#97 - Peter Hotez, M.D., Ph.D.： COVID-19： transmissibility, vaccines, risk reduction, and treatment
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Summary
Dr. Peter Hotez is a renowned vaccine scientist, pediatrician, and an expert on the current coronavirus outbreak. His titles are almost too numerous to list at this point, but I ll make an attempt to do so. He is the Dean of the National School of Tropical Medicine and Professor of Pediatric Pediatrics at the Baylor College of Medicine, where he is also the Director of the Texas Children's Center for Vaccine Development and the Founder of the Tropical Pediatrics Endowed Chair of Tropical Pediatrics.
Transcript
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Hey, everyone. Welcome to the drive podcast. I'm your host, Peter Atiyah. This podcast,
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my website, and my weekly newsletter all focus on the goal of translating the science of longevity
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into something accessible for everyone. Our goal is to provide the best content in health
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and wellness, full stop. And we've assembled a great team of analysts to make this happen.
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If you enjoy this podcast, we've created a membership program that brings you far more
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in-depth content. If you want to take your knowledge of the space to the next level,
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at the end of this episode, I'll explain what those benefits are. Or if you want to learn more now,
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head over to peteratiyahmd.com forward slash subscribe. Now, without further delay, here's
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today's episode. My guest today is Dr. Peter Hotez. Dr. Hotez is a renowned vaccine scientist,
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pediatrician, and an expert on the current coronavirus outbreak. His titles are almost
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too numerous to get into at this point, but I'll make an attempt to do so. He's the dean
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of the National School of Tropical Medicine and professor of pediatrics and molecular virology
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and microbiology at the Baylor College of Medicine, where he's also the director of the Texas Children's
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Center for Vaccine Development and the Texas Children's Hospital Endowed Chair of Tropical
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Pediatrics. I learned of Peter a few months ago for unrelated reasons that pertained to
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microbiology, vaccination, et cetera, and had wanted to interview him at the time and kind
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of postponed it for a number of unrelated reasons. More recently, about three weeks ago, I saw him
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talking about coronavirus, which was really around the time I started to think I had miscalculated.
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This would have been mid-February, the second week of February, and I started to realize at that
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point in time that this was going to be a much bigger deal than I had naively assumed in January.
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I reached back out to him and said, Peter, let's get on a podcast when the time is right,
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and assumed that that would mean when we had enough facts that it was worth talking about.
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But what I did not really anticipate was the past seven days until they were upon us,
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basically about a week ago. So if you're listening to this on the 14th of March, that would have been
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about the 6th of March. A lot of things really changed in my mind. And I reached back out to
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Peter and said, hey, we should probably talk at the end of next week, which gives you enough time
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to manage the very important responsibilities that you have, but also allows us to sort of
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fill in some pretty big gaps in knowledge. And we attempt to do that. And this podcast is actually
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quite short by the standards of our podcast. It's about an hour long. And I think what we'll probably
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do is shorter, more frequent podcasts at this point in time, because the information is changing
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at a very rapid rate, such that anything we talk about on this podcast is likely to be
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background information at best a week out. So we do talk about a number of things. We talk obviously
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about the etiology of the virus, the difference between the virus, which is SARS-CoV-2 and the disease
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state that it causes COVID-19. We talk about how it's spread. We talk about where it came from,
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what we know about it, what we don't know about it, what some of the treatment options
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may be, may not be, why a vaccine is probably not likely in the near term. We talk about something
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called convalescent serum, which is something that looks kind of promising. And at this point,
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anything promising, we want to put sort of all hands on deck with interpreting. So with that said,
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let's just get to this interview with Peter and we'll be following this up with a number of other
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interviews. Also, I should point out on pretty much every day, I'm putting updates up on Instagram,
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where you can find me at peteratiamd.com is the website. And that'll point you to Instagram,
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or you can just go to Instagram at peteratiamd. And that'll be kind of daily updates. But as I said,
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expect to see podcasts at a slightly irregular cadence, just as a way that we can sort of
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communicate with you. This podcast and all podcasts pertaining to the coronavirus will have show notes
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available to all listeners. So these podcast show notes and the subsequent ones that pertain to
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this subject matter will not be behind the paywall for subscribers. So this will be available to
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everybody. We will attempt to provide show notes as quickly as we can. So hopefully that allows
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everyone to access this information without any bottleneck. Without further delay, then please
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enjoy my discussion today with Dr. Peter Hotels.
