This Podcast Will Kill You - COVID-19 Chapter 1: Virology

Episode Date: March 23, 2020

To discuss the ongoing COVID-19 pandemic, we are introducing Anatomy of a Pandemic, a series in which each episode tackles a particular aspect of COVID-19, from virus biology to clinical disease, from control efforts to epidemiological patterns, from vaccine development to mental health coping strategies during this uncertain time. And we’ve got a quarantini (and placeborita) recipe for each installment! In the first episode of this series, we tackle some of your questions about SARS-CoV-2, the virus that is responsible for COVID-19 (aka COronaVIrus Disease-2019). Our episode begins with a firsthand account from Tiziano, a schoolteacher in northeastern Italy who has been living under the strict movement restrictions imposed by the Italian government in an attempt to limit the spread of the disease. Then, we review some of the basics about SARS-CoV-2 and RNA viruses in general. To help us discern fact from fiction, we seek the expertise of a virologist, Dr. Angela Rasmussen (interview recorded March 15, 2020), who answers some of the listener-submitted questions about the virus itself. We wrap up the episode by discussing the top five things we learned from our expert. To help you get a better idea of the topics covered in this episode, we have listed the questions below: What are the origins of this virus? Where did it come from? How can we tell whether this virus originated from one spillover event or multiple? What do we know about the mechanism of how this virus causes disease in humans? Are there multiple strains of SARS-CoV-2, and how do different strains of virus affect disease severity?  Is there a risk of SARS-CoV-2 mutating into something more deadly?  What is Remdesivir and how does it work?  How does handwashing work to reduce transmission risk? How long can SARS-CoV-2 live on surfaces?  What is the minimum infective dose of SARS-CoV-2? See omnystudio.com/listener for privacy information.

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Janice Torres here. And I'm Austin Hankwitz. We host the podcast, Mind the Business, Small Business Success Stories, produced by Ruby Studio, in partnership with Intuit QuickBooks. We're back for season four to talk to some incredible small business owners. The big thing about working at tech is that it's ever evolving, ever changing. everyone's a rookie. That's how fast the industry is changing. So what I'm really excited about is to be part of that change. So listen on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. My name is Tiziano. I'm from the northeast of Italy. I live in a small town in the northeast.

I'm a school teacher. I teach English in a secondary school here. In February, there was, all the attention was on a couple of tourists. around and so on. Then on the 21st we got our first cases here in Italy. They were limited to a small number of towns in the north. What happened was that following week, it was Shrove Tuesday, so schools were already closed for a couple of days. So over the course of that weekend, the first 10 or so towns were quarantined and all the schools in the north were closed. What happened next is that the regions asked for and got an extension of the closure of the schools. So it's been three full weeks now since schools have closed. And there's another three weeks planned ahead of us, at least. I'm a school teacher, so it's been not easy to cope with all of this.

So the thing is, the school stopped, but the rest of the country went on. But things started moving fast. So we are now under this lockdown, which means that we cannot leave our homes unless it's for either work reasons or basic needs. Kind of a soft lockdown because we can actually move, but we have to provide some sort of declaration of written statement or the reason why. We are out of our homes. Until the government came out with the lockdown, I think people didn't really appreciate what that meant. And so it was just a few days before that,

that there were still parties going on and restaurants, so on, so on. For the, let's say, for the lockdown, we are, lockdown we are under now. So if I was to, you know, go out small without the good reason. So if police is going to stop you and check your statement. So if it's for work reasons, they are going to call your workplace and that. So there is the fine or you could face charges. You could go to jail, but that's only for extreme cases.

After the last regulation, so this past week, I think that people are taking the thing more seriously. And from what I see from my immediate vicinity and people, I know we are starting to embrace the social distancing and so we are moving to Skype calls with friends and we are you know the indoors life as much as we can and as a school teacher I maybe have a slightly different perspective than most other people because we started from the very beginning to find ways to still keep doing schooling at some form But there wasn't really a plan for that. So a lot of it was left to our own creativity and goodwill to do things.

There are still issues with that. The first one is that it's very hard to keep in touch with all our students. Because of course not everybody is available. Not everybody has the same resources. and it's hard and it's impacting families, especially families, where the parents are still working, and so they need to take care of the children. Traditionally here, families are very close-knit and this was something that often grandparents did, but parents are, of course, one of the most impacted categories.

impacted categories for the virus. So that has raised some issues. We have one of those flash mobs on the balconies every day basically. You know, I'm in a small town, so there's not a lot of houses around here. Every day there's someone either playing songs or the other day they were tapping for the people in the medical professions. professions which are doing a great job and taking Dublin gifts to cover everything everything so that's that's good there's this other thing that's going on now which is

the kids are making this rainbow paintings and with an hashtag that is basically everything will be fine in Italian and they are you know sharing those pictures on on the social media This is bringing out a lot of, you know, good things. I see that really people care. People care about their neighbors. People care about what's going on. That's a big thing. You just heard from Tiziano, who was kind enough to spare us a few minutes

to chat about his experiences while under lockdown in Italy. Thanks so much for chatting with us. Yeah, we really appreciate it. Hi, I'm Aaron Welsh. And I'm Aaron Elman Updike. And you're listening to This Podcast Will Kill You. Oh, yes, you are. You are.

