Session 1: Covid 19: Translating the Science and Exploring the Path Ahead
// Session Transcript
Dr. Jessica Steier (00:00):
All right. Well, I'm going to kick things off here. Ujust want to welcome you all, and thank you so much for attending today's summit on COVID-19 translating the science and exploring the path ahead. Uthis is my third child. This has been something that we've been working on for weeks, and we're really, really excited to be able to have this opportunity. Ujust for a little bit of perspective. Uwe are living through a modern day plague and we're all doing our best to scramble with the information and the latest science. Uand it's scary. I know we're all really scared and anxious right now. Ubut we're going to get through this together. So science is ever changing and the data changes,uevery single day we're learning something new and it's not a matter of being misleading.
Dr. Jessica Steier (01:23):
It's just that we're trying to catch up to all the information as, as it's hurled at us. So what we're trying to do with this summit is to empower you guys, and we're not just going to hurl the same information at you. We're hoping to empower you to give you context, to explain what's behind the numbers and the statistics. So again, this is not trying to scare you. This is meant to empower you and to get us through this together. There we are. Dr. Love, are you there? I just want to make sure that we can hear you. I am. Can you hear me? Yes. Perfect. We also have to give a major shout out to Montana Mullins, who who's our administrative coordinator. She's been working day in and day out. She's a military wife living at West Point with two boys.
Dr. Jessica Steier (02:09):
She's superhuman. Thank you so much, Montana. We were on the phone last night at 11:00 PM with tech support. This has been an ongoing struggle, but we're here now and we're just so grateful. So, so let's, let's dive in here. I shouldn't be controlling. Andrea's screen bear with us. We want to apologize in advance. If you see any naked toddlers in the background, dogs barking or all living in this new age of COVID and just doing our best. So we, we thank you guys for your understanding. I just want to take 10 seconds to introduce who we are at Vital Statistics Consulting where a woman owned small business certified at the federal and state levels and the state of New Jersey. We were established in 2016, so we've been around her a few years. Now. We have offices in New Jersey, New York and Florida, where I'm located.
Dr. Jessica Steier (03:07):
Our mission is to improve public health, healthcare, quality, and patient safety. Oops, Andrea, I think we're competing here. That's okay. And we, we have an incredible team and so COVID really requires an interdisciplinary approach. So I, myself, I'm a public health population, health scientist. We're joined by Dr. Andrea Love, who's a bench scientist and immunologists more on her in just a second. We have an incredible team of clinicians, pharmacists, health economist, applied statistician qualitative researchers, health services, researchers, you name it, we've got it. And we've all put our heads together and we've tried to organize a summit. That's really comprehensive. And again, you know, the point of this is to translate it in a way that's understandable for non-scientific audiences. So tryna go ahead here, bear with us. All right. So typically we're the ones doing the data analysis. So what we do at VSC is we design healthcare evaluations and we, we do the quantitative and qualitative analysis, statistical analysis number crunching, but we've really shifted our focus in the time of COVID to health literacy.
Dr. Jessica Steier (04:26):
And our goal now is to, as I just said, is to translate the science for non-scientific audiences in a way that makes things more digestible and actionable for the general public. And, you know, I know we're all on social media information is being hurled at us, and it's hard to know what to believe in what to understand. So the whole point of the summit again, is to break things down for the layman, for people who don't have a background in science, so that when you see these facts thrown at you, you understand what's behind them. And again, we're hoping that you walk away with this with an understanding that science changes. Again, we're living in a modern day plague that our grandchildren are going to be reading about, and we've scrambled the past few months to do our best to, to analyze data and to understand the science behind it, things change. It's not a matter of being misleading. It's just a matter of catching up to the latest science. And so, again, we're trying to arm you guys with the tools to really understand what's behind that. So I'll stop rambling. We're going to dive into our first session co Corona viruses and the emergence of COVID-19 primer. We are so, so lucky to be joined by Dr. Andrea Love. Just a little side note. I've known Andrea since we were undergrads at Stony Brook university. And I'm so grateful to have reconnected with her in the time of COVID as I'll explain in a moment she's an immunologist, I'm a population health scientist, and we've really put our heads together to try to to work together in time of COVID. So let me just read a tiny bio on Andrea, and then I'm going to turn things over to you. So Dr. Love, Dr. Andrew Love is an immunologist and microbiologist with over a decade of experience in basic science and translational medicine. She's an expert in infectious disease, immunology cancer, immunology, and auto-immunity, and has authored numerous publications, educational pieces, and subject matter technical documents. Dr. Love believes strongly in scientific literacy from an early age and routinely serves as a guest speaker at K through 12 schools to encourage children toward a career in STEM.
Dr. Jessica Steier (06:41):
Outside of work in her spare time, she also happens to be a marathoner and ultra marathoner, an avid Yogi, and a black belt in judo. And she's always making me feel guilty about my, my lack of physical activity. She's absolutely incredible. She's wonder woman. And we're so, so fortunate to have her as a speaker one final thing before I turn things over to you, Dr. Love just a little disclaimer here. We've done our very best to put together a comprehensive presentation for you guys with the latest data to the best of our ability and understanding. But this is not intended to substitute the the advice from your own medical professionals. Of course, they know your, your personal medical histories and you should defer to them when it comes to your, your own personal decision-making. This is meant to be informative. Glad we got that out of the way. Dr. Love. I'm going to turn things over to you now.
