Session 6: What Makes This Illness Different: Contrasting Covid-19 with Influenza, SARS, and MERS
// Session Transcript
Speaker 1 (00:00):
Thank you guys so much for joining welcome to day two of our summit. I hope some or most of you guys were able to attend yesterday. We've been getting some really great feedback on those sessions. If you do have questions for what was already presented, please feel free to email with additional questions or you can utilize the Hoover app. We've been monitoring it and doing our best to get back to questions as quickly as possible. So definitely feel free to utilize that app. It's also supposed to help us network and keep in touch. Post-Conference as well. So, so that's great. I'm really excited for this particular talk. I'll be introducing the speakers in just a moment but just to be totally transparent. This idea came about based on a lot of misinformation that we saw rampant on social media.
Speaker 1 (00:54):
A lot of people seem to think that COVID is just basically like the flu also questioning why we're having such a strong public health response to COVID and not as strong of a response to to other epidemics and outbreaks. So we're very lucky to have Dr. Andrea Love and Dr. Margaret or like Romanov ski here to talk us through this all beyond moderating. I just want to give a quick background on these two incredible speakers. So Dr. Andrea Love is an immunologist and a 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, she's authored numerous publications, educational pieces and subject matter technical documents. She 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, total transparency.
Speaker 1 (01:59):
It's sometimes Andrea says things that are over my head. She's just too smart for her own good. So sometimes the, you know, the, the the content can be a bit technical, but she always does an amazing job of, you know having takeaway messages and, and so thank you for that, Andrea. Next we have Dr. Margaret Horlick Romanowski. She's an assistant professor at Brooklyn college, part of the city university of New York. She teaches epidemiology public health and social determinants of health. Her research focuses on nutritional epidemiology, dietary acculturation, and health disparities in cult in chronic disease. She's dedicated to mentoring the next generation of public health and epidemiology researchers and engages Brooklyn college students directly in her research activities. And just as an aside I was a classmate of Margaret's at CUNY. We both got our doctor of public health degree together.
Speaker 1 (03:00):
And so this is really fantastic. And as with so many of our other talks, we're trying to present an interdisciplinary approach here. So, you know, Andrea, his background's in immunology Marguerite's is in public health and population health. And so again, we're trying to, to give you guys different perspectives on the same issue. So just if you can go to the next slide, Andrea, so we're putting this disclaimer in all of our presentations, we're doing our best to present you guys the latest and greatest information on COVID. But this is not intended to substitute any advice that you receive from your own medical professionals. And the one other thing I'll add is that the science is ever changing, right. So what we're saying now could change in a month. It certainly has changed from what we've said a couple of months ago, and it's not because the science is wrong or bad, or trying to be intentionally misleading, it's that we're doing studies and we're learning something new every single day.
Speaker 1 (04:00):
So what we're presenting today is what we know now. But again, not intended to replace the advice of your professional medical professionals with that I will zip my lid and turn things over to you after the last thing, if you guys have questions, we're really hoping that this will be as interactive as possible. So please utilize the Q and a function. We'd rather you use that versus the chat function, and then we'll you know, periodically I'll turn things over to to the speakers to, to answer those questions. Thank you.
Speaker 2 (04:35):
Excellent. Thanks Jess. For the introduction, I'm really excited about today's session. So we'll go ahead and jump right in. So I'm going to just give a very short primer about some of the basics of virology. If you guys attended session one, obviously I did a much deeper dive there. Obviously you'll be able to access that information with the recorded sessions, but for anybody that missed it or anybody that wants a quick refresher, this, this will hopefully kind of prime you to, to visualize some of the differences that we discuss later on. So as I discussed yesterday, viruses are a very unique class of microorganisms. They are not a cell in a traditional sense as we typically visualize them other very simplistic structure. So the makeup of a virus is ultimately some sort of nucleic acid that's contained in ultimately the center of the viral particle or virion as we call it.
Speaker 2 (05:34):
And this can be either DNA or RNA, and we discuss that in more detail yesterday. This is surrounded by this capsid and the capsid is made up of a bunch of proteins called [inaudible] that assembled to make this protective coating that, that basically ensures that the RNA or the DNA of the virus remains intact in some viruses. Particularly the ones that we're going to discuss today. They have around that capsid protein shell an envelope, and this envelope is predominantly made up of fatty lipids. And then they have these proteins that are also inserted in that those are what we call the spike proteins. And as again, we talked about those are what facilitate attachment and interaction with the host cells that they ultimately will infect. So this is very different to two cells. How we typically think about them. There's no nucleus, there's no organelles, very simplistic structure. All of this information is contained within the nucleic acids that basically allow that virus to hijack the host cell that infect and use all of the components within the host cell to reproduce.
Speaker 3 (06:44):
Yes,
Speaker 2 (06:48):
Not all viruses are the same. So in addition to having differences versus other cell types, viruses within different classes have differences amongst them. And this is something that I think a lot of people just are not that familiar with. So viruses are classified according to a variety of different parameters. The first is morphology or shape. So these are the four main classes of shapes of virus. You have helical viruses an example of a human pathogen. That's a helix virus would be the rabies virus. You have polyhedral viruses. These are typically in the shape of an ECOSA Hedron. So they're the protein capsid, and they look somewhat irregularly in shape. They're not quite as sphere. And they, they don't have any protective envelope on the outside. Some examples of polyhedral human viruses would be the papilloma viruses. So these are your human papilloma virus that causes genital warts, your papilloma viruses that cause things like plantar warts other polyhedral viruses would be things like the polio virus and also the rhino virus.