Yes, welcome to our first ever minisode series, which we're calling anatomy of a pandemic, which is shaping up to be less of minisodes and more like full-length ones. Yeah, it's maxisode. Sorry, not sorry? I don't know. It's long. Strap in. There's a lot of information.

out there and there's a lot of ground to be covered. So, you know, we're going to do the best we can. And this is the first episode of six that we're dropping all at once. But throughout this pandemic as it progresses, we're going to keep revisiting different topics or visiting new topics to get you all the information that you could ever want about COVID-19. Yep. So we asked everyone out there for questions and hundreds of you submitted your questions. So first of all, thank you so very much because that really helped us to figure out what you wanted to know and how to organize these episodes. And so we are so excited to bring you not one, but six of these episodes where we ask the experts to answer your questions. So today we're starting with chapter one, the virus itself.

And that's what we're going to cover in this episode. But before we get started, we have to report, of course, that if ever it was quarantini time, right now is most definitely quarantine time. Most definitely. Quarantinis have been making the rounds in social media. And first of all, we appreciate everyone shouting us out in that. Yeah, we do. So what are we drinking today, Aaron? We are drinking what we're just calling quarantine one, because.

Because, you know, let's keep it simple. We'll keep it simple. Disclaimer, if you're going to listen to all six of these episodes in one sitting, you don't need to make all six quarantinis. That's probably a bad idea. I personally, so I'm recording this. It's eight my time and I'm drinking coffee. It's 10 a.m. my time. I'm drinking water, but I did drink a quarantini last night while researching.

I drank a couple while taking the pictures of them all. It's important. You've got a taste test. So what is quarantini number one, Erin? Quarantini number one has rum, it has coconut cream, it has lime juice, and, you know, we wanted to make these so that hopefully there are things that you might have lying around the house, more simple ingredients and so on. But I will suggest if you happen to have apricot liqueur, pop some of that in there as well. If your bar cart is as well stocked as Aaron Welsh is. Apricot liqueur is really good in teaky drinks. Yeah.

That's all I'm going to say. I believe you. We will post the recipe for that quarantini, quarantini one, as well as the non-alcoholic placebo-rita on all of our social media pages and our website. Excellent. All right. So. So way back in February, which feels honestly like an entire lifetime ago, we did a

a whole episode about coronaviruses in general. And so we wanted to give you a really quick recap on that. All right. So coronaviruses are not brand new alien viruses. They are large family of viruses that infect a number of different animals. SARS-CoV-2, which stands for severe acute respiratory syndrome coronavirus number two, which is a little bit of a mouthful. This is the official name for the virus that causes the disease COVID-19. You can break that down to see where that comes from. It's coronavirus disease 19, COVID-19. And so this is a virus that is new to humans, and it emerged as it turns out, or as it likely turns out, in November 2019.

Obviously, this is now a pandemic. And so we are going to talk in this episode about the biology of this new virus and some of the characteristics that have allowed it or facilitated it to reach pandemic proportions. Exactly. So let's do a quick primer about viruses in general, especially for any new listeners who haven't heard all of my many virus spiels many times over. So viruses are essentially just packets of genetic material. They're made of either DNA or RNA along with protein. Viruses can't replicate on their own. So unlike most bacteria, for example, which can multiply just by replicating their DNA and then dividing into two, viruses have to infect a cell of some kind, a host cell,

and use that host cellular machinery to actually replicate their genetic material. So in the case of SARS-CoV-2, this is an RNA virus. It's a positive strand RNA virus. So that means that one it gets into your cells, that viral RNA is released into our human cells, and then our cells do two things with this RNA. Number one, they start copying it directly, as if it was our own RNA. And number two, what RNA does in normal cells is it codes for protein. So our cells start to use this viral RNA to make the proteins that that viral RNA codes for. And then the replicated RNA plus those proteins get assembled into new little virus packets. Okay.

And those new viruses can then burst forth from the cell and go on to infect another cell, either in your body or in another host. So that's how RNA viruses work. DNA viruses do essentially the same thing, except that in order to make protein from DNA, your cells have to first translate it into that RNA. So RNA viruses sort of skip that step. And as you'll hear our expert talk more about,

they also tend to make more mistakes in that process of replication. But either way, viruses are using your host machinery to do this. They can't replicate outside of host cells. Cool? Cool. So in this episode, we talked to a virul Dr. Angela Rasmussen from Columbia University to answer your questions about the biology of this virus, how it works, how it infects your cells, and what markers it uses to get into our cells.