Dr. Andrea Love (07:41):
All right. Thanks, Jess. And welcome everybody. I'm very excited to be a part of this. I'm hoping that I can convey some of my expertise. So you guys feel a little bit more prepared and a little bit more well-versed in, in some of the at least in this session, basic biology and virology here. So I'm going to kind of start by giving a primer on viruses as a class of microorganisms first. So they're a very unique class of microorganisms in that they're not characteristically thought of as a cell. A lot of times when you're in basic biology you hear about mammalian cells and plant cells and bacterial cells. Viruses are a specific and unique class. They require a host cell in order to reproduce and survive. Without that, they're ultimately what we call a virion, which is something that can infect organisms, but without a cell to live inside it can't do anything.
Dr. Andrea Love (08:47):
So these are the main components of a virus or a virion. You have this capsid and this is a envelope or protein capsule that coats, the, the nucleic acid in the center of the virion. So every organism, including viruses have a genome that's made up of nucleic acids. I'm going to get into a little bit of some of the differences in terms of viruses. Humans are made up of DNA and viruses have different types of nucleic acids. That's going to basically allow them to carry all the information they need in order to reproduce. So the capsid is a protein coding that surrounds that nucleic acid that is actually complex with the nucleic acid itself. And that forms what we call the nucleocapsid within the capsid itself, which is a series of proteins. Each one of those subunits is called a capsomere.
Dr. Andrea Love (09:49):
These are assembled in order to form this protein coding outside of that, some viruses have what we call an envelope and this is made up of lipids. So fats as well as typically some, some membrane proteins and these, we usually refer to as protein spikes. And we'll get a little bit more into that in a moment. You'll notice they don't have a nucleus. They don't have organelles like Malian cells do so there's no mitochondria, there is no golgi body. They're very simple Instructure and this contains all the information they need in order to spread and reproduce.
Dr. Andrea Love (10:30):
So not all viruses are the same. And this is really critical because they're not classified as we characteristically view mammalian organisms or other things they're classified by a series of different criteria. The first is the morphology or the shape of the virus itself. So I have some examples here on, these are the four main shapes of viruses. So we have helix viruses. And these actually look like a helix. You can see the electron microscopy images below these actually have their nucleic acid in, in a spiral shape and they have their protein capsid that's formed around that. So they look like little cylinders. Polyhedral so typically the, the most common shape in this class are icosahedral. And so these are typically made up of protein sub units and they're non envelope spherical. These are typically polyhedral viruses that have an envelope.
Dr. Andrea Love (11:30):
So the fatty envelope that's around the outside of that is what confers that spherical shape. However, helical viruses can also be spiritual in nature if they have an envelope and then complex are these complicated structures that have these almost look like the lunar module. This is kind of how we were described as them when we were, and these are typically only viruses that infect bacteria, it's a particular class called bacteriophages examples of helix viruses. You can see tobacco mosaic virus here. That's actually a plant virus that infects tobacco plants. But an example of a helix human virus would be something like rhabdo viruses, which actually cause rabies an example of a polyhedral virus. So these are non envelope viruses. This would be your papilloma viruses. So these are viruses that cause regular wards, plantar wards, as well as your human papilloma viruses, which cause your genital warts polio virus is a polyhedral virus and rhino virus, which is a class of viruses that cause some of our common colds are also polyhedral spherical examples are those envelope viruses that we talked about.
Dr. Andrea Love (12:43):
So they have the capsid and then they have a fatty coating on the outside. These would include your influenza viruses, your herpes viruses. So there's a very large family of herpes viruses. These include the virus that causes chickenpox, which is called varicella zoster virus. The virus that causes mononucleosis, which is called called Epstein BARR virus, your herpes simplex one and two and so on. And then the Corona viruses. So the SARS cov two that causes COVID, that fits into the spherical category. They're also further classified by nucleic acid types. So as I mentioned, humans are genes are made up of DNA. Viruses are not always made up of DNA. We're going to talk a little bit more about that in a minute. We also classify them into families by how they reproduce. So because they have different types of nucleic acid, they're actually able to reproduce in different manners. Again, we'll talk a little bit about that. And then finally we classify them based on what organism they live in, what organism they infect, their hosts, and then also the type of disease that they cause.
Dr. Andrea Love (13:53):
So ss I mentioned, viruses differ from typical cell. So the central dogma of molecular biology is the kind of information processing flow. So it typically goes your, your genes are made up of DNA, which live in your nucleus when you're ready to express that gene, that DNA is converted into MRNA, which is messenger RNA. That process is called transcription. And then from there that MRNA is actually converted into a functional protein or a poly peptide, which is called translation. This is the normal flow of information. DNA is a protected molecule that lives in your nucleus. It's the universal language and all organisms, other than viruses exist in that manner, including bacteria viruses are very unique where they can actually have their genes or their universal language be either in or in RNA. One of the major differences between DNA and RNA is that RNA goes directly from that molecule into a functional protein DNA has this intermediate step where it has to be converted into RNA.