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Peter, thank you so much for making time to speak with us. You're in unbelievably high demand. I saw
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you on the news at 530 this morning, your time, and I don't think you've stopped since. And of course,
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you've been nonstop for weeks now, and you've been very generous in making time to speak with me and my
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team prior to today. So again, greatly appreciated on behalf of many people listening. Let's start with a
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little bit of just the nomenclature. People are a little bit confused, I think, about the nomenclature
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between COVID-19, SARS-CoV-2. Maybe explain which one's the virus, which one's the disease, and what
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the history is here. Sure. COVID-19 is official designated name of the disease by the World Health
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Organization. The causative agent is the SARS-CoV-2 virus, SARS-CoV-2. Just like there's AIDS and there's
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HIV, there's the name of the disease, and the name of the virus. And the fact that it's called SARS-CoV-2,
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as I often like to call it, has some meaning because there's a lot of similarity in the type of virus it
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is compared to the original SARS, which I often call SARS-CoV-2, that originated out of southern China
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in 2003 and caused a very serious pandemic, a deadly pandemic, that affected Toronto, Canada,
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among other places. This is a somewhat different type of disease in terms of transmissibility and
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fatality. We can talk about some of the differences between SARS-CoV-2. Maybe we should do that because
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I think transmissibility and lethality are two things that are very important to understanding
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this, and maybe touching on the distinction between SARS-CoV-2 will be helpful.
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Yeah. So actually, we've had now three major pandemics caused by coronaviruses in the 21st
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century. Up until then, when I was being trained in microbiology and infectious diseases, we knew
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about coronaviruses, but they were considered of relatively minor importance. They were coronaviruses
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that caused upper respiratory infections in kids, and rarely they would cause lower respiratory tract
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infections. But we had our first really serious experience with a coronavirus in 2003 when SARS-1
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caused a serious pandemic that disrupted the economy of China and Canada and elsewhere. Another second
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coronavirus occurred in 2012 with Middle Eastern Respiratory Syndrome that emerged out of Saudi Arabia,
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and that was around 2012. And now this is the third one, SARS-2. So the point is we've had a new
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coronavirus pandemic every decade of this 21st century. So hopefully we're starting to realize
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these are pretty serious actors here in terms of global health threats. And that has a lot of
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relevance when we talk about ultimately developing vaccines and why we should prioritize coronaviruses
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Peter, six days ago, I spoke with a colleague of yours who will remain nameless just because we didn't
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speak on the record. And I asked him point blank, what is your level of concern today? And keep in
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mind, this was a discussion on March 7th, six days ago. I said, what is your concern with SARS-CoV-2
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relative to the coronaviruses responsible for MERS and SARS, which were very deadly viruses? And he said
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something to the effect of, I am much more concerned with what I'm seeing today. Do you share that
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sentiment? And do you think that that is an overreaction?
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I think it is an appropriate reaction. And I would have shared that concern six days ago,
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but for very quirky reasons. So you might say, well, everyone knows, or a lot of people know from
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the, from all the public news that SARS-2 is not as deadly as SARS-1 or as MERS, but it's a cause of
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serious mortality. We'll go into that a little bit more. And it's also highly transmissible.
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So while it isn't necessarily the most lethal virus we've ever seen, nor is it the most transmissible,
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it's high in both categories. And that combines in this very unique way. Let me explain that a little
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bit better. So SARS-1, the original one was highly lethal. And if you had it, you were sick as hell and
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you were going into the hospital in the ICU. And that meant that you didn't have a lot of people
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walking around transmitting SARS-1. And that's one of the reasons it tended to burn out pretty quickly,
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although it could cause serious nosocomial outbreaks in hospitals. And MERS-2 more or less
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went by that same playbook. This one is fatal only for certain groups, a serious disease in certain
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groups. And what that means is you have a lot of other, a large segment of the population walking
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around shedding virus, including kids. So kids, for reasons that, and adolescents and young adults,
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for reasons that we don't understand, are getting the infection, transmitting the virus,
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but they're not getting very sick. And there's always the outlier that will,
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but more often than not. So the problem is you have a lot of virus circulating and only certain groups
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seem to be getting serious disease. And those tend to be individuals over the age of 70,
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those who have underlying disability, including diabetes or hypertension or heart disease,
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maybe those on immunosuppressive therapy, although we don't know as much about that.
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Also quite interesting, healthcare workers. So a lot of healthcare workers are getting infected
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because this is so highly transmissible and they're coming into contact with patients.