Speaker 2 (07:53):
And that's another respiratory virus that causes some of what we call common cold. The spherical viruses are basically either helical or polyhedral viruses that are protected by that envelope around the outside. So they have this lipid envelope and this actually facilitates interaction with the host cell. It expresses those spike proteins that bind to host cells. A lot of human pathogens are considered to be spherical that lipid envelope makes them look like they're, they're kind of a a circle. So examples of that would be your Corona viruses. So your, your, your virus that causes COVID-19 the other co Corona viruses that we're going to talk about as well today influenza virus is also a healable spherical virus. And then also the herpes virus family. So those are your viruses that cause her B simplex one and two, your chicken pox virus, that's called varicella zoster virus.
Speaker 2 (08:51):
The virus that causes mononucleosis, which is called the Epstein-Barr and others in that family, the fourth category is the complex viral structure. And these are actually only viruses that infect bacteria they're called bacteriophages. They look like the lunar module there. They have these little legs that allow it to land on a bacterial cell and inject it's nucleic acid. There are any of those that cause disease to humans. In addition to the shape of the virus, they're also classified by the type of nucleic acid they contain. So, as I mentioned, most cells mammalian cells, plant cells, bacterial cells, they all have DNA as their genetic code as their, a universal language viruses are unique in that they could have either RNA or DNA, and that's going to become important when we, when we talk in a little bit they're also classified by how they reproduce. So their method of replication they're classified further by the organisms that they can infect. We talk a little bit about tropism yesterday. So tropism is the the limitation of the scope of the viral infection. And you have three levels of tropism. It can be species specific, it can be tissue specific, or it can be cell type specific. And then, then finally, it's, it's also further classified by the type of the disease that they actually can cause.
Speaker 2 (10:13):
So first, I'm gonna talk about the similarities amongst these viruses that we're going to discuss. So we're going to specifically focus on COVID-19, we're going to focus on SARS and we're going to focus on MERS. And then we're also going to talk about how they relate to influence.
Speaker 3 (10:30):
So
Speaker 2 (10:30):
COVID-19 versus SARS, MERS, and influenza. These are all caused by viral infections. They all cause respiratory disease. So they're also all caused by RNA viruses that are envelopes. So their general kind of overall genetic code is, is somewhat similar in that they are all made up of RNA as opposed to DNA. This is important because it means that they can actually reproduce in the cytosol of a cell. They don't actually have to get into the nucleus. And it also is important with regard to potential mutations in the case of the COVID-19 SARS and MERS, these are all Corona viruses. So they're actually all in the same family. They're, they're somewhat related to each other. COVID-19 is caused by the virus. SARS cov two SARS is caused by the virus, SARS, cov, or SARS cov one, and Merz is caused by the virus, Merz, Coby, and Kovi just stands for Corona virus influenza, although it is an RNA virus, it's actually in a different family and has a slightly different structure it's in the family orthomyxo virus.
Speaker 2 (11:43):
So yes, it is an RNA virus, but it is distinctly genetically different from the Corona virus, family. They are also not diseases, which means that they are all diseases that in animals cause disease in animals. And we're able to mutate over evolutionary mutation, migrate and jump into human species. As we talked about yesterday, 61% of human diseases are caused by zoonotic diseases. So that's not terribly surprising. There, there is some symptom overlap. So we'll get into that a little bit later. Of course, as they are both, they're all respiratory diseases, you would expect some of that. And because of that, they are all they all have the same modes of transmission. So you can see in that figure here, the two main modes of transmission for all four of these diseases are droplet transmission direct direct interaction with, with person to person.
Speaker 2 (12:39):
And then fomite transmission, which means that those infected droplets that you're admitting by talking sneezing, breathing, coughing are transmitted into the air. They land on a fomite, which is an inanimate object or a non-person object. And then that will be picked up by another person. And then that person infects themselves by touching their face or their nose or mouth something else, because they are all viruses. They are not treatable with antibiotics, antibiotics do not treat viruses. They only treat bacterial infections. So those are the big similarities there. I'm going to compare COVID to SARS and MERS first, and then I'm going to compare COVID to influenza. This is all going to be kind of from the science perspective. And then Margaret is going to do a great job talking about the population health perspective of that. So when you take a look at the Corona viruses themselves again, they're also not a diseases.
Speaker 2 (13:39):
We have three viruses that we're going to talk about. So the first is Merz Kovi. This is middle Eastern respiratory syndrome coronavirus. This is thought to have jumped from humans by way of camels. The next one is SARS Kovi, which is severe acute respiratory syndrome coronavirus. This is thought to have jumped from civic cats into humans. And then the most recent that we're talking about is SARS cov two. So it's severe acute respiratory syndrome, coronavirus two. And that is thought to have jumped into humans from either baths or pangolin. All of these three, the original host is thought to be bad. And then they have this intermediate host in either camel's civets or potentially pangolin that then enabled it to mutate further and be able to infect humans. So we take a look at the statistics between these three. So SARS was a significant outbreak in 2002, between 2002 and 2004.