Dr. Andrea Love (15:06):
And there are actually error checking processes that are in place to make sure that new patients are limited. And that will become important when we chat in a little bit. DNA is double stranded versus RNA single-stranded. The RNA strands. So the single RNA strand that's immediately translated into protein is called the plus RNA strand. The mine is RNA strand is the opposite of that. And that has to be converted. These are important because these different components are these different nucleic acid structures will actually change how a virus replicates or their, their ultimate life cycle.
Dr. Andrea Love (15:46):
So as I mentioned, viruses have different genetic material. So you have very distinct differences and different examples between DNA versus RNA viruses. So DNA viruses, as I mentioned, their genes are made up of DNA. This is double stranded. It's formed that double helix that most people are familiar with. It has four different bases, they're all paired and complimentary to each other. I'm not going to get into that portion of things. But also they're located in the new, they typically in fact, and have to be located in the nucleus. So all of your DNA processing occurs in the nucleus of a host cell. RNA viruses are different from that because these RNA viruses with the very few exceptions of, of a couple types of RNA viruses are single-stranded meaning they have this one strand of RNA. This is unprotected ultimately, and because RNA is translated immediately to proteins, this actually occurs in the cytoplasm of cells.
Dr. Andrea Love (16:53):
So they don't actually have to make it all the way to the nucleus. Now they can be located in the nucleus and some viruses do infect the nucleus of host cells, but they don't require it. So as you can see here, we have some common examples of DNA viruses versus RNA viruses. One thing I want to mention, because this question has come up a lot is the ability of this virus to infect us and become latent or dormant. This is something that there's been a lot of mulling about because we've seen this in other viruses, for example chicken pox, right? Once you survive chickenpox, that virus establishes dormancy in cells in your body. And you don't, even though you physically recovered from the illness, you don't actually ever get rid of the virus in your body. And the reason for that is because that virus is actually one of the viruses.
Dr. Andrea Love (17:49):
So you can see that this is a double-stranded DNA virus in this top flow chart, that's the herpes virus family. And what they do is they can, because they're made up of DNA, they can actually integrate into host cells and they can live in the host. Cell is just another piece of our genes. Until one day they become reactivated. And, and then in this case of chickenpox establish a new disease called shingles now with RNA viruses because their genome is made up of RNA. They don't establish themselves. They don't integrate into our genome because our genome is DNA. So they're not compatible. So there's very little evidence to suggest that that would in fact be the case. So once you actually are recovered from this virus it's not going to kind of live in persist inside your body. You'll notice here that within the RNA viruses, you have these plus RNA and these minus RNA viruses.
Dr. Andrea Love (18:45):
Again, I'm not going to talk too much about that. I do want to point out that within the RNA viruses, you have some that are envelope, some that are not envelopes. And one that I want to draw your attention to is the minus RNA orthomyxo viruses. Those are the influenza viruses. So these are actually very distinct from each other. Genetically, and we're going to talk more about that in session three more about what makes the disease itself different, but obviously I've circled the Corona viruses here because we're going to talk about those. And those are envelopes positive RNA viruses.
Dr. Jessica Steier (19:25):
Andrea, if I could just jump in for one second. I'm sorry. We're all I know. I was just commented. We're all having flashbacks to, to our undergrad biology classes and wishing we had you as a TA back then. If, if you all have any questions, please do use the Q and a function. And we'll do our best to answer. If there's time. Thank you. Sorry, Andrea.
Dr. Andrea Love (19:50):
Oh, no problem. All right. So now that we've got a little bit of the fundamentals of the virus, we want to talk about how the virus is actually infect us. We know that they can't live, they can't reproduce outside of host cells. They have to find a host to live in. So viruses exhibit, what we call tropism and tropism is a phenomenon that, that basically dictates what type of organism and what type of cells a virus can live in. We know that not, we don't get infected by all viruses that exist. We know that certain viruses can't infect us. We know that certain viruses only infect certain parts of our bodies. And this is this tropism effect. So we have three different levels of tropism. We have cellular tropism tissue, tropism, and host tropism. And so working from kind of the top-down host tropism is basically a virus can infect one species, but not another.
Dr. Andrea Love (20:42):
And an example of this here is myxoma virus. This is a disease in rabbits, but it can't infect humans. Tissue tropism is when it can infect certain tissues of our body, but it can't infect others. So for example, influenza virus, it can infect lung tissue, epithelial cells in your respiratory tract, but it can't infect brain tissue which is significant in terms of thinking about the disease itself. And then cellular tropism is kind of at the bottom tier on a more microscopic level where that viruses can only infect certain cell types. So as an example, HIV, so human immunodeficiency virus infects, macrophages, and T-cells, but it can't infect neurons. And the reason behind this is due to the way a virus gets into a cell. So cells express specific proteins on the surfaces of them that a virus recognizes and binds to.