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And for reasons that we don't understand, healthcare workers are getting a higher level
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of serious disease than you would expect given their age groups. There's been a lot of medical
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mysteries about this virus, why kids are not getting seriously ill, why adolescents, young adults not
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getting seriously ill, but why healthcare workers are getting seriously ill. So we saw this
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in Wuhan in China, where this virus emerged, at least a thousand healthcare workers became infected,
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and about 15% of those developed serious illness or in the intensive care units. So they seem to get
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much sicker than you would have expected. And whether that's due to a higher level of exposure or a higher
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inoculum of virus, and whether that is reproducible in the US, we'll have to see. So those are the people
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that seem to be the most vulnerable, the very old, those with underlying disability and healthcare
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workers. And that also is a perfect mix because you're knocking out a lot of people out of the
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healthcare workforce that have to self-quarantine or are getting sick. And we were seeing these tragic
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situations play out in China or elsewhere where healthcare colleagues are taking care of healthcare
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colleagues in the ICU. And that is also highly destabilizing.
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Yeah. And it's also very non-linear because if you lose 10% or 15% in that situation of your healthcare
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workforce between physicians, nurses, respiratory therapists, et cetera, the knockoff effect of that
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is much more than a 15% hit to the ability to provide care. So...
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That's right. And then the other population we're seeing at high risk, we're getting sick,
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are the first responders. And the first responders are coming into contact with
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very severely ill people, they're getting infected, and then they have to self-quarantine.
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So we're seeing large numbers of first responders knocked out of the workforce. And then it's going to
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reach a point, potentially, where we're going to have this perfect storm of not having enough healthcare
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workers and first responders to help us. And so for all of these really odd features of the virus,
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it starts adding up to become a very serious epidemic and highly destabilizing for any country
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that has large numbers of people. And of course, we didn't help our case at all by the US being so
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behind in diagnostic testing and allowing this virus to circulate for long periods of time.
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As of today, Peter, do you know how many tests are available? I know that as of yesterday morning,
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we were at about 75,000. How long until we hit a million, which in theory was promised as of yesterday?
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Who knows? The promises keep coming. And this also has a lot of serious consequences because
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my colleague, Mark Lipsitch, has done some nice studies with his doctoral student, Ruan Li,
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in China showing that the cities that get hit hard in terms of depletion of healthcare workforce and
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run on hospital beds and ventilators are those that allow transmission to go on for long periods of
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time without intervening. So whether or not you're a city that is totally overrun in terms of having
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patients on ventilators and hospital beds and depletion of healthcare staff is very much depends
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on how quickly you picked up transmission. So in Wuhan, where transmission went on for six weeks,
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without people intervening, it was a catastrophe. So it was, and we all heard the stories of what went
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on in Wuhan and creating 10 cities of hospitals as opposed to Guangdong, where they picked it up after a
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week and there were 20 people in the ICU. So it's night and day. And in the U.S., now we probably
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think transmission likely began in the middle of February if our first known indigenous case occurred,
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I think it was around February 26th. So back date around five or six days, the average incubation period,
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we're getting up there now three, four weeks where transmission has been going on undetected because
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we haven't had the testing available. And that's what I'm worried about is in two weeks from now,
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all of a sudden we're going to see hospitals inundated with large numbers of sick people.
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We don't know for sure, this is a new virus, but that is the consequence of the failure
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that our government has had in terms of getting testing available.
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And Peter, that's a really important point that I just don't think can be overstated,
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which is coming back to this point of the importance of social distancing now to buy time.
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Because if we could do anything at this point, there is no stopping this. The opportunity to prevent
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this virus from entering this country or reaching a sufficient number of the population seems pretty
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slim at this point. It's a question of if 100,000 people are going to be infected and it happens over
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a year versus a month, that has enormous consequences. Do you think there is still an opportunity to shift
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that curve? If we can get a big order of magnitude level of testing in the next week and we can see
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which communities have significant levels of transmission, potentially we could intervene.