And then we also chat about its mutation rate and what that means for disease severity to its longevity on surfaces and whether the existence of multiple strains is a concern. So she'll introduce herself to you right after this break. Dinner shows up every night, whether you're prepared for it or not. And with Blue Apron, you won't need to panic order takeout again. Blue Apron meals are designed by chefs and arrive with pre-portioned ingredients so there's no meal planning and no extra grocery trip. There, assemble and bake meals take about five minutes of hands-on prep.

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Go to quince.com slash this podcast to get free shipping on your order and 365 day returns, now available in Canada too. That's Q-U-I-N-C-E.com slash this podcast to get free shipping and 365-day returns. Quince.com slash this podcast. I'm Dr. Angela Rasmussen. I'm on the faculty at the Center for Infection and Immunity at the Columbia Mailman School of Public Health. I'm a virologist who studies, I specialize in studying the host response to infection. So when you get infected with a virus, your body responds to that.

There's an immune response, an inflammatory response. Sometimes there can be metabolic responses, and I study those. And sometimes those responses, depending on what they are, can mean the difference between getting rid of an infection and having, you know, a mild, short illness versus having a chronic illness or a more severe disease. So the viruses that I've been studying lately are Ebola, MERS coronavirus, influenza virus, other hemorrhagic fever viruses, and of course now, like many of my colleagues, I'm also studying SARS coronavirus 2 or COVID-19. That is the reason that we brought you on today. So thank you so much, first of all, for agreeing to be on the podcast.

And yeah, so jumping right into the SARS-Co2, what are these? origins of this virus? Where did it come from? So we don't know for sure. And I suspect that that's going to be my answer to almost every single one of your questions today. But we do know that there was a very, very similar virus found in a bat in a cave in China in 2017. And this virus is a member of the same genus as SARS coronavirus or SARS classic. and SARS-Coronavirus 2, this novel coronavirus that we're all dealing with now. There are a number of these viruses that have been discovered. They're called bat SARS-like coronavirus, is a very clever, original name

because they are very much genetically like SARS-Coronavirus and now SARS-Coronavirus. We do know that this virus probably, based on our analysis of the genome, evolved from one of these bats SARS-like coronaviruses. We don't know if there was another animal involved in the spread of this virus from its wildlife reservoir, the animal that had it in the wild to humans. What we do know is that this spillover, which is the transmission of a virus from its wildlife reservoir into humans, was probably a single event, meaning that there weren't multiple instances of animals infecting people. After the first patient or patients weren't infected with this

from whatever animal it came from, it's been transmitted human to human ever since. The reason why it's important to understand eventually if this came directly from a bat or if it came from a different animal is that both SARS classic and MERS coronaviruses were amplified in an intermediate species. So both SARS and MERS are thought to have also originated in bats. However, SARS classic was transmitted into humans most likely from an animal called a civet. And MERS coronavirus is known to be transmitted primarily from dromedary camels to humans. So we don't know if there was another animal in between the bat and the human that also was involved in the spillover from it's wildlife reservoir.

To follow up on that, so you mentioned that this likely came from one spillover event. So from one infected animal, whether it was a bat or a different intermediate host, into a human, how can we tell whether it's one spillover event or multiple? Yeah, so you can tell that by looking at the genome. And one thing that's been really incredible and also really hard to keep up with about this particular epidemic is that this is really the first time that we've had sequence data from the virus genome really, really soon after the first patients were reported. So the first viral sequences were uploaded and shared with the international scientific community in early January. So we've been

able to analyze the genome of this virus since before we actually were able to even isolate the virus. So we can look at the genome of this virus and we can look at the specific individual changes in one isolate of the virus versus another. And by looking at those changes, we can deduce how many different viruses came out of the bats versus went from person to person. There are specific genetic signatures that are associated in many cases with bat coronaviruses and coronaviruses that are transmitted within bats, including some sequences that are part of the envelope glycoprotein,

which is called spike. And that molecule is on the surface of the virus, and it allows the virus to enter a cell that it's going to infect. That protein spike has changes sometimes that are specific to bats versus specific to humans, and we can look at that as well to determine how recently the virus, the virus emerged from a bat versus emerged from a human. Awesome. Thank you. Did that make sense? Okay. Yes. Absolutely. Okay, good.

So kind of along those lines of the proteins on the surface, are those related to how the virus gets in and actually causes disease? What do we know about the mechanism of how this virus causes disease in humans? So that's a very excellent question because it gets into what I study. The response. So there are two things to any virus infection to keep in mind. The virus can infect cells and that determines whether it can establish an infection get inside versus the viruses, what we call pathogenicity or ability to cause disease. Not all viruses cause severe disease. Some viruses, most viruses that can cause disease, which we call pathogens, those pathogens in some people will cause very mild disease and in some will cause very severe disease. And we're seeing