Dr. Andrea Love (21:42):
It's kind of like a lock and key or a puzzle, a puzzle piece. Those viruses and those receptors on the host cell have to be specific. So once they bind, it basically unlocks the ability of that virus to then infect that cell. So once the virus is able to actually recognize that host cell, it's going to attach to it, and then it's going to infect it and ultimately reproduce once they actually are done reproducing, we're going to go through those steps. They'll able, there'll be able to spread to neighboring cells to then kind of propagate that infection, you know, having a single infected cell in your body does not mean that you're actually going to have disease. It has to actually have the ability to,
Dr. Andrea Love (22:27):
Spread,
Dr. Andrea Love (22:30):
So how viruses infect us. So again, this is kind of a schematic. I really love this where it really walks you through this whole infection process. So there's five steps, and this is very different from how our cells reproduce or how, you know, other organisms reproduce, but the virus life cycle starts with attachment and that's that recognition of the virus with the receptor. And that's based on that tropism. So certain, certain viruses have receptors for certain cell types. And these are very specific and very distinct both within a human, within an organism from cell type to cell type, but also across organisms, as we just discussed, once they attach they bind through that lock and key, they're going to penetrate the cell. Sometimes we call that entry. There are different methods of entry. I'm not going to talk too much about that, cause it's not, it's not that relevant.
Dr. Andrea Love (23:25):
But there are some methods that are called phagocytosis or endo cytosis where they actually are part of the cell membrane and they're budded in sometimes they just actively just release their material into the cell itself. From there, you have what we call uncoding and replication. So that uncoding step is the dissolution of that, that membrane, that lipid membrane, if it's an envelope virus and then also the capsid. So in any virus, the capsid will dissociate those, those pieces of the protein are going to go off to one side and then that releases the genome. So whether it's an RNA or DNA virus, that's going to lead to replication of the genome. So of the information. So if it's a DNA virus, that's going to go into the nucleus and it's going to be reproduced through the host cell method. If it's RNA can stay right in the cytoplasm or the cytosol and be replicated that way from there, you're also going to be making those viral proteins and those are going to make new capsid proteins, new capsule mirrors.
Dr. Andrea Love (24:32):
So you're going to make more copies of the genome. You're going to reproduce that you're going to make more viral proteins that are the components of the capsid. And then once those are all synthesized, and this is all using hijacking the host cell. So the virus is not bringing most of these things with it, other than the original capsid and the nucleic acid from there, it utilizes and it hijacks everything else. The host cell has to offer all of the enzymes to make proteins. And then once it's done, it's going to become reassembled in more viral particles than you started with. And then it's going to be released. That's the final stage. Once it's released, it's now free to go find another cell in your body to infect.
Dr. Andrea Love (25:17):
So why do we
Dr. Andrea Love (25:18):
Symptoms when these viruses actually infect us? So there's two main reasons we get symptoms. So the first is our immune system. So there's three main branches of the immune system. You have physical barriers, things like the skin, things like mucus and saliva and molecules in our saliva that that can actually inactivate pathogens. And then of course you have other sorts of things like the acidic pH and enzymes in your stomach and GI tract. Once a pathogen breaks those barriers, then you have the first line of defense, which is our innate immunity. These are immune cells and chemicals that constantly are circulating in our body. They're not specific for a particular pathogen, but they recognize pieces of cells or organisms that are foreign. So things like, you know, free floating viral RNA. So we know the genome is made up of RNA that shouldn't be outside of the cell.
Dr. Andrea Love (26:16):
So when that's recognized that will activate the innate immune system cells in the innate immune system are things like dendritic cells, monocytes, macrophages, neutrophils, et cetera. They produce inflammatory chemicals called cytokines. And chemokine that actually activate that third branch of the immune system, which is our adaptive immune system. And that adaptive immune system becomes very important when we talk about recognition or memory protection against a future infection, and those are your T cells and your B cells, your B cells are responsible for making antibodies against a pathogen and your T cells participate in directly killing those cells. Those are our cytotoxic T cells or helping or establishing memory in order to regulate and, and maintain these, these crosstalk between the different cells of the immune system. Now, the immune system, as I mentioned, produces these chemicals that activate the other branches of the immune system, but they also produce inflammation.
Dr. Andrea Love (27:22):
And so these inflammatory chemicals, your cytokines, and chemokine often contribute to your physical symptoms. Things like fever, things like swelling, even when you get a cut or an injury that's not related to an infection, that's all because your immune system is mounting this wound healing response. So one branch of the symptoms are directly caused by the immune system, recognizing this invader and then mounting an attack against it. In other instances, and in, in other, in other parts of disease pathology, the pathogen itself. So pathogen is basically just any, any organism that caused disease. So pathogen could be a virus. It could be bacteria. Just want to kind of clarify that. I'm going to use that term quite a bit. So the pathogen itself damages your cells. So some symptoms are direct result of tissue damage or cellular damage caused by the pathogen.
Dr. Andrea Love (28:21):
And those symptoms typically coincide with the tropism of the virus. So the cell types that the virus infects. So for example influenza, which we'll talk more about later, that actually kills epithelial cells in your upper respiratory tract. And that's partly why we have coughing and things like that as symptoms, but it also makes us prone to secondary bacterial infections like pneumonia because you killed off those cells and now it's easier for other things to infect you. So two main reasons that we get symptoms. Usually there's a combination of both. And that's important to keep in mind as we talk about the disease itself.