Speaker 2 (14:39):
And that was the first of these three emergent Corona viruses. We have four other Corona viruses that infect humans that cause very mild respiratory illnesses. These were first categorized in the 1960s, and I'm not going to talk too much about those today. If you want to learn more about that session one recording we'll have that information. The, our knot of SARS was somewhere between two and four. And what that means, if you recall, is the, are not values, the reproductive value. This means that for every one person that's infected, they can go on to infect between two and four additional people without mitigation efforts. And so this, this is the potential for significant spread. It means it's very contagious. It was first reported in China. It led to about eight, a little over 8,000 total infections before the outbreak sort of died off.
Speaker 2 (15:32):
And it had about just shy of a 10% mortality rate. The next one that emerged was Merz. This was an outbreak in 2012 and they are not here was actually less than one. And this is important because in our not that's less than one means that it's going to be a self-limiting outbreak. If, if a single person is transmitting to less than another person, ultimately, eventually that outbreak will soar will eventually die out. Ultimately this was first reported in Saudi Arabia. It caused about 2,500 infections and a little bit less than 900 deaths. So it actually had a very, very high mortality rate when compared to, to what we're looking at here. And of course the current outbreak that we're dealing with this started in 2019. So COVID-19 stands for Corona virus disease 2019 for the year that it was first identified. The are not that we're working with right now is about two to two and a half.
Speaker 2 (16:31):
So somewhat similar to SARS in terms of infectivity. It was again, first reported in China. We have this is actually those stats. Don't look at those. We have the updated numbers as of this morning when this data was originally pulled. We were only at around one and a half million. We're now well above 4 million infections and almost 300,000 deaths right now. One other thing that's important here is we want to look at the velocity of the viral spread. So if you look at the numb the time it took for a thousand people to become infected, it took two and a half years for this to happen with Merz because it has a very low are not value. It doesn't spread that easily. SARS was a little bit faster moving. It took about 130 days for a thousand people to become infected.
Speaker 2 (17:19):
However, with COVID-19 it only took 48 days with the are not of about two and a half without mitigation efforts. It will take 30 days for a single person to infect 406 more people by way of exponential spread. So when we take a look at the additional parameters of these Corona viruses, so we have COVID-19 caused by SARS cov, two SARS caused by [inaudible] and then murders caused by Merz Kovi that are not value that we just discussed is obviously very important. Looking at COVID-19 versus SARS they're somewhat similar SARS has the potential to actually be somewhat more infectious. Merz has a much lower or not value. Now, if you look at the case fatality rate, and we're going to talk a little bit more about that later. But the case fatality rate of MERS and SARS were significantly higher than what we're seeing for COVID-19.
Speaker 2 (18:16):
In addition, they actually have shorter incubation periods. The median incubation time of COVID-19 is about 5.1 days with a range of about four to 14 days. But the biggest factor here is that with COVID-19 25 to 50% of cases are asymptomatic. We did not experience that with SARS or with MERS. And what that means is that you could be infected unknowingly and be spreading that around the population, in addition, SARS and MERS, ultimately the majority of those cases were very severe illness. So what ends up happening is that when those people are infected, they're hospitalized, so that you've stopped that chain of transmission, because that person is not walking around in the general population. So that, that significant morbidity there is going to actually reduce the potential spread because those people are going to be ultimately out of commission while they're receiving medical treatment.
Speaker 2 (19:16):
With the case of SARS, what we saw in that outbreak, although we did have a reasonably sized outbreak, most of those cases were in healthcare workers that were in direct contact with both each other and with ill patients. And so that was somewhat self-limiting as well because here in COVID-19 because you have this asymptomatic population these people are people in the general public. So people that are interacting with other folks ultimately around each other, so all told, although they are similar you know, in the viral family, they actually cause very different disease, as well as have different demographic characteristics.
Speaker 2 (19:59):
So now I'm going to quickly touch base on influenza. So what about influenza? We have a lot of people that say, Oh, it's just a flu it's, it's just the flu. And it is not a flu. It is not in the influenza family. They are not the same viral type. And they cause very distinctly different disease, both in the cell types. They, in fact, and, and the pathology and spread of it. So influenza is a catch all term for many, many viruses that are in this orthomyxo virus, family. There are different strains and subtypes within each class. And there are three categories of influenza viruses that normally infect humans. We have influenza a, B and C influenza C is a less pronounced human pathogen. But in very rare instances, it can infect people influenza a and influenza B are the common ones, influence a are the ones that are classified by the H and the end.
Speaker 2 (20:54):
So when you hear H one N two or H two and three, or things like that, those are the influenza A's influence a B is called influenza B. And there are two main subtypes that are categorized by name. I'm not going to get into that. Key thing is that the influenza genome although it is, yeah, both made up of RNA, just like the Corona viruses it's made up of pieces. So it is eight different segments. And what that means is that these are shorter pieces of RNA, and it's very, very easy for these to exchange amongst other influenza viruses. This is called antigenic shift. What this means is that if you have two different subtypes of influenza, a that are in the same cell or near each other, they can very easily exchange pieces. And this is why the influenza viruses mutate so quickly.