that in terms of the fairly broad range of disease presentations of COVID-19. So the ability to get into the cell is just one part. And of course, in order to cause disease, a virus has to be able to infect the cell. So those proteins on the surface of the cell, or on the surface of the virus particle called spike. Spike binds the host cellular receptor, which is, in humans, the molecule we know about anyways is called ACE2. And ACE2 is on a variety of different tissues, but there's a lot of it in your lungs, which is why this causes a pulmonary disease. So certainly in that sense, the virus spike protein is involved in determining that this is going to be a pulmonary disease. Similarly, we know that ACE2 is expressed in the gastrointestinal

tract, and there have been reports that infectious virus has been found in stool of some patients. Also, people have reported diarrhea, which may, again, suggest that the ability to infect the intestine because of that receptor binding the spike protein on the surface of the virus particle allows this virus to cause a gastrointestinal disease. But when you're talking about what is the difference between a virus in two different people causing a mild cold-like illness in one person versus causing severe pneumonia in another, that difference is often related to the host response. And that can be determined by a lot of different things. It can be determined by genetics. It can be determined by the health state of that

individual, which we, again, already know as a risk factor because people with preexisting medical conditions are more susceptible to severe disease. So really, a lot of the disease is likely caused by a sort of out-of-control inflammatory response in infected tissues. And that largely depends on the person who's infected, as well as their overall health condition and sometimes the circumstances in which they're infected. That was so beautiful. Thank you. Such a great answer, yeah.

Thank you. I get passionate about the host response. So recently there was a paper that was public. that found that there were two strains of the virus, and they named these strains L and S. And these strains, according to this paper, seem to differ in their virulence, one being more aggressive than the other. And this finding has seemed to be a little bit controversial. So can you talk about why it is controversial and whether the possibility of multiple strains is a real concern, and maybe whether this finding is actually valid, are there multiple strains of SARS-Co-V-2?

Right. So this definitely gets down into the inherent property of RNA viruses like coronaviruses. And that is that every time the virus copies its own genome in order to replicate or make more viruses, the virus makes mistakes. The enzyme that that copies the genome does not have proofreading capability the way that the analogous enzymes that we have that copy our DNA genomes do. So that means that the virus makes mistakes. we call these mutations. Many of these mutations are silent. They don't have any effect on the way the virus works.

Many more of them will have a negative effect on the way the virus works and make it so that the virus can't work, essentially. And some of them will confer an advantage. These mutations occur randomly. So there has to be a selection pressure to maintain mutations from generation to generation. And some of these advantages can be an enhanced ability to replicate in various host cells. It can be the ability to evade the host immune response. It can be something that would make the virus more capable of infecting cells or capable of

inducing a response that would lead to more severe disease. So right now, we don't know what a lot of those theoretical mutations would be that could make the virus more virulent capable of infecting more cells or more pathogenic capable of causing more intense disease. The paper that you mentioned is controversial because essentially it's grouping these two viruses into what they're calling strains, but what are normal groupings of RNA viruses that have replicated in multiple hosts. What makes a virus a different strain, often depends a lot on which virus you're talking about. In this case, if we're talking about two different genotypes

or virus genomes that encode virus genes that result in differential disease or more severe disease in one person versus less than another, whether that's a strain or not is sort of up for debate. What I think is controversial about this paper is that essentially they were just grouping a variety of different clinical isolates of the virus, and then going back to the clinical data that had been recorded about those patients and making assumptions that these genetic changes that distinguish these two groups

were responsible for any differences they found in the patient's conditions. That is, it's really hard to say. first of all, the group, the viruses and the L group versus, I think, what is it, the S group? Mm-hmm. Yeah. The differences between those viruses, they're not all, it's not just two viruses. They're groups of viruses that cluster together when you look at their genomes and compare them. So it's really difficult to say that any one of the specific genomic changes that are characteristic of either group are directly responsible for causing increased or decreased disease severity. Gotcha. So it's possible or likely that there might be multiple, quote unquote, strains of this virus, but whether or not that translates into any

manifestations in terms of disease severity is not yet clear, and we probably won't know it for a while. Yeah, that's fair to say. And this is really also a question that needs to be addressed in terms of doing experiments to understand what are our features of the virus that make it more pathogenic or able to cause disease. So the only way to really look at that is either through human volunteers or patients who at least could be identified very early after infection and then followed over time, we call longitudinal observations, or by looking in animal models to try to understand the various mechanisms of pathogenesis. My personal suspicion, and again, this plays to my bias for the host response,

but when you're looking at humans who are genetically diverse, you will see the same virus, the same identical strain of a virus, cause two different types of disease and two different individual people. So even when you're looking at a fairly large patient population, and you're just making correlations between certain clinical features that were recorded by their doctors during clinical care, as well as the genomic sequence of their disease, you're not really able to look at any of those mechanisms

that might distinguish a host from one from another. So you can look at the differences in the virus, but you're never going to know what's different from one person to the next. So it's really difficult to conclude, even on a data set of hundreds or thousands of patients, that a genetically different strain of a virus is the only thing that is causing one person's disease to be more severe than another's.