Dr. Andrea Love (29:05):
So we're going to talk about Corona viruses specifically now. So Corona viruses are very large family of viruses. There were hundreds of them. They were first described in 1931. Most of these caused disease in birds and other mammals. We first isolated the first human Corona virus in 1965 and characterized it, there are four human coronaviruses. These are ones called HCOV on this table here. Seven known Corona viruses currently cause disease in humans. And that's aside from the hundreds of others that cause disease in other species. So birds and mammals, the four human Corona viruses that are listed here, 229E, NL63, OC43, and HKU1 these are lumped into the common cold. So this includes other families of viruses, but also these four Corona viruses cause just very mild respiratory infections. Umost people have been infected with them at one time or another in their life.
Dr. Andrea Love (30:09):
The three that we're going to talk about most, and obviously one in particular are these new or what we call emergent Corona viruses. So we have SARS CoV, this caused SARS. So that's severe acute respiratory syndrome. That was a new disease outbreak in 2002. The next one is MERS CoV. This one causes MERS, which is middle Eastern respiratory syndrome that causes that caused a new disease outbreak in 2012 and SARS CoV 2, which is the one we're going to talk about most causes COVID-19. So there's a big difference between the name of the virus and the name of the disease. So I like to be very clear about that. I know we call this COVID-19 for, for brevity sake. But the virus is called SARS CoV 2, which is SARS coronavirus two. Now this image here is the structure of the SARS coronavirus specifically, or SARS CoV 2.
Dr. Andrea Love (31:05):
So you have that, that RNA in the center of that virus. And then you have your nucleocapsid, which is that complex of RNA and nucleocapsid proteins. And then on the outside, you have that fatty envelope and then you have these proteins that are listed. The one that's most important or has probably garnered the most attention is what we call the S protein or the spike protein. This is very important in terms of how the virus can infect us. But that's kind of the structure of the virus. It's pretty, pretty simple. Especially considering how significant a disease is able to cause. So SARS, cov V two. So this is the newest of the Corona viruses known to infect humans. If we did a genetic study of this virus and we identify that as closest in genetics. So it's most similar to Corona viruses that are known or identified in bats and pangolins. Pangolins are these mammals.
Dr. Andrea Love (32:02):
They have these kind of scaly armor. They, they kind of look like an Armadillo they're, they're one of the most poached and traded animals on the planet. It's very, very sad, but ultimately this virus, these viruses that were originally in bats and pangolins it mutated and jumped, jumped into humans. So normally the, these original viruses were not able to infect humans, but something happened as it replicated and it was able to now infect human cells. And the reason for this is that that S protein that I just mentioned, the spike protein is able to bind a protein that human cells express called ACE2. And this is a receptor that's expressed on certain cells in our body, mostly epithelial cells, also cells in our renal systems or in our kidneys, as well as in the GI tract and actually also expressed in, in testicles in testes. So this receptor is the protein that's expressed on the host cell and this spike protein on the virus interacts, recognizes and binds that. And that's how it's able to get in and infect ourselves. Once it's infecting ourselves, it then causes this disease that we've now named COVID-19, which stands for Corona virus disease 2019. That was the first year it was identified. And
Dr. Andrea Love (33:24):
Described.
Dr. Andrea Love (33:27):
So where did COVID-19 come from? So, as I mentioned, it's closest in genetics, so it's most similar to viruses in bats and pangolin. So COVID 19 is what we call as zoonotic disease. Zoonotic diseases are illnesses or diseases that are present in animals, but can be transmitted to humans. And something that's very important to keep in mind is that about 61% of human diseases are zoonotic. Even more interesting is that 75% of new diseases discovered are zoonotic. So those are diseases within the last 10 years. So the prevalence or the emergence of these new diseases that are typically animal born, but now we're being transmitted to humans is increasing in prevalence, MERS, and SARS are also zoonotic diseases. So they also were able to mutate and to jump into humans. MERS is mutated from camels and SARS is mutated from civic cats.
Dr. Andrea Love (34:30):
Now, something to keep in mind is that those were the host that immediately transmitted to humans. All of these coronaviruses have originally thought to be started in bats. So bats transmitted to camels camels, then transmitted to humans that's transmitted to civet cats, civets then transmitted to humans. And then the case of SARS cov two, which causes COVID again, bats may be transmitted directly to humans, or maybe they went through pangolin first. A little bit of that is unknown because we haven't been able to identify which genome and actually mutated from the key thing to keep in mind is that these zoonotic diseases are transmitted through a variety of methods it can be airborne, meaning just close proximity to, to animals might be able to transmit if that animal is in fact infected. This could be you know, through just being near them.