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So yeah, we still have to try, but boy, it would have been nice to have that three or four weeks ago
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when there was maybe just a handful of communities that had transmission. We could have focused all of
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our energy on that. And so we did lose an opportunity, I think, to prevent this from becoming a large
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epidemic. And I get asked about this a lot. For instance, I got Alison Camerata on CNN asked me this
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morning, whose fault is this? And I think my response to her was a bit surprising. I said, look,
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now's not the time to start assigning fault. There's going to be time for that later and
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we can have a federal investigation of where the breakdowns occurred. But I think right now,
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we've got to focus on what the task at hand is. And I introduced this new concept this morning,
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both on CNN and on Fox News. And I did it after calling my friend and colleague, Arturo Casa Duval,
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who's a professor at Johns Hopkins, who's been pushing this idea for a few weeks that there is a
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low-cost intervention that we could apply right now. And that is identifying patients who've been
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infected, recovered, and looking at their convalescent serus. In other words, people develop
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antibodies, an antibody response to varying degrees, collecting that serum, isolating antibody,
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and then using that as a treatment. Because that's all we're going to have right now. I already think
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the window is passed when we're going to start having significant numbers of people sick from
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this virus in hospitals and intensive care units. And this is the one thing we can offer them given
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the fact that we're not likely to have any effective antiviral drugs for a while. And it could be very
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effective based on what we learned historically from things like the 1918 flu pandemic, the Spanish flu,
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or even from experiences that we've heard about from SARS and MERS or even this virus in Wuhan,
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both as a treatment, which would require large amounts of antibody, but also as prophylaxis.
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So you can give a small amount and keep healthcare workers and first responders on the job because
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it's preventing them from potentially from getting sick. Peter, when it comes to convalescent serum,
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I want to make sure I understand something, which is from a technical standpoint, this is easy.
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Obviously, from a theoretical standpoint, it makes sense. This is, as you point out, not a new trick.
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However, when we start to think about bottlenecks in the supply chain, it does require apheresis,
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correct? Yeah, it looks that way. And so we really need the help of blood banks and any,
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I don't know if you do this only in academic health centers or whether every community hospital
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would have this capability. And we would need some guidance from the drug administration,
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from CBER, the Center for Biologics Evaluation Research. So this is kind of a 30,000-foot aerial
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view of the problem. Speaking to Arturo, he thinks putting together a federal task force to really
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look into this and to help with standardizing it and figuring out what we can do. But it has,
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if we have, wind up having a situation similar to Italy in the United States or even part of the United
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States, having this at our disposal is going to be really important because otherwise we've got
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nothing. Otherwise, we go back to the 14th century in terms of using quarantine methods and that kind
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of thing. And we see what happens when we have to do that. It's not a good look for our country.
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Peter, do we have a sense of how many individuals could be helped by the serum of one convalesced
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patient? How scalable is it? The kinds of numbers people are throwing out are 300 mils,
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300 to 600 mils for someone who's potentially seriously ill. So that looks like a one-to-one
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donor per patient. But for the prophylaxis, if we're talking 5 mLs, a single donor could potentially
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prophylax dozens or maybe even 100 individuals. And who knows how often those numbers really are. But
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given the fact that it's relatively low technology, doesn't need to bring in a lot of specialized
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equipment, I don't think. I think it's something we need to look into. And Arturo gave me the
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permission to sound the alarm on CNN and Fox News. And we'll see how it resonates in the coming days
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and weeks and see if it catches fire. What about remdesivir, which seems like one of the more promising
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things that could be repurposed? Do you buy that argument that this drug, which has been developed
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by Gilead for Ebola is potentially, I mean, it's being used now on compassionate exemption. Do we have
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a sense of its efficacy? Or is it too soon? I haven't seen those numbers. And so it will require
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a clinical trial. And whether you use combination therapy, certainly antivirals will go a lot faster
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than vaccines. And we've developed a recombinant protein vaccine, but it's, you know, we'll see how
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quickly that can come up to speed in terms of clinical development. You've said in the past,
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a vaccine is really not something we're going to have in the next 12 months. And it might even be
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longer than that. Can you just explain to folks two issues? One, the technical challenges of
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vaccinating against this coronavirus per se versus say an influenza and the lessons we've learned from say
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RSV viruses. And then secondly, the logistics of getting a vaccine tested, vetted from a safety and
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efficacy standpoint to be used on asymptomatic people. Those seem to be two separate issues
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that are both stacked against us. Well, yeah. I mean, vaccines are about the highest bar there is
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in terms of testing because you're essentially, typically you're immunizing well individuals
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or healthy individuals. So you have to be pristine in terms of its safety. And historically, it's been
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very difficult to compress those timelines to something quick. So it's not unusual for a clinical
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development plan for a vaccine to last a year, two years, sometimes three years to go through
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the series of phase one trials for safety and then graded trials for phase two to show that those
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are expanded safety studies, maybe getting a hint of efficacy, and then the phase three pivotal study
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for licensure in an area of transmission. So even under ideal circumstances, that will take time. Now,
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I think there are opportunities to streamline this. So my colleague, Rino Rapioli, who's one of the real
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thought leaders in vaccines, he's at GlaxoSmithKline, has drawn up a lot of interesting roadmaps for doing
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more things in parallel rather than serially and accelerating those timelines. And I think that
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there's a lot of interest in applying that for this vaccine. But I've made the statement that I'm
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not sure this is the one you want to do it with, even though there's so much urgency. And the reason I
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say that is coronavirus vaccines have, at least in laboratory animals, shown that they could create a
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problem known as immune enhancement, where the vaccine could actually make things worse. This is a
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phenomenon that was found originally with the respiratory syncytial virus vaccine, the RSV vaccine,
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that was a killed virus vaccine, a formal and inactivated vaccine that was tested by the National
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Institutes of Health at Children's Hospital in Washington in the 1960s, where vaccine recipients
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actually did worse than the non-vaccine recipients after they were exposed to the natural virus
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living in the community. And the mechanism is not still entirely clear, but those who were vaccinated
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had more hospitalizations than there were even two deaths. And there was the added layer of complexity
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that this study, when you look at the paper, I only realized this recently, was done among almost all
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African-American kids as well when it was done in Washington, D.C. And there were potentially two
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deaths. So this squashed enthusiasm for RSV vaccines, appropriately so, for a long time.