Speaker 2 (21:48):
So you actually have these new subtypes that emerge simply because of this genetic shuffling that we call it. In addition to that, because these are small pieces of RNA they are very prone to mutation. And so you get this other phenomenon called antigenic drift, and these are random mutations and these lead to potentially different strains. And one of the reasons that we have this annual vaccine is because of the speed of these mutations occurs very rapidly. Every time it infects a human and it's reproducing, you have the potential to have these mutations. And so by the time you get to kind of the next year of disease those, those strains that you encountered last year are actually very different from the ones that you're encountering now. So big difference between that, and then the Corona viruses is that the Corona viruses RNA is a single piece.
Speaker 2 (22:41):
So it's, it's not, it doesn't have this capacity to randomly shuffle it's pieces of, of genome. The other thing that influenza that's unique about influenza is that it exhibits a seasonality. It exists year round in every country ultimately, but you see peaks during kind of the fall winter months where we call it the flu season. You always have this kind of sub threshold of, of people that do get influenza during the summer and things like that. And so that's something to keep in mind as well. Now, the other thing is that you have an annual vaccine, so a vaccine will generate herd immunity. We're going to talk more about that in session 11 of course. But this actually reduces the morbidity and mortality of influenza because this generates protection in populations. So as I mentioned, influenza is a very complex group of viruses.
Speaker 2 (23:38):
As I mentioned, there's three main classes that infect humans, influenza, a, B and C. They have obviously different hosts, as I mentioned, influenza is also a zoonotic disease. The genome is made up of segments. And so this causes that, that high rate of mutation, and that's why we need a new vaccine every year. You'll notice that influenza a and B are the ones that cause the most disease in humans. Typically in a, in a season, we see a seasonal influenza strain with both influenza a and influenza B. Generally the influenza a strains are the ones that cause pandemics. And, and every now and then you can have very severe outbreaks with influenza B for example, this year's influenza B was, was quite severe.
Speaker 2 (24:28):
Now I'm going to kind of compare COVID-19 to influenza in the context of the science. So when you compare COVID-19 versus the flu again, influenza is caused by many different viruses. These change every year, this is very important. COVID-19 is caused by one virus, SARS cov two right now, no, no additional strains. It's just SARS cov two. Based on where those patients were were from, we have different isolates of the virus, but they're all the same virus, a big parameter that's different between the two is the incubation time. So COVID-19 has a very long incubation time, immediate incubation time of 5.1 days, which means that while that person has gotten infected and while the virus is reproducing, that person is contagious and doesn't have symptoms for almost a week. And it actually can be up to 14 days. In addition, you have a significant population that actually will have asymptomatic disease, which means that they can be full on infected, not know they have it and be a spreader influenza.
Speaker 2 (25:36):
However, has a short incubation period of about an average of 48 hours anywhere from one day to three days, really. And what that means is that you have the potential to infect less people because you're going to develop symptoms much faster, and ultimately you're going to stay home, or you may need to get medical attention. In addition that are not value that we talked about, the number of potentially transmissible people, an individual can infect COVID-19 right now, we're estimating between two and two and a half. Flu is only 1.3. So while it can be transmitted and you will have an increase in, in the outbreak, it's much, much less as far as potential spread than COVID-19. In addition, the hospitalization rate is much lower with the flu versus COVID-19 and the case fatality rate is also significantly lower right now we're observing about you know, on average 3.4% case fatality rate with COVID-19.
Speaker 2 (26:40):
Now, again, that is based on how many tests were being able to administer. So we may not actually be capturing the total number of cases because there are so many asymptomatic people. However, and I'll, I'll mention this in a moment in more detail. Even when you look at the bottom level estimate, that case fatality rate is still significantly higher than, than compared to the flu. Now, again, you do have some symptom overlap and that can be very challenging when you're trying to determine, you know, diagnostics whether or not I qualify for tests and things like that. So here's a nice Venn diagram that kind of compares and contrast the two. So again, you look at that incubation period, incubation period for COVID-19 is much, much longer. There's only a single virus. Complications are much more common in COVID we're seeing even aside from the common symptoms, there are other significant symptoms such as blood clots, pulmonary embolisms there's some very pronounced inflammatory responses in children now that we're observing lots of GI issues, et cetera.
Speaker 2 (27:49):
A lot of the severe symptoms and COVID-19 are actually because of the overreaction of the immune system. It leads to a condition called cytokine storm. And this often leads to some of these fatal cases that we're seeing. Now you do have a little bit of symptom overlap, as you can see here, where we have things like congestion, the Teague fever, aches, headache, et cetera. But again the biggest factors are, are the, the S the incubation time, the are not value. And of course the severity of disease. As I mentioned, again, they are transmitted in both methods, dry respiratory droplets, and fomite, that is true for, for bolt. Now, the biggest thing here that I want to emphasize is that with influenza, we have a flu shot. We have a vaccine. And what this does is it prevents and protects us from the most common strains of the flu that, that we have identified for a given year.
Speaker 2 (28:46):
Now, although the flu mutates very quickly, even if you get a strain that the shot does not protect specifically for you actually will have reduced severity of illness, even if you end up getting the flu if you have the flu shot as protection. In addition, we do have some antivirals such as Tamiflu. These will, these will help to inhibit the viral reproduction and ultimately reduce symptoms severity as well. So treatment with those, if you do get the flu, they can also help reduce disease severity. In the case of COVID-19, we have no flu shot, we have no effective treatments yet. We're trying to repurpose some existing treatments and clinical trials to see if they're effective. Again, we're going to talk a lot more about that in session 11. But right now, the only prevention is social distancing and self isolation.
