoV-2 yet, so we can't say that definitively for this virus. I see.

Now, in regards to actual cases of this happening, one of the first major outbreaks that we saw that was driven by kids was an overnight camp, a YMCA camp in northern Georgia, at What happened there is these kids went in. Nobody really thought that they were sick. And then there was 260 kids that ended up falling sick from COVID when they came out of the camp. All of them had been, except for the ones that brought it in to begin with, but all of the other ones had caught it there. And the average age of the kids that were spreading it there, I believe, if I remember the study correctly, was eight years old. So these are school-aged kids that are spreading the virus to one another.

And as I mentioned earlier, these kids, they didn't really suffer very badly. There was a few kids who had to be hospitalized. But the kids that were infected here didn't suffer tremendously because of the COVID infection. But what we want to keep in mind here is that if we're thinking about transmission that would take place at schools, if these kids are infected, there's a few things that can happen. They can infect their teachers. How many of the teachers are elderly? Elderly people suffer very badly from COVID. The teachers can be infected.

Or, if the kid is exposed to the virus and is infected at school, they come home, they infect their parents, they infect their aunts and uncles, they infect their grandparents, anybody that they're exposed to. And those adults are going to be the ones that suffer, and they would have got it because of the school, even though the kids themselves didn't suffer particularly badly. So it's possible to open schools in a safe way. But if we don't have really strict testing regimens and strict social distancing, strict mask wearing, making sure that the kids aren't hugging each other and licking each other's face during recess, it's a recipe for disaster if those things are not being strictly followed. But there is a way to do it the right way.

It's just I fail to see many schools actually implementing really, really strict policies. Now, to get to the other point that you made about this rare inflammatory disorder, This is, and I want to emphasize rare, there was a study that was done by the CDC that was looking for this one inflammatory condition in children that's called multi-system inflammatory syndrome in children, or MISC. It's basically like Kawasaki disease, but I don't expect that to mean much to most people. So what this MISC is, it's a disease that kids get that isn't necessarily directly linked to a virus. It's not the virus itself that's causing it. It's like an after effect from the virus. And it is associated with fever, rashes, conjunctivitis, which is swelling of the outer layer

of the white of your eye as well as your inner eyelid, redness in your mouth, cracked lips, swollen lymph nodes. Those are the things that are in similar to Kawasaki disease, but there's also more severe things associated with us, like peripheral edema, which is when fluid accumulates in the tissue of your peripheral vasculature, so think your lower legs, GI problems, shock, which is where there's not enough blood flow to your tissues, and that's an incredibly severe thing. And elevated markers of inflammation and cardiac damage. So these are things that are really, really bad. And the reason I wanted to say that it was rare is the CDC

looked from the beginning of March until the end of July to see how many cases there were. And this is strictly in children. It's under the age of 18. They only found 570 kids that had had this condition. In the U.S., in the U.S., 570 kids in the U.S., between March and the end of July, and they were basically just pulling hospital records and seeing what kids were diagnosed with this inflammatory syndrome. Then what they did is they wanted to see if those kids had been tested for COVID, and the vast majority were. Something like 565 of the 570 had been tested for COVID. And guess how many of them tested positive for COVID? every single one of them, all 565 kids that were tested that had this inflammatory syndrome

had had COVID just prior to having this inflammatory syndrome. So we know, at least we have incredibly strong indications that this really, really severe disease is directly linked to COVID in children. So even though the kids didn't suffer particularly badly from COVID, a lot of them were asymptomatic and the ones that weren't asymptomatic generally just had the sniffles or something like that for a few days. But afterwards, they ended up getting this really, really severe condition. So, no, kids are not just given a free pass and they have nothing to worry about. It's rare, but they get this really, really terrible condition afterwards sometimes.