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And the question is, was this unique to respiratory syncytial virus or is there others that do it? Well,
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after SARS in 2003, there was an initial effort to again develop killed virus vaccines to test in animals.
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And unfortunately, after virus challenge, those animals also exhibited a lung pathology that bore
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some resemblance to what we saw in the kids with RSV in the 1960s. And we said, oh no, this is,
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are we going to be faced with this again? And so the thinking was, well, okay, maybe that was unique
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to a killed virus vaccine. Let's do this with the whole spike protein. So if you look at a cartoon of what
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coronavirus looks like, you always see these little spikes all around it, that's the part that docs
00:24:12.520
with the receptor. So a recombinant protein vaccine was made with the whole spike protein. Sure enough,
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we also saw immune enhancement, although it was more in the liver than in the lungs. But the thinking was,
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can we get around this? Is it going to be impossible to develop coronavirus vaccines? Well then,
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our colleagues at the New York blood center, Shibu Jiang and Lanyin Du found that if they only use the
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receptor binding domain, the smallest part of the S protein that docs with the receptor, the
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acetylcholinase 2 receptor in the lungs, they seem to get protection in laboratory animals without all
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the immune enhancement. That was pretty exciting. And that's the concept that we partnered together to
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write a grant to the NIH together with the Galveston National Laboratory where they had the virus for
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potentially doing preclinical studies and Walter Reed. And we wound up making a vaccine, manufacturing it
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that showed pretty good levels of high levels of efficacy and seemed to get around the problem
00:25:13.080
of immune enhancement. And that's why we got so excited at the prospect of maybe we could develop this
00:25:20.680
receptor binding domain as a vaccine. And we did. And we got funded by the NIH. It took us several
00:25:26.200
years to do it to show all of the safety, none of the immune enhancement and the efficacy had it
00:25:33.320
manufactured. But after then, by then nobody was really interested in coronavirus vaccines anymore.
00:25:39.720
And we couldn't attract any investment in moving into clinical trials. We kept it on stability studies,
00:25:46.520
but that project more or less was done until a few weeks ago when this new coronavirus emerged.
00:25:54.120
And we began looking, the Chinese were really good about putting up their data. Everyone says how
00:25:59.640
non-transparent they were, but I disagree. They were very transparent. They were putting up all their data
00:26:05.560
on these preprint servers like BioArchive, MedArchive. And we were able to see
00:26:09.960
that the SARS-2 coronavirus bore a lot of resemblance to SARS-1. It was about 80% similar in terms of its
00:26:18.520
genetic code bound to the same receptor. We realized, oh my God, we might actually have a
00:26:24.840
vaccine that we could repurpose for this epidemic. In the meantime, we also started trying to make the
00:26:30.360
new one as well, the receptor binding domain for the new one, but this was already manufactured. And
00:26:35.240
now we've been in this hunt to try to identify prospective donors to see if we can now move
00:26:41.880
this into clinical trials. That's been a few weeks now. And I'm, you know, it's sad to report we've
00:26:46.680
still not been able to raise the money to move it into clinical trials, which is really tragic. It's
00:26:52.120
already manufactured. We can move as fast as anybody, but this really goes to show you the problem of
00:26:57.960
dealing with vaccines, either for neglected diseases that I've devoted my whole life to.