Right, right. That makes sense, yeah. SARS as being a much deadlier coronavirus, I think a lot of people that wrote to us expressed their concern about whether this virus, SARS-CoV-2, might mutate into something more deadly such as SARS, classic. You mentioned, or you talked a bit about the mutation rate of this virus and mRNA viruses. Can you say anything to our listeners about whether there's a risk of this

virus mutating into something more deadly? And especially maybe also in the context of control measures or how behavior might influence viral evolution. Right. So this is a concern. And I think one of the reasons is that mutation is a very scary sounding word. And it's not been helpful. I think that a lot of movies are always like, oh my God, it's mutated and it's now airborne or something. And the thing is coronaviruses are RNA viruses. RNA viruses mutation is an inherent property that they all have. Because the enzyme that replicates the genome is prone to making these mistakes, every RNA virus will have the normal mutation rate for an RNA virus is about one in every thousand units of the genome that gets copied is a mistake or a mutation. Coronaviruss actually have an enzyme that does

some limited proofreading. So their mutation rate is lower than many other RNA viruses, but it's still higher than for enzymes that replicate DNA. So it still has a relatively high mutation rate. And there will be mutations every single time the genome is copied. In terms of mutating to become more virulent or more lethal, it's really, really difficult to predict that. Because mutations don't stick around unless there's some sort of selection pressure, it's hard to imagine what the selection pressure would be to make the virus more lethal. If anything, viruses are selected to become less lethal only because viruses can't replicate without a host. And if you kill your host before they can transmit the virus to another host, that pretty much

cuts off that virus's evolutionary chain. So I think that it's likely, certainly, that the virus could mutate or has mutated. And there will be mutations every time the virus copies itself within a single person, much less is transmitted to another person, but it's very difficult to say that the virus would be evolving on its own the capacity to be more lethal. Now, however, if there is an antiviral drug developed, for example, and that targets a specific part of a viral protein, then it's possible that that would be a selection pressure for the virus to evolve resistance. That's one example of how viruses can become more lethal by evading countermeasures. If there's a vaccine, it's possible that the parts of the virus, the vaccine recognizes, could be a pressure for those

parts to mutate. The way that your immune system works for most vaccines is by making antibodies. And those antibodies recognize a shape on the surface of the virus. So if you think of a virus as a three-dimensional sort of ball that's covered with spikes, antibodies would recognize the shape of those particular spikes. It's possible that a virus could evolve a slightly different shaped spike that those antibodies from a prior infection or from a vaccine would then not be able to recognize. So that is another way in which a virus could potentially evolve to be.

more lethal in the sense that it would be able to, again, evade a countermeasure that we had developed for it. Will that happen? I don't know. A lot of that depends on the types of antivirals that we find are able to work against this virus, as well as the vaccine strategies that are being tested right now, how well they work and how well they are able to induce immunity. We do know from some other viruses, though, that certainly antiviral drug resistance is something that happens. We know that from influenza evolving to be resistant to Oseltamivir or Tamiflu. We know that influenza normally it's surface antigens or the proteins that are recognized by vaccines change all the time.

So that's why we have to get a flu shot every year. So there are certainly examples in the wild world of virology that viruses can do this. But on its own, I don't think that there's any particular pressure that I've seen any ways that would cause SARS-coronavirus to spontaneously evolve greater lethality or virulence. Gotcha. So speaking of antivirals, remdesivir is going around the news. There's potentially trials happening. It seems to be maybe promising. for looking at treatment for SARS-CoV or for COVID-19, the disease. Could you tell us a little bit about what this drug is and how it works?

Certainly. So ramesivir is a nucleoside analog. That means that it is shaped a lot like the ATCs and Gs that make up a given virus genome or human genome for that matter. When viruses are replicating the enzymes that copy the genetic material, is reading the existing genome so it knows where to put which ATC or G. Remdesivir works by fooling that enzyme into thinking that it is an ATC or G and gets inserted into the genome, and then when enough of that happens, the genome doesn't work.

It's also thought that some of these so-called nucleoside analog drugs can also activate components of your innate antiviral immune system, making your cells more capable of responding to and resisting viral infection. So that's thought to be the mechanism of action for remdesivir, as far as I know. So these nucleosite analogs don't always work for some RNA viruses. But there is data in non-human primate

suggesting that remdesivir is effective at treating MERS coronavirus, and now some people have showed, I think, in vitro, at least that it's capable of reducing virus titers of SARS-Coronavirus too. So we do know that these nucleosite analogs can be effective against certain RNA virus infections. We just won't know if it's effective in people until the clinical trials have been completed. Gotcha. Our sign off for this podcast is wash your hands, you filthy animals. We've been saying it for years.