And is that condition, I mean, you talk about obviously all of them having COVID. Is this an immune over-response to COVID that people think is the ultimate cause of the? the inflammatory disease, or is it just not enough data to back that claim up? That would be the speculation. So again, there is no, there's no studies that are experimental, seeing like they had somebody that was infected with COVID. They put them into a lab, and then they just studied their inflammatory markers starting when they were infected with COVID all the way through when they ended having this inflammatory syndrome. Those studies just don't exist. So, and you can imagine why. But the idea here,

would be, you're right, the body is responding to COVID, and then something goes wrong in its response where it's able to clear the virus and in children, typically very, very efficiently. It clears the virus, but then something's, you know, wrong in terms of how the immune system is then keyed up, and the immune system then starts to just kind of go nuts and attack different stuff in their systems or dump these, as I said at the beginning, pro-inflammatory cytokines into their system and that increases inflammation, which can cause a lot of damage in their systems. That's the speculation. But again, there's no experimental studies that have shown that that is the mechanism, but it's

fairly likely that's the case. Yeah. So it is rare, but the point here is that kids are not wholly spared from suffering from the disease directly. And even if they don't suffer directly from it and they don't get the inflammatory disease, they can obviously spread it to more susceptible immunocompromised or elderly people in their families or their immediate spheres of influence. And so on different levels, there's different forms of risk.

Exactly. And, you know, it really is sad because in lieu of any competent federal government response, and even in a lot of these, like I live in a deep red state here in Nebraska, in lieu of any response or meaningful response from our governors, all this shit falls onto the school districts and often individual teachers and staff in these schools and these are obviously people that are not trained to be medical experts and so you know just another tragedy of this botched response

is that so much of it falls onto the shoulders of people in our society who are already overworked and underpaid and now have to have this extra burden put on top of them when it comes to the health of the kids which teachers, you know, love and they hate to see this happen and they're scared for themselves and do they bring it back to their family. So just another layer of just absolute depravity in America's response to this virus. But speaking of effects that take place after the virus has cleared, what long-term effects

have been reported in adults specifically? Yeah. So we've seen several long-term effects that have persisted after the infection is already passed. So after there's no more virus left in your body, we're still seeing some effects. So we're seeing respiratory failure in some people who have already cleared the virus. We're seeing cardiac problems, heart problems, cardiovascular problems, which is the vessels that go to your heart and around your body. We've seen these in a bunch of people, including asymptomatic people. There was just a study that came out of Germany maybe two weeks ago. 70% of the people who

showed up to the clinic after having been infected and after they have cleared the virus had myocarditis, which is inflammation of the big muscle in the heart. That's a really serious thing to have happened. And 70% of the people had had this myocarditis and something like 62% of them had not had it previously or had any cardiac problems previously. This was something that just came up regardless of whether it was severe or not. And of course, these people were in the hospital for whatever reason. So it's not necessarily a good. look at the general population but let's look at uh there was just a report that came out either yesterday or the day before i think the day before that showed big 10 athletes these are like

just about the healthiest people that you can possibly imagine when they tested these big 10 athletes because all of the student athletes were being tested for covid one third of the athletes that had been that had tested positive for COVID-19, either active infection or an antibody test, which would indicate past infection, a third of the people who had tested positive were showing this myocarditis on their heart scans. And these people were really healthy, and a lot of them were asymptomatic, and we're still seeing this heart condition. And we don't know how long that's going to persist for, because the virus is new. We don't have long-term data on that. Other things that we've seen, we talked earlier about clotting disorders, thromboembolisms, these blood clots

that go around the body, including going to the lungs and causing people to die. We have cases of young people having strokes that had no risk factors for strokes before we're talking like 30-year-old people having strokes after having recovered from COVID because of these clots that are being thrown in their system. We have inflammatory problems. increased inflammatory markers, pro-inflammatory cytokines. We've talked about a bunch. And one of the more interesting things is a lot of young people are actually spontaneously developing type 1 diabetes after they've recovered from COVID.

So they get the virus out of their system and they should be fine. But all of a sudden they get diabetes, type 1 diabetes for seemingly no reason other than the fact that they had COVID before. And then the last thing that I'm going to mention is just something that's in common with a lot of other respiratory illnesses is that you get secondary infections, particularly in the lungs after the virus has been passed. So think about when people have a really bad flu and then they end up getting bacterial pneumonia afterwards because their flu was really bad and it made them really susceptible to any bacteria being in their lungs or sometimes fungi. We're seeing the same thing in COVID. We're seeing a lot of secondary infections in the lungs of people that have recovered from COVID. Yeah.