00:27:02.440
We've made vaccines for schistosomiasis and hookworm and Chagas disease and moving them
00:27:08.600
into the clinic through our National School of Tropical Medicine at Baylor College of Medicine
00:27:14.600
and Texas Children's Hospital Center for Vaccine Development taking on this coronavirus. But you'd
00:27:19.720
think that people would be pretty eager to support us to move this forward, but so far it hasn't happened.
00:27:25.480
Should that change? I assume people can pretty easily get a hold of you if there's
00:27:29.800
interest in this. What's the easiest way for people to get a hold of you at this point in time?
00:27:34.040
I assume just through the university? Yeah, just send me an email. My email is
00:27:38.200
pretty public. It's just HOTEZ last name at BCM stands for Baylor College of Medicine.edu.
00:27:45.240
And we can do this through either the college or Texas Children's Hospital and be fantastic.
00:27:51.000
What do we know about the ACE2 receptor and its role here? Certainly a few weeks ago,
00:27:59.320
I remember seeing a paper that discussed this in the context of the first SARS outbreak. This was a
00:28:05.640
2005 paper and that got us very interested in looking at angiotensin receptor blockers and things like
00:28:11.400
that. But is the following still our understanding, which is that the virus gains access to these cells in
00:28:18.120
the lung, the type 2 pneumocytes that make surfactant? Probably through this ACE2 receptor,
00:28:23.240
though there may be a co-receptor, once the pneumocyte is infected, it reduces its capacity to
00:28:29.880
produce surfactant, which is one of the more telling pieces of the pathology. Is that still largely
00:28:35.880
accurate to our understanding? Well, I think there's a couple of things. I think first of all,
00:28:39.400
the receptor is not only in the lungs, it's also found in the intestinal tract, and you can see
00:28:43.880
intestinal pathology with this. And that may even be... And even myocardial, potentially.
00:28:49.000
And it's in endothelial cells as well. And that may partly explain some of the diverse pathology
00:28:55.720
that we're seeing. So for instance, patients who are very ill with this, if you look at the
00:29:01.400
MedArchive reports coming out of China and elsewhere, a lot of them are getting acute myocardial injury.
00:29:07.080
And we don't really know if that's from myocarditis or whether just getting myocardial infarction is a
00:29:13.080
consequence of the infection. But I think that's probably a major mode of death for a lot of these
00:29:18.600
patients. And it's very confusing because there's a lot of things going on at once. You have
00:29:25.080
acute myocardial injury, but you're also seeing acute respiratory distress syndrome, ARDS.
00:29:30.760
So therefore, is the heart injury due to the ARDS and shock, or is it occurring in parallel? And then
00:29:37.480
what's the basis for the ARDS? Is it overwhelming virus invasion in the lungs, or is there a huge
00:29:45.960
inflammatory component to this? And there's differing opinions on that. And that also has implications
00:29:52.360
for treatment. Then the intestinal pathology as well. And we've seen patients, at least 10% of the
00:29:58.520
patients reported in some hospitals in Wuhan, they presented with GI symptoms and were erroneously
00:30:05.640
admitted to the surgical suite. And those are the ones that wound up actually infecting large numbers
00:30:11.480
of healthcare workers because nobody suspected this was SARS-2. So that's confusing as well. And you can
00:30:18.600
imagine how well the confusion that would create for monitoring and figuring out who should get tested.
00:30:24.920
So my colleague, Paul Offit, is of the opinion that he thinks the GI route is actually a major
00:30:32.440
mode of transmission, is noted and speculated. Well, at least he's talked to me on the phone about
00:30:39.320
whether the fact that cruise ships are so widely affected, he says it reminds him a little bit of
00:30:45.720
norovirus when it affects large numbers of cruise ships. So is it getting into the food? So we don't
00:30:51.480
really know the modes of transmission of this. We know droplet contact is going to be important.
00:30:56.120
People are coughing micro droplets onto surfaces and then people come into contact with them with
00:31:01.960
their hands and auto-inoculate themselves in the mucous membranes of their eyes and mouth or
00:31:07.880
whether they're coughing directly onto people's faces. But the other modes of transmission are also
00:31:13.240
interesting. Is there a lot of fecal oral transmission? I don't think we know that.
00:31:16.840
Is there a true airborne transmission where the virus can travel on microparticles long distances?
00:31:23.640
It turns out not many respiratory viruses do that. We know measles does, chicken pox does.
00:31:29.640
So we're still in this deep learning curve about this virus.
00:31:33.000
Which again brings us back to this point of can you buy time? Because time presumably brings clarity,
00:31:39.800
reduces uncertainty. Did you see the paper today that just came out from the New England Journal of
00:31:43.960
Medicine that looked at the fomite transmission? No, I didn't see that. What did it find?