Yeah, we started it. Just kidding. So can you tell us why hand washing is a great way to reduce the risk of getting a respiratory infection? Yeah, that's a great one. And this is so both for enveloped viruses, which coronaviruses are, the envelope that I'm talking about is a membrane that is derived from your cells on the surface of the virus particle. The spike protein that I talked about that's needed to bind. the receptor and for the virus to enter the cell is embedded in this envelope in the membrane. That's why spike is called an envelope glycoprote because it's part of the envelope. So either alcohol-based hand sanitizers or soap will disrupt that membrane. If you disrupt that membrane, wash it away. There's no more spike. The virus can't get into your cells.

The virus isn't activated. Soapy water is more effective than hands. sanitizer because that also has the added effect of physically washing things off of your hands. So in addition to disrupting the membrane and making any viruses or some bacteria or other microorganisms that have a membrane that can be disrupted by soap or hand sanitizer, that's great. But in general, there may be other things. There may be non-enveloped viruses on your hands.

Soap and water washes them away. physically so that they're no longer on your hands at all, whether it disrupts the envelope or not. For that reason, washing your hands is by far the best thing you can do to reduce your own risk besides practicing, of course, social distancing. Hand washing is better than hand sanitizer, although it is important to note that for this particular virus, hand sanitizer, as long as it's 60% alcohol or more, will work in between hand washes. So one of the other questions that we've gotten a lot, and I'm also curious to know and have been sort of keeping a good amount of skepticism with whatever I read, is just how long

this virus can survive on different kinds of surfaces. So hard surfaces, soft surfaces. And maybe how does this compare with some of the other common respiratory viruses? Yeah, so a great preprint just came out. I'd like to pitch my collaborators at Rocky Mountain Labs. This is Nilcha Van Dremelan, who is with Vincent Munster at NIAID. Rocky Mountain Labs have just released a preprint with some of their colleagues, I believe, at Princeton, showing that SARS coronavirus 2 and SARS Classic have some different properties, as well as some similar properties for remaining infectious on various surfaces. So they looked at experimentally generated aerosols, which for SARS-Coronoviruses, is only an issue

for the most part in hospital settings where there are aerosol-generating procedures. But they showed that for both of these, the aerosol half-life is only about three hours. So that's good news in that, you know, if somebody that you love or care about is working in a hospital or an ICU or is getting treated there, these aerosol. are not going to persist for days at a time in the environment. They also looked at survival of the virus on copper, stainless steel, plastic, and cardboard. And the virus lasts the longest on stainless steel and plastic.

So it lasts 48 to 72 hours. And it can potentially be there for longer than that. But what's important to note is that there was a three log, reduction, so a thousand times less virus that was infectious after 72 hours. So even though you can detect infectious virus on surfaces, plastic or stainless steel surfaces after three days, it's a greatly reduced amount of virus. Compared to SARS-Classic, SARS-Coronavirus 2, lasted longer on cardboard. However, it didn't last longer than 24 hours, so before everybody gets worried about getting packages in the mail or opening letters or ordering stuff from

Amazon, it also was essentially undetectable after 24 hours. So cardboard is probably not a surface that's going to retain the virus for days and days at a time. What we don't know is that the effect that temperature and humidity and other environmental conditions would have on this because they didn't look at that in this paper. However, the same group had previously done work with MERS coronavirus, and that showed that temperature and humidity were also really, really important factors in terms of the virus being able to persist and remain infectious on various surfaces. So my take home from this is that I assume that the virus under ideal conditions can last for a couple days on surfaces. So I just try to, again, wash my hands and where I can disinfect shared communal surfaces,

like tables, take precautions to avoid being exposed to virus that may be on shared surfaces, but it's probably not going to persist in the environment for more than a couple days. Awesome. And you mentioned that this is a virus that spread by respiratory droplets. What do we know so far about the minimum infective dose of this virus? Well, that's a great question, and that is definitely a question for which I will say, I don't know. Okay. And this has been discussed a lot in the context of that reduction I was talking about

on surfaces after 48 to 72 hours, depending on the material. If you have a thousand times less virus after a couple days, is that enough virus to establish an infection, it's really hard to say. And probably a lot of that also depends on the root of infection, too. So if you are touching your hands to your nose, the inside of your nose, your nostrils is a mucus membrane. It's a mucosal surface. Mucous itself acts as a barrier that prevents virus particles from coming into contact with the cells that are in your nose to infect them, that's going to be different than in your mouth and in your eyes. And all of these different mucosal surfaces that could potentially be infected, there are inherent mechanisms,

barrier mechanisms that protect those surfaces from being infected. So it's not enough to necessarily have one infectious virus particle. You may have to have a certain number of those infectious virus particles to overcome these other obstacles to infects. that your body has. We don't really know what that is. I don't think that anybody has looked at that and because the animal model work is still in development, we can't really look at that in the context of a controlled experiment where we would be able to look at different amounts of virus on different surfaces and see which animals got infected and then how sick they got. Gotcha. Gotcha. So in our first episode on coronavirus, we ended our interviews by asking,