So, you know, all that stuff is on one level incredibly scary. And I think it pushes against this idea that I think is widespread in our society of, you know, this is an old person disease. This is something that hurts people that are maybe obese or immunocompromise. And if I'm relatively young and relatively healthy, it's not going to be a problem for me. So who cares? I'm going to go out and go to bars. and I'm going to do my thing and live my life, blah, blah, blah. And what this is showing is even in situations where, like you're talking about the athletes,

where they're completely asymptomatic, they still have these downstream long-term effects that are still fundamentally in a lot of ways mysterious as to why they're caused, how long-long they last, what the long-term effects of these things are going to be. And so all of this, you know, speaks to the idea not that we're trying to, you know, scare people or anything like that, but rather to give people. people a real understanding of the dynamics of this disease and give you the tools to not only understand, but to take action to prevent yourself and others from getting it. And especially when we live in a society where one of the most effective mechanisms, masks, have been hyper-politicized.

So, you know, I went to Seattle to visit my, a close friend this summer. And Seattle, obviously, very left liberal sort of city. And everybody's wearing masks. People out walking. their dog by themselves are wearing masks or whatever. I come back to Nebraska and I go into a grocery store or a gas station or heaven forbid I like to fish so I go to like a bass pro shop so you can see the demographic shift in a place like that and you're just seeing 90% of people know masks, people that are old, people that are out of shape, people in line standing a foot behind the person who's standing a foot behind the person in front of them.

And so it's just it's a horrific sort of social. situation, but insofar as we can control what we do and insofar as we can educate those around us to take those proactive steps. I think that's what we're really urging people to do and not get sucked into some of this more ignorant stuff about, this is just a concern for old people or because I'm relatively young and healthy. I have nothing to worry about. That's just not the case. And even if that were the case, spreading it to other people is a problem. Think about others, not just yourself. I know I'm speaking to the choir here, but it just, to see how so many people in our society take this so unsuriously is really sad and disheartening.

And so anybody that does take it seriously, we should, we have an obligation to do everything we can to protect ourselves and others. Absolutely. The political class is using the virus as a way to disrupt solidarity between people. This is something that really we should be pulling together around. Regardless of political orientation, we should have solidarity as humans, but if nothing else, the working class, the people that are disproportionately affected by this. This is something that should pull the entire working class together is something that we can fight together and make a better society together. But the political class insists on dividing us on a virus, a virus, something that we should be fighting together. They make it so that everything is us versus them.

And that is what's inhibiting our public health response right now more than anything. Yeah. And that speaks to the mentality of fascism or reactionary conservatism or whatever. Us versus them, problems in our society are never solved by these far right figures. They're only turned in to mechanisms of division. There's only scapegoating. You can only point out the enemies and go and attack them. But there's never, ever any solutions to the actual core problems of our society.

And that's something I think that's worth definitely noting. when it comes to this pandemic and when it comes to all the other issues in society that we're facing and countries around the world are facing. But let's go ahead and move on. And I know you mentioned antibodies a little bit earlier, but it might be helpful just to talk about them and sort of the role they play in all of this. Yeah. So antibodies, most people have heard of them.

But basically what antibodies are, they're little proteins that are pooped out of our B cells. So our B cells, again, remember, are part of our adaptive immune system. So that's happening later on in the infectious process, something like a week plus after we first have the infectious particles within our system. So after that week or so, our B cells have already been presented with an antigen. They recognize what's in, that one specific B cell that recognizes that antigen from that specific pathogen. Then that B cell has, after that period of time, built up enough clones of itself that all recognize that pathogen. that they can go around and these B cells will then differentiate into different types of B cells, but the one that we're looking at here is called plasma cells. These plasma cells will go

around and they'll just start pooping out all of these antibodies. Now antibodies, just briefly what they look like, think of them as a why. It's got a long, you can say tail and then two tips on the top. And the tips bind to the epitope, which is a long, you can say tail, and then two tips on the top. And the tips bind to the epitope, which is to say the specific thing that they're meant to recognize, right? So in this case, let's think about antibodies that would respond specifically to the spike protein of COVID. So these two tips of the Y recognize the spike protein. They get pooped out of the B cells. They just start floating around.