00:31:48.760
Well, here, I'm going to pull it up. The telling figure in this sort of looks at four different
00:31:53.720
surfaces, actually several plastic, steel, cardboard, copper surfaces, and it looks at the median and
00:32:01.080
half-life survival on these surfaces. And not surprisingly, I think, based on what you just said,
00:32:07.560
Peter, there's pretty reasonable survival. So until you reach a level that they think is
00:32:13.000
not compatible with transmission, takes about 72 hours on plastic, takes 48 hours on cardboard,
00:32:20.120
takes about 24 hours on steel, and takes about eight hours to 24 hours on copper.
00:32:28.920
So a couple points I'd make there from a public service announcement. I've seen a lot of talk on
00:32:33.720
Twitter of all you need to do is have copper on your door and nothing gets in. Well, apparently not.
00:32:38.920
And we have evidence that at least a day of survivability on these fomites. And again,
00:32:46.760
I think that speaks to the R-naught being as high as it is. And maybe this is a reasonable time to
00:32:52.840
explain exactly what R-naught is and what we think our best estimates are of it and why it probably
00:32:58.040
feeds into what you've been saying about the concern over the transmissibility.
00:33:02.040
I think all of this put together presents a picture of why this virus is so highly transmissible. You
00:33:10.840
have the fact that this virus can live on surfaces. So the droplet contact motor transmission is
00:33:19.480
significant because it depends on the virus being able to survive on fomites and surfaces. And the fact
00:33:26.840
that this virus will often land on people's face and they can auto-inoculate themselves,
00:33:32.120
that's the mode of transmission, maybe fecal-oral and maybe airborne transmission as well. And so
00:33:37.400
what does that all add up to? It all adds up to the fact that when people have looked at it,
00:33:43.240
it's a pretty high what we call reproductive number, or what the Brits call R-naught, what we call R-sub-zero,
00:33:50.040
which refers to roughly the working definition is the number of people that will get infected
00:33:57.640
if a single individual has this virus. So the number that I carry around in my head is between
00:34:05.240
2.24 and 3.58, roughly between two and four people infected for every single individual.
00:34:13.160
And some people will shift those numbers around more or less. And I think that level of transmission
00:34:19.000
varies depending on location and a number of other factors, but it's pretty high. If you look at
00:34:26.760
seasonal flu, for instance, which is around 1.2, 1.3, so this would be two or three times more
00:34:33.640
transmissible than seasonal flu. Clearly not as transmissible as measles, which is up to 12 to 18,
00:34:39.880
but still quite high. So as I mentioned before, every new emerging pathogen has its own little shop of
00:34:47.240
horrors. In the case of this one, it's pretty highly transmissible. And there are a lot of people in
00:34:54.440
this case who are running around who are not sick that are spreading this virus around and infecting
00:35:01.240
a subgroup of individuals who happen to get very ill and with very high mortality rates. So the case
00:35:07.720
fatality rate of this virus is between 0.6 and 3.4%, which may not sound all that high, but that's
00:35:17.640
easily between 4 and 20 times higher than influenza. And that, given the fact that there is a group
00:35:24.120
walking around with this, means you're going to have a lot of people in hospital in intensive care
00:35:29.480
units, and especially among older populations where that mortality rate is between 10 and 20%.
00:35:35.240
And that's what's so devastating is the fact that when this virus goes into areas where large numbers
00:35:43.480
of older people congregate, especially older people with underlying disability can have some
00:35:49.480
devastating effects. And the Chinese told us this was going to happen. They told us about what happens
00:35:55.240
when this virus goes into a nursing home or affects older people and large numbers of deaths of those
00:36:01.640
individuals over the age of 70. And I don't know if it was because we didn't believe them or we just
00:36:07.320
had to learn it on our own. But when we had our first community transmission in Kirkland, Washington,
00:36:14.360
we saw how this virus raced through that nursing home and killed 13 people in a nursing home of about
00:36:21.960
100 individuals. So 13%, which is exactly right in that area of 10 to 20% that the Chinese told us about.
00:36:29.640
And then I became very concerned, not only from the lack of government response from
00:36:35.080
the debacle with the testing, but also that there was not a lot of guidance being issued around nursing
00:36:41.640
homes or assisted living facilities. And I had the opportunity to testify to Congress about our vaccine
00:36:49.480
to the House science space and technology committee. But I hear I had the attention of Congress and it was being filmed on C-SPAN
00:36:58.600
to or C-SPAN. And I said, look, this is my chance to really sound the alarm on what's not happening to protect our old
00:37:06.760
people. And as I was saying it, I knew it was being very provocative and I was being deliberately provocative.