our interviewees, what about this disease concerns you? And what about the response or how the epidemic has been progressing reassures you? Oh, boy. The second part of the question, nothing. Yeah. Gosh. No, I've been, what scares me the most by far about this is the federal response here in the UFS. It has been unacceptable for a variety of reasons. And I suspect, that largely because the response has been heavily politicized and influenced by considerations that should not be a factor in public health responses, worrying about case numbers from, you know, an electability point of view is a really, really terrible way to approach an effective public health response. That concerns me greatly because,

initially I felt, you know, I was concerned about this, but I felt that if we were on top of it in terms of surveillance and testing, then we could really limit and contain spread. In January, when there were a few patients coming into the United States with travel history who were identified and rapidly sequestered and there didn't seem to be a ton of secondary transmission, I felt pretty calm that we were responding to this correctly, identifying and isolating patients, which is what you should do, doing contact tracing back when it was manageable to do that. Then it turns out through genomic analysis that it looks like here in Seattle anyways, we've had community transmission since that first patient arrived and potentially transmission

from other patients who may not have even been identified. And some of this has been the absolutely unacceptable slow rollout of effective testing. and the continued failure to adequately increase testing capacity and throughput, I think that that has really, really harmed our ability to contain this outbreak. And while where we can, we should still make efforts to contain it by doing contact tracing and isolation and quarantine on these, you know, tried and true public health methods, part of our focus now has to be mitigation. and that has to be the so-called flattening the curve,

trying to limit and reduce spread or the speed of spread to avoid overwhelming hospitals, trying to make sure that there is a safety net in place for people who can't afford to work from home, who don't have sick leave, who may not have adequate insurance. We need to make sure that all of those things are addressed so that we can at least mitigate the effects that this is going to have on our health care systems and on our public health, as a country and really as a species on this planet, we really need to have all hands on deck, including full engagement from the public. And I'm concerned that with the amount of misinformation that our federal leadership has provided, the constant still downplaying of the seriousness

of this situation, I'm very concerned that some of these measures won't even work. And I'm not so much concern for myself. I'm not in a high-risk category. I do have asthma, but I still, you know, I don't think that I would be personally likely to die from this. But of course, I'm concerned about all those other people who do have pre-existing health conditions, who are immunosuppressed, who are older, who have underlying medical conditions that would cause them to have a bad outcome or other people who may not even have coronavirus but are unable to access medical treatment that they need for other things because our hospital systems are overwhelmed. So my concerns, really my concerns about the virus are the least of my concerns with regard

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this podcast at checkout. This is Bethany Frankel from Just Be with Bethany Frankel. Listen, I have a bone to pick with these dog food brands calling themselves fresh, natural, healthy. Sounds great, but a lot of these quote-unquote fresh dog foods in your fridge are not even 100% human grade, which is why feed your babies, just food for dogs. It's good enough for big and smalls, my precious babies, so it's good enough for your babies, 100% human grade, real ingredients, beef, sweet potatoes, green beans, delicious.

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No code, no gimmicks, just real fresh food. Janice Torres here. And I'm Austin Hankwitz. We host the podcast, Mind the Business, Small Business Success Stories, produced by Ruby Studio, in partnership with Intuit QuickBooks. And we are back for season four. We're talking to small business owners who are doing incredible things in their industries, achieving their dreams, being their own bosses, putting in the work, and enjoying all the benefits that come with it.

This is our most exciting season yet. We're talking to more entrepreneurs about how they launched their vision, and more importantly, how QuickBooks on the Intuit platform helps them do more in less time. Working in QuickBooks just makes it easier to run the business, right? There's so much that you need to do when it comes to running a business, building products, setting up marketing campaigns. And to run a business, you have to make sure that your finances are in order. So it removes my anxiety from one side of it so that I can focus on everything else. Whether you're a long-time listener or just getting started, tune in and join.

us. You'll be so glad you did. Listen on the IHeart Radio app, Apple Podcasts, or wherever you get your podcasts. Awesome. Thank you again so much, Dr. Rasmussen for joining us. We really appreciate you taking the time out of your busy schedule. And it was really lovely chatting with you. Thank you. It really was. All right. So we wanted to wrap up each of these episodes with a what did we learn section. And we wanted to take the top five things or the five key things that we learned from our conversation with these experts. So we'll go through each of these five things. We've already talked about this. This is different than our normal episodes where none of what we're saying to each other is a surprise.

Yeah. I don't know. It's how we had to do it. It's how it's I think it's important because like, you know, we go over, we went over a lot in this episode. we're going to go over a lot in every episode. And I think that kind of trying to wrap it up and see what are the most important points is going to be. It was helpful for me even to go through.

Absolutely. It's very easy to get lost in the details of this. And so let's big picture this situation. All right. So one of the biggest things that we learned is that this particular virus, SARS-CoV-2, because of the specific receptors that it uses to get into ourselves, so that ACE 2, this virus can and does infect the lower respiratory tract. So that's why we are seeing as severe of disease in some cases as we're seeing.