And if they see the spike protein, they stick right to it. Now, once they stick to it, there's a bunch of different things that can happen in terms of what they actually do to prevent us. from not clearing, in this case, the virus. One of them is, again, remember that the antibodies have two tips. That means that they can each bind two viral particles. And if you've got a bunch of antibodies binding to a bunch of viral particles, and those antibodies are binding to different viral particles, and again, specifically the spike protein in the example I just gave,

you end up with a big clump of antibodies plus viral particles that are just clumped together and it actually makes it so heavy that it basically falls out of solution and those viral particles can no longer go around and look for cells to infect the more common thing that we typically think of antibodies doing so that's just a fun one what the thing that we typically think of antibodies doing is looking for the part of the virus that has a function for how it's actually causing an infection. So again, we talked about the spike protein being essential for getting entry into our cells.

If you have antibodies that are targeting the spike protein, this is a process called neutralization. One of those tips of the why will find the spike protein, stick onto it. Now all of a sudden that spike protein can no longer bind to our ACE2 receptor. And because it can't bind to our ACE2 receptor, it's no longer dangerous to us. It can't get into our cells and it can't do anything. So that's what we hear neutralizing antibodies. That's the idea behind neutralizing antibodies.

They stick onto the dangerous part of the pathogen and make it not dangerous. And there's a bunch of other things that they do. Just one other fun one. Well, I should also mention they also help increase inflammation, which is a good thing in a lot of cases for immune response. But one of the more fun ones is called the complement system. The antibody will stick to cell membrane. This is more common in bacteria. Actually, it's pretty much only in bacteria, but we'll talk about it anyway, just because it's fun.

The antibodies will stick to the surface of that cell, either an infected cell or the bacterial cell. And they will call these complement proteins to come on in, and those proteins just punch a bunch of holes through the membrane of that cell, causing the cell to just kind of explode and fall apart. So it's just kind of fun, you know, bring in the proteins, yeah, to punch holes through it. like a paper punch is basically what they're doing. It's just absolutely amazing. And as somebody that I'm just fascinated and I've studied pretty deeply, just evolution by natural selection and just thinking how the complexity that goes on every moment inside of our bodies is forged over millions and millions of years through the interaction between the organism and its environment and nature really crafting this complexity.

It's just truly, truly astounding, and this is just one small example of that. Can I add one quick thing here? You're going to love this. It's not related to COVID specifically, but it's something that we like to think about in terms of evolution of the immune system. So you can actually, if you want to look up more into this, because I'm not going to go through a bunch of the different parts of it. But if you Google evolution of the immune system, you'll find where exactly different components of our immune system came about in our predestinal. creatures. But one of the interesting things is you've heard of CRISPR, I'm assuming by this point. Crisper Kast9. It's used for gene editing. Right. Crisper actually was part of the

bacterial immune response because bacteria can be infected by viruses. And what happened is these bacteria had to have a way of preventing the viruses from coming in and killing them. Because if they didn't, they would die and they don't like that. So they developed something of an immune system themselves. And they have other components of their immune system as well. But one of the things that they developed was this CRISPR-Cast-9 system that was used for preventing bacteriophages, which are viruses that infect bacterial cells. What we did is we discovered this part of the bacterial immune system and figured out how to adapt that for gene editing. It's not actually something that we came up with on our own, and it's some synthetic process that we devised in the lab.

It comes from the bacterial immune system. So you're right. It's a super interesting story of immune evolution through time, because those are just in little bacteria, and it's now the cutting edge of human science. God, so amazing. Absolutely amazing. All right. Well, let's go ahead and finish us up with one last question, and that is what you hear a lot, sort of even in the political realm. And in the early days of the pandemic, I think a country like the UK was even flirting with letting the virus ravage the population to reach what is called herd immunity.

So for those that don't know, what is herd immunity and what do we know about the potential for reaching it and what the cost perhaps would be in trying to reach it? Right. Heard immunity is the idea that enough people are immune to a virus or bacteria in this case of, virus, either through having been infected and then developing immunity to it through that or a vaccine, enough people are now immune to that disease where that disease can no longer spread efficiently through a population because every time it tries to spread to somebody, it finds somebody that's immune to it and it kind of snuffs out transmission. You can think of this like if you put a spark into a pile of wood shavings,

that spark is going to catch some of those wood shavings on fire, and then it's just going to spread through the wood shavings, and you're going to make a fire. On the other hand, let's say you take those wood shavings and replace some of them with pebbles of sand. So now you've only got a few wood shavings, like let's say 10% of them are wood shavings and 90% of them are grains of sand.