Speaker 3 (29:39):
Andrea, we do have couple of questions. Do you think we should take a couple now or wait till the end? It's up to you?
Speaker 2 (29:48):
We could take a couple now I have just this one more slide and then I'm handing it over to Margaret for the population health aspect.
Speaker 1 (29:55):
Perfect. Okay. well let me just jump in because some of the questions pertain to what you just covered. So first we have a question, is there asymptomatic flu? And if so, can it be spread while asymptomatic?
Speaker 2 (30:08):
That's a great question. So, you know, there is, there are very mild cases of flu in some instances, and some clinicians may categorize that as, as asymptomatic or mild, those cases of course can still be contagious. And even though it's a short incubation time, you still can be contagious during that 48 hours as well. So, so that's very similar amongst them. The biggest thing is the duration and the proportion of asymptomatic cases. Even if you get a mild case of the flu, you're, you're gonna feel it generally, you're going to have a fever. You're gonna feel pretty crummy. So you'll probably take a day or two off work, even if you have a mild case. Whereas with, with COVID-19, you know, now we're seeing that it might be almost 50% of cases that could be completely asymptomatic.
Speaker 1 (30:59):
Thank you. Just a couple more, and I know we want to leave time for Margaret. So just quickly we understand why the flu mutates so quickly, but do we know what causes viruses like COVID to mutate and affect humans?
Speaker 2 (31:13):
Absolutely. So that all comes down to the fact that all of these viruses that we're talking about are RNA viruses. So the reason that mammalian cells and generally evolution has led to most organisms, having their genes encoded in DNA is because DNA is a more stable and protected molecules. DNA is made up of two strands that are complimentary to each other. They're like mirror images and they're protected in the nucleus by both the nucleus itself. And then also by the complex structure of the DNA. So it's typically tightly wound in a ball it's not kind of floating around in strings. For that, that DNA to actually be expressed, it has to go from the, the DNA to the RNA portion, through the process of transcription. And then the RNA is turned into proteins, which are the functional component through a process called translation.
Speaker 2 (32:09):
This is, this has multiple checkpoints and you have error correcting mechanisms when you're specifically going from DNA to RNA, with viruses that are made up of RNA, you skip that DNA to RNA step. So you don't have these error checking mechanisms. And so RNA viruses in general are more prone to mutation than DNA viruses because you're missing that step. So it's going straight from that RNA to a protein. So what that means is over time as these viruses are mutations are going to accumulate. Now, a lot of those mutations are going to be evolutionarily disadvantaged for the virus, meaning it's, it's either going to be detrimental to them. It's going to, it's going to reduce their infectivity or it's going to not enable them to infect their, their host anymore. But some of those will be advantageous, meaning it will lead them to have a new mutation that now and now allows them to infect a new species or a new cell type. And that's what we're observing here is that just through random error mutation eventually a strain popped up that was able to jump into a human, and then it took advantage of that because we are a susceptible population.
Speaker 2 (33:20):
Thank you, Andrew. We do have other questions, but let's pause. I want to make sure we have enough. Absolutely. All right. So the last thing I want to talk about right now is the case fatality rate. And I know Margaret is going to talk a lot more about that. I do want to have the caveat that these numbers are based on obviously estimates that we have from the tests that we're implementing. So of course we're not testing every single person, but if you look at by demographic or by age group here, even at your high-end and your high risk you know, elderly population with the seasonal flu, you really have an upper limit of about 0.8% fatality rate. Now, of course, we do have a vaccination which helps protect. So that's going to reduce that as well. When you look at COVID-19 if you're in your high demographic group, you're seeing on average 6% case fatality rates.
Speaker 2 (34:10):
So this is four to seven times higher than the flu. When you average this out, based on all populations, you're seeing an average of 2.3% versus 0.1% across the entire age group. And that's 12 to 24 times higher. Now, of course, that's the caveat here where if you actually look at your, your range of estimates, so because we're not testing everybody, we have asymmetry in asymptomatic carriers that we're not capturing as part of our total case burden. That could be a range. So if you look at the seasonal flu with an estimate of a point, 1% overall mortality rate, your bottom of estimate range for COVID-19 is 0.5%. So that's still five times higher, even if we assume that we're missing half of all the cases. If you look at the top of the estimate range, we're up to about 4% and that's including factors like access to medical care demographic issues that were discussed in, in very great detail during session five yesterday and things like that. So even if you normalize for the fact that we're not capturing probably all the cases, it's still significantly more, more fatal than the flu. So now I'm going to pass it over to Margaret. Let me give you control.