Dr. Andrea Love (35:23):
It could also be through fecal oral route or bodily fluid transmission from an animal to, to a human. It can also be transmitted through vectors. So vectors are usually insect, transmitting organisms where they're going to pass a disease from an animal to a human, a direct contact or, or foodborne by consuming infected products other zoonotic diseases of note. So there's a lot of viral bacterial and even protozoan diseases that are zoonotic, but examples are in the viral category. We have rabies that's obviously transmitted by a bite from an infected animal. HIV and AIDS is thought to evolve, have evolved from a a primate similar disease called SIV, a West Nile virus, yellow fever virus. These are also not diseases. Bacterial ones are things like plague that's caused by a bacteria called yersinia pestis by way of a fleet salmonella, salmonella, or salmonellosis. Again, that's typically in chickens and other organisms easily transmitted to us. Eco-Line again, cows, other organisms transmitted to us a lot of tick-borne diseases such as Lyme disease, Babesia, et cetera. And then a protozoan one that might be familiar with some is toxoplasmosis. That's the reason why pregnant women can't scoop litter boxes. That's a cat parasite that can be transmitted to humans.
Dr. Jessica Steier (36:50):
Andrea, if I could just interject. And I think you're, you're probably going to cover this, but we got a question and actually this was emailed to us by several people. We've been hearing a lot about the Corona virus being created in a lab, but scientists have stated that this is not possible based on the structure of the virus. Can you explain a little about how scientists are able to determine the source of a novel virus? Obviously you just took us through the, the origins, but can you speak at all about why we don't think it was created in a lab? Maybe.
Dr. Andrea Love (37:22):
Absolutely. Yeah. So if we go back to this image here, this bottom image that looks like a bunch of color-coded stripes. This is actually looking at the, the genome, the, the, the the protein sequence of the binding region, which is this square region that's identified in the top right image. That's the receptor binding domain. So the portion of that spike protein that interacts with the host cell. And so what we're looking at here is actually the protein sequence or the amino acid sequence that actually creates this functional protein. And so we're looking at the SARS CoV sequence compared to these viruses that circulate in the wild that are related to other, other diseases caused in other animal species. And so by looking at what we call homology we can actually determine that this was likely the result of a single or a couple of particular amino acid mutations. Further when we look at functional characteristics, such as the ability to in fact, the infectious factor, which we're going to get into in another session these sorts of parameters that caused the pathology of the disease itself. It's, it's almost impossible for this to have been genetically engineered by, based on all of these parameters. Does that answer the question, Jess?
Speaker 4 (38:45):
Sorry,
Dr. Jessica Steier (38:45):
I muted. I, I think so. If there are any follow-up questions or any related questions, please do submit them using the Q and a function. Thanks,
Speaker 4 (38:54):
Andrea.
Dr. Andrea Love (38:56):
So why do we have so many zoonotic diseases? Because this becomes very important when we're thinking about our regular behaviors. So of course, globalization and overpopulation just puts us in close proximity to other species. And this is, you know, global you know, we're probably 3 billion people over carrying capacity of the planet, and that's not how many people you can cram into, you know, square footage, but it's using resources you know deforestation building in wildlife habitats and things like that. So that's a big thing. Of course, other factors such as climate change as the climate is changing, you have expansion of the geography of vectors that transmit diseases less relevant here in the case of, of COVID, but definitely relevant in the case of things like Zika virus, yellow fever virus, West Nile virus, et cetera. As you have mosquitoes and other sorts of organisms expanding their geography, now you're increasing the potential spread of disease.
Dr. Andrea Love (39:54):
Of course wildlife trafficking, wildlife poaching, and then of course, wild animal markets that facilitates close interaction. And this is actually really critical because not only do you have people near wild animals that they would normally would never interact with when you have wild animals interacting with other wild animals that they would never interact with in the wild themselves, you have animals coming from various different geographies that would normally never encounter each other. And through a series of new mutations, one of those mutations enables that virus, for example, to jump into a new species, this is all random. So viruses, mutate regularly, every replication every time they reproduce mutations are, are generated most of those mutations or either what we call silent or nonsense, meaning that they won't allow it to do anything. It's either going to not change the virus at all, or it actually will be an evolutionary disadvantage and that virus just won't be able to reproduce. And it will become an activated when you have a mutation that's random that actually enables it. You recognize a new host cell or a new host that becomes an evolutionary advantage because now it has this whole new pool of, of hosts that it can now,
Dr. Andrea Love (41:09):
Infect. So
Dr. Andrea Love (41:11):
Of course, any sort of behavior that's going to facilitate interaction with other species new areas, new geographies, et cetera, that can contribute to the emergence of these zoonotic diseases.
Speaker 4 (41:26):
So
Dr. Andrea Love (41:26):
The danger with a zoonotic disease, why, why is this such a big deal? Why is the emergence of a new pathogen really important? The reason for this is that when you have a new disease that you've never encountered, that means your body, your immune system has no recognition of it. You have no way to fight it off. You have no memory, you have no defenses built up. So once that happens, once this virus jumps into a new host, now the entire population is susceptible. Everybody's just as prone to being infected as another. And that allows the virus to spread extremely rapidly. And again, as I mentioned, it's all about an evolutionary advantage. So if a virus lives in say civets but all the civets have gotten ill and they have immunity. Then it has nowhere to go. You block this transmission chain.
Dr. Andrea Love (42:12):
So it needs to find a new way to continue to reproduce. And so these mutations and this ability to jump into a new host species allows that to propagate. And as you can see you know, every single country around the world have cases of COVID now because of this susceptibility of the population. So as of this morning, we have almost 4.2 million confirmed global cases and almost 300,000 confirmed global deaths. I say, confirmed here because these case numbers are a function of diagnostics. And as we know, there are some issues with testing and access to testing. But this is kind of the numbers we have to work with. So it's extremely prevalent, it's spread extremely rapidly. And so it's, it's important that we address it and slow it down. So I'm going to quickly review what we chatted about. And then I'm going to open it up to questions.