And you put that spark into that pile. Not only are the 90% of the particles of sand not going to be able to be burned by the spark, but you're also going to be less likely that those wood shavings are going to catch on fire too because the sand particles are blocking a lot of those wood shavings from the spark. Hoping that that makes sense because I just came up with it in the moment, but that's basically what the idea of herd immunity is. And the idea here is that viruses work the same way.

They have a specific number of people that they would generally infect from each infected person. We call it the R not value, which is, it looks like R within a little zero after it. That number denotes the average number of people that would be infected by an infected person. So if you have an R not of, let's say, three, you have one person that's infected. That person would, on average, infect three other people. And you can see how it would spread through the population that way. The R not is if everybody was susceptible to the illness. What the idea with herd immunity is, is you can make an R not effective, which is a different number, which takes into account things like existing immunity in the population. And you want to bend that number to being under one, because if every infected person is infected less on average than one other person, eventually the number of new infected people is going to drop to zero.

So herd immunity is the idea that you would have enough people immune that eventually the virus would just kind of burn out because there's no long. people that it can infect. So the idea behind vaccinations would be exactly this. You would want to vaccinate enough people that the virus would no longer be there because there are some people who are not able to be vaccinated for immune efficiency problems or whatever religious beliefs, which, yeah, that's a different discussion entirely. But the point is that there are people that either cannot or have,

what they believe to be strong, compelling reasons to not be vaccinated. So you would vaccinate enough people where that wouldn't matter and the virus would go away anyway and those people still wouldn't suffer despite not having been vaccinated. But what the UK and Sweden were looking at particularly is instead of having the slow burn of the virus through the population because they didn't know when the vaccine would be available, they would try to have all of the people who would not suffer particularly badly so young strapping men like you and me we would we would get infected right away early on in the pandemic and then that means that well we've been infected now we're immune that means that no longer we can we can we can't be infected again and we're not going to be able to spread

it again we only have that one time so they wanted everybody to go about their daily lives like usual get infected and then hopefully be immune to it what we didn't know at the time and frankly we should have known better and it was something that I and another immunologist that co-hosts a COVID town hall every week on the David Feldman show with with me have been saying is that we didn't know how long immune memory to COVID infections would last because SARS COV2 is not the only coronavirus. We have coronaviruses that cause seasonal colds, just regular colds. A lot of them caused by coronavirus. And then we also had the original SARS back in 2002, 2003. You might remember that outbreak. Hong Kong and then also in Canada, there was quite a few cases. That was

much more severe, something like 9.5% of the people that got SARS 1 back in 2002-03 died from it. So that's a very severe disease. And there's another coronavirus in the Middle East called MERS, Middle Eastern respiratory syndrome. That kills something like 30% of the people that get it. So much more deadly even then. But if we look at how long the antibodies in our systems last after the infection with these other coronaviruses, with the seasonal cold coronaviruses, we've seen that we have a drop, massive drop in antibody levels after just a few months, which is why some people are infected with the exact same coronavirus causing the same cold multiple times in the same year because their memory to that does not last.

It doesn't generate that sort of immune memory that's maintained in memory B cells, which then in subsequent infections would then upregulate and then be able to produce antibodies to really prevent us from being infected to begin with. And even if we look at the case of SARS, one, the one that killed almost 10% of the people that got it, even with that, you'd think that a really severe disease

we would have good memory against, but we saw drops and antibody levels of people that survived SARS after between two and three years. So based on these previous viruses, we knew that best case scenario, we were likely to have two to three years of memory, but it could have been as low as a couple of months. Then we had papers start coming out about a month or two ago that had looked at people, some of the first people that had been infected in China and their antibody levels to the causative agent of COVID, SARS coronavirus too. And, and And they found, so guess what, a drop in antibody levels after two to three months, which is really bad news.