Speaker 3 (35:29):
All right. Should we good? Okay, great. Oops, something happened. All right. Let me restart for you. Let's see. Hold on. I'm going to take control back for a sec. Sorry about that. No, no, not at all. All right. You should be good now. Okay,
Speaker 4 (35:53):
Great. Thank you so much, Andrea. And thank you so much. Jess, and thank you for the organizers and everyone who is here much appreciate the opportunity. I'm going to keep it brief. But I have the story of New York city as a case study. And so the question that's circulated in many places, and that sort of seems to give people some sense of comfort is to like in COVID-19 to the flute. And so I'll take you through just looking at the case study of New York city to say, well, what is it actually just like the flu, the late January public health officials in the U S were in the midst of the flu season and concerns about COVID-19 were actually limited. In fact, the general assessment that we made at the time of the outbreak was that with the efforts in China, the flu was probably still the biggest threat for the U S population, but this position changed relatively quickly is us cases emerged in various locations at the same time.
Speaker 4 (37:00):
And community dispread was also identified and very rapidly became clear in New York city in particular that this was going to be much worse than the flu in more ways than one. So before we look at it exactly how they compare in a population and thank you, Andrew, you really set this up for I have little to explain but I'd like to establish two things when we talk about death. And there are many more things to talk about, but mortality is the state of being mortal. And I went to the dictionary because I thought, okay, let's get this clear. But it also means that the death of large numbers of people, but neither of these, give us a good sense of the severity or magnitude when we talk about populations. So in epidemiology, we use a number of measures of death and severity but to compare epidemic impact on a population specifically we may speak of mortality rates because we have two known numbers or, and mortality is the number of deaths.
Speaker 4 (38:09):
We're pretty certain when people have died and we are pretty good at establishing cause of death. And so we would establish the rate of number of deaths due to a specific disease or a cause divided by the total population at risk. And those, we are pretty certain about how many people we have. And that last part is really important because by establishing a proportion, we're able to compare impact of a disease in large and small countries, States, cities, et cetera. We can compare Luxembourg to the United States by establishing these rates and we can get a meaningful number and then multiplied by a hundred thousand and get how many people die per 100,000 population. Now this factor we multiply with varies greatly depending on how rare or common the disease is, but in the case of flu and COVID-19 a hundred thousand works pretty well. So, so let's take a look at the us usual flu season.
Speaker 4 (39:14):
The annual mortality rate from seasonal flu, the, we used to publish that they estimate of the us population was about 329 million people. And the estimate of flu deaths is about 44,510. And I want to just clarify that estimated influenza deaths actually includes influenza and pneumonia. They're aggregated in the data because influenza very often progresses to pneumonia and there's a whole classification issue. But let's for simplicity sake, say that the flu deaths are 44 or five 10. And that gives us a us flu mortality rate of about 14 deaths per 100,000 persons in the population. Now let's take a look at COVID-19 mortality rate. So as of this morning at seven 32, am I the number of COVID-19 deaths in the United States are reported at 82,389, Which is approximately 25 deaths per 100,000 population.
Speaker 3 (40:33):
That's 1.8 times greater mortality from COVID-19 compared to the flu. When we look at the U S population as a whole, now I promised I would talk about New York city as a case study, and one of the country's largest mics with tropical ease as an example of what could happen and how this actually compares. So in New York city each year, there's an average of 2000 flu deaths. And again, the department of health in New York city department of health and mental hygiene also aggregates because they're reporting to the same system influenza and pneumonia together in a population that's estimated to be about 8 million, 175,000. We have about 48% of the population that's vaccinated for the flu. And what else would I'd like to insert? Is that the food season's about 21 weeks from November through April, March or April depends on the year and each year 2000 York city residents died due to the flu.
Speaker 4 (41:50):
So if we calculate the flu mortality rate for a hundred thousand, so we take the number of cases over the population and multiply by a hundred thousand, we get a case, a flu mortality rate of 25 that might sound familiar. I don't have to tell you that 2020 has really dealt as an unprecedented global challenge and New York city has taken a toll. So as of this morning, the New York city department of health has reported 20,237. COVID 19 deaths, 15,100. One of those are confirmed by a COVID 19 positive test. And 5,136 are probable classified based on COVID-19 consistent symptoms and progression of disease. But unfortunately, due to limited access to testing, these patients were never tested so far. The COVID 19 season has lasted 11 weeks since the diagnosis of the first case on March 1st.
Speaker 4 (43:00):
And so to 20,237 new Yorkers have died from COVID-19. If we relate that to the total population, we've arrived at a mortality rate of 247.5 per 100,000 population now in New York city. That means that 200, if we rounded up that 248 versus 25 people have died from COVID 19 versus the flu. Now with these numbers were progressing, it was a little harder to see the relationship, but it's getting clearer and clearer. How, what the ratio is between these two lumbers. So I don't have to tell you really, you can do the math in your in your head that the mortality ratio, the ratio between the mortality numbers in these two from these two diseases is 10 times. So in New York city, so far COVID-19 has caused 10 times more deaths than the regular flu. And this of course is an addition to the flu season. We just end it.