Dr. Andrea Love (43:08):
So viruses, as I mentioned, they're a unique class of microorganism. They require a host cell in order to survive and reproduce without that host cell, they have limited ability to survive before they'll ultimately become inactive. Virus types are very distinct and diverse. They're classified by the nucleic acid type. They contain the shape, the type of animal they infect and the type of disease they cause specifically with Corona viruses. These are family of RNA viruses. There are seven species that cause human disease with over hundreds that cause disease in other animals, particularly other mammals and birds. The new outbreak is a virus called SARS cov two that causes the disease. COVID 19 zoonoses are diseases that jump from animals to cause disease in humans. The majority of human diseases that we know of are caused by zoonotic diseases COVID-19 is thought to have mutated from a bat. Corona virus by way of a pangolin as an intermediate host, and was able to infect humans as a result of this random mutation the spread of disease with a new disease, something that we've never seen before, everyone in the population is susceptible, which is why we have such rapid spread of this within the human population.
Dr. Andrea Love (44:29):
So that's my about the basic virology and Corona viruses. And I'd be happy to take any questions,
Dr. Jessica Steier (44:43):
Andrea, thank you so much. Um, I learned, learned a lot just now the beginning was a little scary and then you, you, he's just into things. So thank you so much. So we do have a bunch of questions, a couple here, and then a couple that came through in social media. So let's start with do we know why the virus has been very slow to spread on the African continent? My sister is a doctor in Central African Republic. They have a few hundred cases and no deaths so far.
Dr. Andrea Love (45:09):
That's a great question. And I think you know, we're, we're, we have a session where we're going to talk about some population health but part of it is because of the demographics in terms of population density. So the virus and of course I don't want to jump the gun for session three, but we're going to talk about transmission. The virus needs to spread human to human, ultimately. And there's a few methods of that. So there's no vector that transmit it. Which is why in say African Subsaharan Africa, you have things like malaria that can be very prevalent because it's transmitted by way of mosquito. This is a person to person infection. So in areas where you have low population density, you don't have a population dense hub. That's going to be a big pool of potential vectors of transmitting that disease. This is very distinctly different to something like New York city, which has millions and millions of people packed into a very small geography, which is really prime conditions to spread a respiratory disease such as this. You'll notice even here in the US in more rural situations, we have very, very low case loads. And that's ultimately because of the predominance of person to person interactions.
Dr. Jessica Steier (46:25):
And just one thing to add here from a, from a public health perspective, I'm really not I don't know enough about what's going on in Africa to comment on it specifically, but I wonder how widespread their testing is which would affect our understanding of the spread and whether or not the mortalities are due to to COVID or not. So just want to throw that in there as another consideration.
Dr. Andrea Love (46:49):
Great point. Yeah.
Dr. Jessica Steier (46:51):
Okay. Andrea, how can someone be infected without symptoms when they have no immunity?
Dr. Andrea Love (46:57):
That's a great question. And that has to do with some of the, the viral load or the infectious dose. You have some, and again, that also has to do with the host immune system. So when you get physical disease, there's a lot of factors involved. There's the pathogen itself, there's your immune response. There's how those two things interplay. People are genetically diverse, right? Not every single person is the same as another. And so when you get an infection, some people's immune systems are more active. They they react very strongly. They get very high fever, they have a very pronounced inflammatory response and other people's immune systems are a little bit less less active. Now there's a lot of reasons behind that. But ultimately that can be the reason why you would have say what we call subclinical infection, where you're technically infected, but you don't have physical symptoms. And this is actually really important because we're gonna talk about this later again, but there are people that are asymptomatic that can actually infect other people. So it's a little bit of a combination of how many viral particles are, are in your system at the same time. But a lot of it is, is the diversity in people's immune systems. Everybody is very, very different when they, when it comes to responding to them.
Speaker 4 (48:16):
Thank you.
Dr. Jessica Steier (48:17):
Okay, next question. Is it true that the latest mutation of the virus is more deadly?
Dr. Andrea Love (48:26):
That's a good question. So there's some preliminary information that suggests that and this is not a new thing. This is the, the virus that's in the U S so I don't want to suggest that this is something that happened a day or two ago. This has been around for awhile, but there've been obviously a few mutations. It's still the same virus. But ultimately there is some limited data that suggests that it might be more infectious and it, and as a result, it might have a slightly higher mortality rate. Now that was one study that was published. Again, we have to wait a scientist for confirmatory studies to emerge. Right now we have a variable case, fatality rates, depending on a lot of parameters, which we'll talk a little bit more in the public health capacity, but some of that is access to healthcare. And some of that is demographics of the population and things like that. As of right now, we still want to, you know, go with the understanding that there's a range of fatality rates. And this certainly is not a new virus,
Speaker 4 (49:30):
So to speak
Dr. Jessica Steier (49:34):
A rumor going around is that people previously infected with H1N1 could be immune to COVID-19. Could that be possible, or the viruses? Similar.