Now, more recently, there was some papers that found that this drop happened at the beginning. And then it kind of leveled out at a high level where they thought, oh, you know, it dropped at the beginning. But there's still enough antibodies floating around where the people should be protected from subsequent infections. And just one caveat, not everybody develops antibodies after they're infected. Something like 30% of asymptomatic cases don't generate antibodies at all at any point afterwards. So theoretically, no memory there at all. But they thought maybe, maybe, you know, the antibody levels drop after two to three months, but then they level out and they'll still be fine. But just this last week, at least when we were recording, it's the last week, we've seen, I believe we're up to six or eight cases of people that have been infected.

twice with COVID and pretty definitively infected twice with COVID. And the reason I say that is we had had some people that had tested positive multiple times. There's different kinds of tests. There's the RTPR test, which detects current infection, and then the serology tests, which look for antibodies, which would detect past infections. There were some people that tested positive multiple times with RTPR tests, but the speculation was that there was just still some viral junk left in their

system after they had gotten rid of the virus and that second positive test was just picking up the junk and they weren't actually infected again because they weren't sick the second time. But this last week what they found is people that have tested positive a second time, they can do genetic sequencing on the virus that's in their system and look to see if there's mutations between the first time that they had the virus and the second time they had the virus. And sometimes it's possible that over time, you would generate mutations within your own body, but not very many. The longer you go in time, the more mutations you're going to rack up. And they found that these people that had been reinfected more than once had had two different strains of the virus, because there was

enough mutations where they figured out there was basically no way. I mean, it was infinitesimally small chances that it was the same virus that had been originally in their system. They'd been infected a second time. If you can be infected a second time, that means there's not really much opportunity for herd immunity, because the idea with herd immunity is that you have these grains of sand that are preventing the other people from being infected. But if you put grains of sand in there, and then after a little bit of time, you take them back out and stick new pieces of sawdust back in, you're not ever going to get to the amount where that fire is not going to catch. so that's the fear that we have now is that we really don't know how long this memory could last for

in the in the majority of people it might last for you know a couple years we don't know yet it's still early on but we have had these cases in the last week or so of reinfections occurring which really throws into doubt the idea that we would be able to reach herd immunity and it also throws into doubt the idea that a vaccine would be effective for a really long time we don't know yet. It might only be effective for a few months to a few years. We just have no idea. And if you want to read more about this, I just had a piece published in WSWS on it. You just Google mounting evidence for COVID reinfections or something like that and you'll find my article on it. It goes more in depth. Yeah, I can definitely link to that. I do have a question. You mentioned vaccines

and broadly speaking. I mean, we probably don't know enough about, you know, this particular virus, but viruses generally, is there a difference when it comes to reinfections? regarding whether the person was infected with the disease sort of naturally or given a vaccine? Or is that functionally the same thing? And so we'd expect reinfections to be similar between those vaccinated and those who actually were infected with the virus? That's a great question. And it depends on the disease that we're talking about.

There's some where the vaccine is not as effective as being infected naturally with the virus or bacteria. There's some where the vaccine is much stronger than being infected with the virus and bacteria. But we don't know in this specific case because we don't have any sort of data on any of the vaccine candidates long term. But there are cases where if you're getting a vaccine, let's say you get, I don't know, I'm not even going to pick a specific example, but let's say you get this virus. And if you get the virus, you're immune from it for 40 years before you'd be susceptible to getting it again. And then you get, on the other hand, if you get the vaccine,

for it, you're only immune for 10 years. Actually, one that jumps to mind now is smallpox. The smallpox vaccines start to wane in terms of effectiveness after about 10 years, whereas if you're infected with smallpox, you're generally immune forever. I mean, for all intents and purposes, you're immune forever from smallpox if you're infected, but only 10 years if you've been vaccinated. And that, it depends on the type of vaccine. There's a bunch of different types of vaccine, whether it's inactivated or live attenuated or acellular or subunit vaccine, there's a bunch of different types of vaccines that would influence how effective it's going to be. But yeah, we don't know for these current vaccine candidates yet whether or not we're going to see better immunity

than natural infections or worse immunity compared to natural infections. There's one paper out on a vaccine that I'm hearkening back to now off the top of my head. where, and again, this was only in their, I believe, their phase two, where they saw that there was more antibodies after the injection, like immediately after the injection and after a booster, a second shot, there was more antibodies in the system than there were in the average person who was actually infected with the virus, which would be good news in terms of having a robust response that we might have some lasting memory for, but there's no data on that, whether or not that initial higher level of antibodies. is actually going to mean that we're going to have longer lasting antibody. So we just don't know. I see. Fascinating. Wow.