Speaker 4 (44:13):
So what about time when we speak of seasons? Right? What about the duration of these outbreaks? So let's just revisit the numbers. New York city has seen 20,237 deaths from COVID-19 over 11 weeks and 2000 flu deaths over 21 weeks with the respective mortality rates. So if we divide by the time and then find the ratio between the two new mortality rates. So 22 and a half or 23 people have died from COVID 19 per week per 100,000 people. And only a little over one food case has died per week over the over the 100,000. So then we find that in reality, it's not 10 times, but it's more like 19 times more deaths were caused by COVID 19 than the flu. And this is in the context of extensive shelter in place, closed schools, closed colleges, universities closed businesses, closed playgrounds and parks, and only essential workers and services and operation since the middle of March. So nine of the 11 weeks, New York city has literally stayed at home. And in this situation, COVID-19 has already caused 19 times more deaths than the regular flu. And that of course is in the context of the larger country in the U S where similar efforts have been in place to varying degrees, the total death toll as of today, as I mentioned earlier, is over 82,000. So with that sobering picture, I'd like to turn the slides over to Andrea.
Speaker 2 (46:08):
So just to quickly summarize and Margaret, that was, that was wonderful. That was a great summary. It was so clear. You know, I think New York city is obviously a case study, you know, to be looked at when we see some of these other maybe less populated, but certainly more chomping at the bit to reopen you know, County States, et cetera. You know, obviously we don't want to see this sort of spike amongst those places as well. So yeah, so just to reiterate as of right now globally, we have just shy of 4.3 million cases as of seven 30 this morning, and just shy of 300,000 current confirmed deaths. Now, again, I reiterate the confirm because this is all based on the testing access that we have. I'm just going to quickly summarize, and then we're going to spend the last 10 minutes going through the rest of the questions I see there's some coming through.
Speaker 2 (47:03):
So again, viruses are unique class of microorganisms. They hijack and require a host cell in order to survive and reproduce when we compare SARS, MERS and COVID to each other. These are all in the Corona virus, family. These are all recently mutated and emergent diseases that are zoonotic in nature, meaning they started an animal species and they were able to be transferred to humans. Because of that, we have complete susceptibility. We were never encountered them before. We have no baseline immunity. Everybody in the population is susceptible when you compare influenza versus COVID. In addition to the statistics, in terms of case burden, mortality rates, et cetera, both spread through similar mechanisms, droplet and fomite transmission, both cause respiratory illnesses. There are some shared symptoms amongst the two of them. Obviously there are very distinct differences between them, both are not treatable with antibiotics.
Speaker 2 (48:00):
When we look at symptoms COVID-19 and influenza do share some common symptoms, such as fever, cough, fatigue, myalgia, which are muscle aches headache and chills. However, we are seeing that COVID-19 has some very unusual and severe additional symptoms. We have a lot of GI issues. We have inflammatory responses, things like cytokine storm and autoimmune responses in children. We're seeing things like blood clots, pulmonary embolism, stroke, et cetera. And that's all contributing to the increased morbidity and mortality and demand on hospital resources. When you look at infectivity, the median incubation time of COVID 19 is much longer than influenza. It has a range of two to 14 days with a median of 5.1 days. This means you can be walking around unknowing, infecting other people with influenza. It's a much shorter incubation time of 48 hours as a median and a range of one to four days.
Speaker 2 (49:00):
When you compare prevention, COVID-19 has no effective treatments and no vaccine yet influenza has an annual vaccine which reduces morbidity and mortality as well as potential antiviral treatments for severe cases of influenza. So we pulled a lot of that data from these sources. Again, we're happy to share those. I've been responding to a lot of questions in the Hoover app. I found it really fun and interactive. So if you do want to chat and get some of that data, feel free to reach out to us there. And we can take any questions now.
Speaker 1 (49:33):
So we have a bunch of questions here in the Q and a, and also on social media. So just a couple of things I want to, you know, we, we have some questions here about questioning the origin of COVID-19, you know, there's been a lot of chatter. We know in social media, some people are wondering whether this started it in the lab. And you know, Andrew, you did comment on that in yesterday session. Just in the interest of time, I'm going to say, if we can go back, you know, we, we do have that answer. Do you know the session was that session session one that was session one recordings of all sessions will be disseminated and made available on Friday. So we encourage you to go back to that. So just in the interest of time, I'm going to ask that you do that. Okay. So if this is the mortality, when we are staying at home, what is the projected, when things open back up we actually have a session tomorrow, the final session of the summit session, 15 we're on a walk through different scenarios belonged story short. We're obviously terrified of that, right? If we can look at other countries and they're experiencing, you know, when they opened up, even once the incidents of COVID really dwindled, they saw a resurgence and it simply recycled, you know, it looks like this, like a rollercoaster and they're seeing, you know, the epidemic start again. So that's why we're so cautious about reopening society. We're trying to avoid that. You know, I know there have been tons of modeling about projected mortality, projected incidents, prevalence if we open up and those numbers are very scary. So again, definitely tune in tomorrow session 15 for more details on that. Okay. Next question. Why didn't stars take off in numbers the way COVID-19 did, did SARS have an asymptomatic state?
Speaker 2 (51:27):
That's a good question. And I think I touched a little bit on that, but I definitely am happy to elaborate. So the biggest reason that this didn't take off is that the majority of cases of SARS were in hospital workers. So you have somewhat of a self-contained outbreak there where you don't have, you didn't have an asymptomatic population in the general population walking around. In addition, the incubation time of SARS was much shorter. And once people became ill with SARS, the majority of those patients ended up in the hospital as patients. So they're, self-contained from there, they limit that transmission chain because they're not just mildly ill or asymptomatic and still interacting with other people. So diseases that typically have a very high morbidity, meaning they cause significant disease. They actually generally are less contagious because you basically limit the ability of that pathogen to spread to the next person in the chain of transmission. Thank you. Okay. Next question. How does COVID compare to the 1918 flu in New York city? Margaret, are you able to comment?