And that is something that sets this virus apart from a lot of other coronaviruses, the more common ones that circulate and cause the common cold. But this is a similarity that SARS-CoV-2 shares with its closest relative, if viruses have relatives, and that is SARS classic, SARS 1. Number two, we also learned that this novel virus can definitely survive on surfaces for at least some time, and we're going to provide a link to that paper that Dr. Rasmussen mentioned on our website and in the show notes. But what we still don't have a great handle on is what exactly that means for transmission, because we don't know how many viral particles it takes to actually

make you sick. Or how different environmental conditions like temperature and humidity, how these might affect the longevity of the virus. But what we'll touch on in another episode in more detail is that we don't even know how much virus people are shedding. So really the best thing you can do is just kind of assume that your saliva and the saliva of everyone around you is infectious. So wipe down surfaces, wash your hands before you touch your face. These are the basic steps that will protect you not only from getting this virus, but also from spreading it to others. And it'll also do those things for so many other viruses, too. Yeah, absolutely. Number three, we also learned, I like this one, that viruses are not evil creatures intentionally setting out to kill you.

There's no malice. There's no malice there. They're just... As far as we're aware. I guess we haven't asked the viruses, but still. And the thing about this is mutation doesn't have to be a scary word. So yes, because this SARS-CoV-2 is an RNA virus, it does have a higher mutation rate than a DNA virus might or than a bacterial disease might. And certainly it has a higher mutation rate than our cells have. But that doesn't necessarily mean it's going to mutate to become more virulent or make you more sick. and it's probably uncommon that it would mutate in really drastic ways. There's been a lot of talk about this is going to mutate to be airborne.

And we'll talk in more detail in a future episode about what respiratory droplet versus airborne transmission really means. But in general, it's very uncommon for viruses to mutate in that drastic of a fashion to change their mode of transmission. Okay. Okay. Number four. So the other thing that Dr. Raspinson helped clarify is that we don't know for sure yet if there are different strains of this virus. But even if there are different strains, we don't know if that will actually result in different virulence or infectivity between those strains. Because so much of what goes into disease severity is related directly to our individual host response. And so it's really hard to tease apart the individual effects of certain virus strains and how much. much a particular viral strain is going to affect us or cause disease or be more infectious than another. And so that's something I think is really important to remember as this talk of strains comes into the news is that this is also something that's going to probably take a bit

to figure out whether there are any differences in the infectivity or virulence among any of the strains that we might detect. Yeah, absolutely. And finally, the fifth and I don't know, maybe most important thing that we've learned from this episode is something that all of our listeners already knew. And that is wash your hands, because washing your hands is really effective at reducing the spread and the chance that you're going to get infected or spread an infection to somebody else. Washing your hands really works. And alcohol-based hand sanitizers also work as well if you don't have the availability to wash your hands in a certain time. But we do want to note that hand washing is better because it actually washes those little viruses and bacteria off of your hands,

whereas the hand sanitizer just kind of leaves a sea of dead bodies on your hands. A sea of dead bodies. Dead cells and viral particles. Exactly. Aaron, do we have any? references that we'd like to shout out for this episode? We do. So we've got a couple of papers. One is by Van Dormelan at all from obviously 2020 because we're talking about SARS-CoV-2. And we also have, and that's titled aerosol and surface stability of SARS-CoV-2 as compared with SARS-CoV-1. And so this is the one that Dr. Rasbussen mentioned that looked at how well the virus survives on different surfaces. And then the other paper that we mentioned in our interview that referred to the L and S strains of SARS-CoV-2 is by Tang at all. And that's also from

2020. And it is titled On the Origin and Continuing Evolution of SARS-CoV-2. And as always, we'll post the links to all of our sources for this episode and every single episode on our website. We're also working on a specific COVID-COVID. section of our website where you can get answers to frequently asked questions to share with friends and family. And thanks again to Dr. Rasmussen for dropping some knowledge on us and on all of you out there listening. Absolutely. I will say too, if you want lots and lots of detail on the virology of this virus, there's a whole podcast series called This Week in Virology that has been doing a lot of updates about COVID-19 and SARS-CoV-2.

and they have a lot of details. It's hosted by a bunch of virologists. Ologies also had a great virology episode that interviewed another expert about this virus. And there's a whole bunch of other podcasts out there, too, if you just can't get enough. Thanks to Bloodmobile for providing the music for this episode and all of our episodes. And thank you for listening. We'll see you soon for Chapter 2. Until next time, wash your hands.

You filthy animals. This is Bethany Frankel from Just Be with Bethany Frankel. Listen, I have a bone to pick with these dog food brands calling themselves fresh, natural, healthy. Sounds great, but a lot of these quote-unquote fresh dog foods in your fridge are not even 100% human grade, which is why feed your babies just food for dogs. It's good enough for big and smalls, my precious babies, so it's good enough for your babies. 100% human grade, real ingredients, beef, sweet potatoes, green beans, delicious. These are foods that you would want to eat. Not that the babies would ever share.

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