Last question. I just thought of this was you were answering the previous question. It's the sort of two parts. And we'll wrap it up. I really appreciate all the time you've given to us today. You mentioned that there are other coronaviruses that pretty much are just a common cold. We come into contact with them on a yearly basis, sometimes multiple times in a year. Two-pronged question.

The first prong is, did those coroner? coronaviruses initially start off as pandemics to humans 10,000, 20,000 years ago. And the second prong of that is, given everything we know about this coronavirus, specifically, is that a likely fate for this COVID-19 virus, that it would just eventually work through the population, vaccines, natural infections, whatever it may be, mutations, and then slowly just become sort of included in that normal yearly coronavirus sort of attack in the wintertime? Yeah. So what you're describing there is whether or not the virus becomes what we would call endemic,

as opposed to epidemics. Epidemic means a massive outbreak all at once. Endemic means it's just naturally circulating through the population all the time. We don't, at least to the best of my knowledge, understand the past history of coronaviruses in terms of these common cold coronaviruses, how severe they were, you know, hundreds of thousands, if not millions of years ago. We don't know. It's really hard to tell.

Viral phylogenetics is a really interesting thing. My research that I do on Ebola is related to that in terms of looking at Ebola precursor genetic information from 24 million years ago inserted into different mammalian genomes. We don't know what kind of effect that had on there. We just know that there was something that was exactly like Ebola or very similar to Ebola that was infecting these different animals 24 million years ago, whereas we only actually found the virus in 1976. There's a huge gap between 24 million years ago in 1976 where we have no idea what it was

actually doing in animal populations. And then in 1976, we saw it in people for the first time. Similarly, coronaviruses, these viruses have been around for, ever, not literally forever, but you get the point. They've been around for a long time. What we don't know, to the best of my knowledge, is how, whether or not these exact cold causing coronaviruses were more severe in the past. It's possible that some of these were much more infectious or deadly in the past, but I don't see them as having the massive, uh, severe cases that we're seeing with with these new coronaviruses SARS one SARS two and MERS these these are really

kind of unique at least in terms of human coronaviruses there's animal coronaviruses too that cause a lot of weird things there's a cat one that causes GI problems and cats that's quite severe for cats also a coronavirus and that doesn't infect people so coronaviruses are really interesting viruses and is it possible that this coronavirus could become endemic was your second part to that question. And that's a really interesting question. If we didn't, if we stopped looking for a vaccine, I could see that becoming the case. Because as the standard of care for somebody that's infected with COVID is getting better, we are seeing the rate of death of people that are infected dropping. Now, of course, it's also dropping because the average person being infected now was

younger than it was early on in the pandemic, where most of the people being infected were old, nursing homes particularly but we're getting better at treating it even without having an actual drug for treating it just we know how to keep these people alive if they do develop severe COVID so if we didn't have a vaccine or really good therapeutic agents it's it's possible

that we would be able to at least prevent people from dying from it too often over the course of time and eventually we would find therapeutic agents that would reduce the risk of death even further or even reduce the likelihood that somebody would suffer severely from it, but not die. That's highly possible.

But because of the race for the vaccine and because of how much economic incentive there is to just get rid of this virus, I don't see it being endemic except in the circumstance where you have pockets of people who aren't vaccinated. And I'm talking large pockets of people. One of the cases that springs to mind, did you ever hear about the case of the polio vaccine after the killing of bin Laden?

No, no. Okay, I'll run through that really quickly because I know that we're way over time. So I apologize for that. Totally fine. What happened is in Pakistan, they were looking for bin Laden. And one of the things the CIA was doing to try to find bin Laden is they set up a fake polio vaccine operation. where they were going around and instead of giving people the vaccine, they were taking DNA samples from people

and then testing them to see they had samples of Bin Laden's DNA from the past at some point. And they wanted to see if they could find any of his kids, people that had his DNA in them, because if they did, they would know roughly where he is and then they could go in and kill him. And this isn't eventually how they found bin Laden. It was a completely different scenario,