Speaker 4 (52:38):
Yeah. Yeah. So I actually thank you for that question, but sort of a secondary level, right? Cause that's the Seminole pandemic that we seem to refer back to. So I pulled the numbers from the New York city department of health, and I want to preface this by saying that the, the way of, obviously we didn't have the same kind of confirmation of flu strains or even the presence of the virus, but the data from the health department of the actual flu deaths was about 12,000 activates an exact number 12,562. And if we relayed that to the population at the time, which surprisingly was five, 6 million people living in New York city at the beginning of the 20th century, the the mortality rate was 224 per 100,000. So you may remember that I said 248 per 100,000 was the COVID-19 deaths and 224 from the, the 1918 flu pandemic. So that means that COVID 19 at this point is affecting New York city much more severely than the entire duration of the 1918 pandemic or flu.
Speaker 2 (54:02):
Thank you. Thank you very much. Okay. Next step. How do we know we, aren't counting COVID deaths as flu deaths and vice versa.
Speaker 2 (54:15):
I can kind of comment on some of that. So you know, typically at this point in the year, the, the seasonal flu has, has dwindled pretty significantly. We have pretty good testing available for influenza, both a and B strains. And generally fatalities from influenza are caused by secondary bacterial pneumonia. This is a very different pneumonia that then we see in COVID patients. What happens is the influenza virus kills certain cells in your respiratory tract, and then you become more prone to additional secondary infections because those cells no longer can protect you. So identifying a bacterial pneumonia versus an inflammatory pneumonia that we're seeing in COVID is very distinct different, both pathologically and, and also tests test wise. So it's very easy to kind of distinguish the two different mortalities. In addition, a lot of the COVID cases in terms of mortality are due to other factors, things like pulmonary embolism, we're seeing some stroke related deaths, and a lot of these are characterized by overreaction of the immune system, which is, again, something we can characterize by taking clinical samples.
Speaker 2 (55:25):
So in that same vein, we got a bunch of questions about the classification of COVID depth. So there's been a lot of misinformation out there about how we're over counting deaths, how, you know, physicians and hospitals are being paid to classify in that, you know, people who have underlying conditions such as diabetes for example, are being classified as COVID depths. So they're asking, are we overestimating? It sounds like you want to answer. I just want to, if I could just chime in and say, sure, I would say that if anything, it's the total opposite. You know, if anything, we're underestimating the number of COVID deaths, because so many people are at home. Now we are under counting all the people who have died in their homes. So if anything, and just want to debunk hearing now that hospitals and physicians are not getting payments to classify deaths as COVID deaths Andrew, it sounds like you wanted to chime in.
Speaker 2 (56:20):
So, yeah, and I agree with that completely. I would say we're actually underestimating deaths. Now, when you look at a cause of death, you're looking at the finite thing that ultimately killed an individual. Now, those things are not in a vacuum that, that, that complication or that ultimate cause of death is, is due to something else. So it's something like we look at influenza, for example, people aren't dying just from the flu virus, they're dying because of secondary bacterial pneumonia. And those are in the high risk populations like infants and the elderly who have weakened immune systems. And they can't fight off that second infection. It's still because of influenza. If they didn't have influenza in the first place, they wouldn't have gotten the bacterial pneumonia and they wouldn't have died. It's the same situation with, with COVID, if they weren't infected with COVID their diabetes wouldn't have been a cause of death, at least at this point in time there atherosclerosis or other underlying conditions it's because their body is under attack by the virus. So ultimately even if they died because of cytokine storm, the cause of death or the cause of that cytokine storm is the virus is COVID-19.
Speaker 1 (57:33):
Exactly. So we're, we're coming up on the hour here. So we, we have a question about, would we open college campuses in the fall? Andrea and I are actually giving a talk later today on the do's and don'ts of COVID that's at 3:00 PM Eastern time. And I think we could touch upon that there, perhaps. So tune into that and if you can't attend live B be sure to access the recording. We'll make sure we touch on this. But just the last question, Andrea, and like 30 seconds. Do you believe that once flu becomes prevalent again, that an individual would be able to attract both the flu and COVID at the same time?
Speaker 2 (58:10):
Yeah. And that's the biggest concern about the reopening is that the timeline for potential spike would likely happen around kind of the end of summer early fall when we're starting to see flu cases now, because they infect different cell types, they have different infection mechanisms and they are distinctly different viruses. They're not going to say, Oh, well, you know, I got this person. So you kind of go onto the next person. What ends up happening is it becomes a co-infection and then you have these comorbidities where the infection from one is basically taking all of the energy from your immune system. And now you're more susceptible to another infection. So what we're going to expect to see is actually higher rates of potential morbidity and mortality when those two viral infections or outbreaks align with each other.
Speaker 1 (59:00):
Thank you. Thank you both so much. We hope you enjoyed this session. If you have any other questions, definitely do reach out by email or via the HUV app. And we hope to see you in the next session. You should have a link in your email waiting for you, or you can use the Hoover app. Thanks again.
Speaker 2 (59:17):
Bye everybody.