Dr. Andrea Love (49:46):
Good question. So, H1N1 is an influenza virus. And as I mentioned, although they're both RNA viruses, they are in different families. These are the Corona viruses, influenza viruses are the orthomyxo viruses. They're very distinct. They have very distinct genomes. They infect different cell types. They have different receptors. Other than the fact that they both cause respiratory disease, they are very, very, very different. There is no evidence that previous infection or previous recovery from H one N one influenza would give you any sort of immunity to a coronavirus.
Speaker 4 (50:20):
Okay.
Dr. Jessica Steier (50:22):
As an RNA virus, did you say Corona virus can stay in the body manifest later? What are the implications of that?
Dr. Andrea Love (50:31):
Yeah, thanks for bringing that up. So DNA viruses require the host nucleus to reproduce. Those are things like the herpes viruses. Some of the viruses in that family are your Epstein-Barr virus, which causes mononucleosis your chicken pox virus, your varicella zoster virus that causes a chicken box and later shingles, DNA viruses can establish latency or dormancy, meaning they can persist in your body after you survived or recovered from the primary infection. And those can become reactivated later. And re-established disease, RNA viruses can't do that. They don't actually get into the nucleus for the most part. And so they don't really have the capability to integrate with our DNA because of course they're made of RNA and not DNA. So in the case of RNA viruses is very unlikely that they will be able to establish a latency or dormancy within our body and reactivate later. Okay. So I guess that's good news. Good news is good news. Absolutely.
Dr. Jessica Steier (51:38):
Do we think rates will drop in the summer due to temperature and humidity?
Dr. Andrea Love (51:44):
Yeah. So there's a lot of obvious theories behind this something that I want to kind of emphasize, and maybe I'll go back to one of my slides if I can figure out how to do that. Here we go. We take a look at this global map. So these are obviously the cases here. You can see that we have cases all around the world, in every climate, in every geography. Now it is true that, and I'm going to talk about this more in session three today viruses have preferred climates that they're most transmissible usually because of their mode of transmission or where the vector lives or whatever the case happens to be generally speaking, respiratory viruses thrive a little bit better in lower humidity and lower temperature environments. However, there's no indication that it's going to just disappear in the summer. We may see slightly lower rates of transmission. Partly because of the weather itself, partly because of some of the social distancing measures we've taken. But it will be able to still persist in the summer as temperatures increase. And as humidity increases now in a lab, when you UV rainy that very, you know, high doses of UV radiation, you can inactivate a virus, but that's not the same as simply just sitting out in the sun. Yeah,
Dr. Jessica Steier (53:13):
I'm really glad you said that because I have seen a lot floating around social media about how exactly what you just said, sitting out in the sunshine is, is going to kill the virus. And so you just confirm that, you know, in a lab setting and tends to be radiation for, for prolonged periods of time that might kill the virus, but that's not the same thing as simply sitting out in the sun.
Dr. Andrea Love (53:36):
Yeah. And you certainly wouldn't be able to get that dose, even if you just lived outside. You know, these are levels that are going to cause you know, significant health effects, if you were ever able to be exposed to that.
Dr. Jessica Steier (53:48):
Right. Okay. Do different countries have different mutations, thus affecting fatality rates? Okay.
Dr. Andrea Love (53:58):
So as of right now, there's one SARS cov, two virus there are different slight different variants. These are called isolates. These are classified by where the patient was and how they were isolated. There are no unique strains. There are no different variants or serotypes or subtypes. That's very different from the influenza virus. There's a single source COVID virus. Right now there's no evidence that, that different countries have different mutants or different versions are different isolates that actually confer different, different disease pathology, or different case fatality rates. A lot of what we're seeing in terms of variation of, of our fatality rates are ultimately through what population is getting infected. Certain people are more susceptible. Certain people are more prone to having pre-existing conditions or co-morbidities that can cause, you know, fatalities as a result. And then of course, access to healthcare access to, to hospitals, things like that. Those are the biggest determinants in, in the demographic differences amongst the fatality rates.
Dr. Jessica Steier (55:07):
Interesting. Okay. Thank you. Thank you so much. I don't see any other questions on here. If folks have any other questions, please send them in.
Dr. Andrea Love (55:18):
I will put up my email address again. Oh, cool. So anybody does think of something, please feel free to email and ask
Dr. Jessica Steier (55:28):
And just I guess a logistics comment if you wanted to join our next talk I'll be co-presenting session two basic COVID 19 statistics. How to interpret the evidence. I promise. I, you know, for those of you who hate math, I promise we'll, we'll break it down. I know in a way that's that's really understandable. So you should have received an email with links. Each of the links for each of the sessions is distinct. So you could either go back to that email and click on the link for session two or you can, you should be able to access session two via the Whova app, if you did download it. If you have any questions, whether they be for Andrea about the content you just presented or the any tech questions, logistical questions, please feel free to shoot us a question in the Q and a function or the chat, and we will be happy to answer. If not, we thank you so much for attending our first session. I'm so excited and again, so very grateful to you Dr. Love for your time and expertise. . And, and Andrea is giving multiple talks.