but they did this for a long time where they had these fake vaccinations going on. Now, polio was almost eradicated in Pakistan and Afghanistan. There was only three countries in the world of the time that still had active cases. Nigeria was the other one, and Nigeria was just declared polio-free this last week. So now it's just Pakistan and Afghanistan. But it was almost eradicated there, which means that it would almost be eradicated worldwide now. But after they got bin Laden and it leaked that this was the method that the CIA was using to try to prevent people, or not to

prevent people. But to find bin Laden, it caused such a backlash that people stopped getting the polio vaccine in those areas, either because they thought that it was a scam set up by the U.S., they thought that the U.S. was just genetically profiling them. I mean, those are valid concerns. It was literally what the U.S. was doing. But there was also groups from the Taliban, for example, that also saw what the U.S. was doing and then threatened people that were either giving the vaccines or people that wanted to be vaccinated. So vaccine usage dropped dramatically. And there was an uptick of cases of polio, which only just now is starting to come back under control. I mean, we're down to very low numbers of cases in those two countries again.

But there was a huge uptick in cases because the U.S. set up this CIA fake vaccination program that just ticked everybody in the area off. Oh, my God. Now, if you have a pocket of people in the world that are not getting vaccinated for either geographic reasons, you know, it's hard to get the vaccine to them or because of political reasons. They think that Bill Gates is trying to poison them with the vaccine or whatever. Then you could have the virus circulating within that population and it could in theory keep circulating for a long, long time and it could become endemic. But as long as we were able to get enough people vaccinated within a period of time that that vaccine would be effective for, I wouldn't say that that would be a super likely outcome. Okay. Interesting. I take two main things

out of that. One, even though coronavirus is a family of similar-looking viruses, they are very unique and different and you can't really elaborate from one to all the others. And two, the CIA is a terrible organization. Those are both incredibly valid points, Brett, and I would second each of those. Well, wonderful. Henry, thank you so much for having this conversation for enlightening me and my audience on the cutting edge of where the science is at with regards to this virus. in this pandemic. I really, really appreciate the clear, concise way that you transmit scientific knowledge. And thank you so much for coming on. Before I let you go, can you please let listeners know where they can find you and even support you in your work online? Yeah, sure. So if you want to

follow me on Twitter, I'm not the most active person on Twitter, but I do use it. You can find me at Huck, H-U-C-N-95. Patreon, similarly is patreon.com slash Huck-1995. I put content up there breaking down new science articles basically what we just did here but in written form and I've got different tiers of support and I'm going to emphasize the Patreon simply because this pandemic hit at the worst possible time for me and I fell through every crack imaginable in the social safety nets I got stuck here in the U.S. instead of being in Germany and wasn't eligible for unemployment or anything like that so yeah this is this is pretty much the only way that I have of keeping my insurance payments going at the moment.

So if you're feeling charitable and or are interested in public health information, check out my Patreon at Huck, 1995. And the last thing I'm going to mention is if you're interested in this kind of conversation, really breaking down what's going on with COVID in a not too rosy way, which is what we see in a lot of the media is every time there's a paper that's even mildly optimistic, They start losing their minds over it and then kind of forget all of the negative papers. If you're interested in that kind of coverage, check out the David Feldman show. David Feldman's a leftist, prime time Emmy award winning comedy writer.

He's got his own podcast that seems like it goes about 80 hours a week. But I've got a segment down there a couple times a week. And worth checking out. And yeah, I think that it's important for us on the left to, support our different left media in order to keep us all flourishing and thriving. So check out that show. Feel free to check out my segments there. Follow me on whatever you want. And if you have any questions, just shoot them over to me. Perfect. I'll link to that show. I'll link to your Twitter and I'll link to your Patreon, urging people to go and support you at this time. You don't even get

the bare bones help that the rest of us get. So if you can pitch a few dollars to Henry to help them get through this pandemic, be much appreciated. And then also that paper that you mentioned earlier, if you want to shoot me an email, you don't have to, but if you get the time to shoot me an email the next couple days, I'll make sure to link to that as well so people can go and read that. Thank you again, Henry, so much for coming on. Let's keep in touch. And as this pandemic progresses, perhaps I can have you back on to talk about where the science goes from here, how it develops, and where we're at in a few months. Anytime, Brett. Thanks a lot. Well,

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