00:37:11.480
And I knew it was going to be on the evening news and be on the news the next day, but I felt I had to say something.
00:37:19.960
And that's when I used that expression, this is the angel of death for older people. And indeed that had that effect,
00:37:27.560
but it was a wake up call to people. And now we're starting to see nursing homes across the country take those extra measures to
00:37:35.320
carefully screen people going in and out of nursing homes to review all of their preparedness plans.
00:37:42.520
And now the health and human services secretary is mobilizing inspectors around infection control.
00:37:49.400
And that's an example of where I, over the years, I've always had this interesting career that balances being a working
00:37:57.560
scientist and MD-PhD vaccine scientist developing vaccines and for neglected disease interventions with
00:38:05.160
that advocacy in places where I've seen gaps. So I saw a gap in getting people to care about these
00:38:12.920
poverty related and neglected diseases in the early 2000s and helped raise awareness that's now led to
00:38:19.160
treatment of more than a billion people annually for neglected tropical diseases, raising awareness about
00:38:25.800
diseases of the poor in places like the United States. And now we've been working with Senator Booker,
00:38:31.080
Cory Booker around this issue, getting people to counter the anti-vaccine movement. So I'm a parent of an
00:38:39.000
adult daughter with autism and wrote this book called Vaccines Did Not Cause Rachel's Autism to kind of
00:38:45.720
counter the false narrative and the misinformation from the anti-vaccine movement. And here was another
00:38:51.480
example of using my voice to really help people who didn't have a voice otherwise.
00:38:57.160
Peter, what geographies in the United States are you most concerned about? And then I guess I also ask you that
00:39:04.120
question at a global level, but we'll start maybe in the United States.
00:39:07.000
Well, I mean, right now, it's all bets are off. I think any urban area of the U.S. now is vulnerable. And we've seen
00:39:16.200
this now take off in Seattle. We've seen this take off in New Rochelle in Westchester County. We're starting to see some
00:39:25.160
uptick in New York City. And there's nothing really unique about those cities other than there are
00:39:31.000
congregations of a big urban population. So on that basis, I have to believe any large urban center is
00:39:38.120
vulnerable. And it could be any place is vulnerable. It's just that urban areas tend to have more
00:39:44.200
physicians and so more health care, better public health infrastructure. So maybe it's just being picked
00:39:50.360
up there for. So I said last week, this is going to be a difficult week for America because the testing is going to
00:39:57.160
start to gear up. And now that it's in the hands of Quest Diagnostics and LabCorp and Roche, we're going to get a much
00:40:04.840
more full picture of the extent of this virus in the United States and North America. And I think we're starting to see that
00:40:12.040
the numbers are going up 1,600. Who knows what it'll look like by next week? Is it going to be 10 times
00:40:17.640
that number? I think that's quite possible or even more. And with that, we'll undoubtedly be picking up new
00:40:24.360
foci of infection. That's a pretty frightening thought to have a log increase in a week. But when you look at
00:40:30.480
other countries that have not done well, that's exactly what we have seen, isn't it? Well, the question is whether
00:40:36.460
that's a true log increase or whether we've had that transmission all along. It's just that now we're
00:40:41.540
cherry-picking communities to detect it, or maybe both going on simultaneously. But I suspect we're
00:40:49.480
going to see those numbers steeply rise again. And so this gets back to what I was talking about with
00:40:57.020
Mark Lipsitch's paper, where he says the more sustained community transmission goes on, the health
00:41:04.540
burden's going to be in terms of hospital beds and ICU beds and the demands on healthcare staff.
00:41:10.780
I think as we pick up these new levels of transmission in places that's been going on for
00:41:16.040
a while, next week, so the horror this week was we realized we're seeing a lot more cases and maybe new
00:41:22.220
areas of community transmission. I would say the same for next week with the added piece. Now we're
00:41:27.680
going to start to see hospital beds fill up. And that's why I'm really pushing now for blood banks
00:41:34.080
to implement this new antibody therapy, because I think the need's really going to be there. And if
00:41:40.020
you don't offer people any hope of anything, I think that's where panic starts to spread, where you
00:41:46.200
start seeing panic, not only among the population, but among the healthcare workers. And we've got to be
00:41:53.020
able to stop that. So I think just like this week was challenging because we're starting to see an
00:41:57.740
increase, I think in the next two weeks may be the critical period when we may start to see
00:42:02.640
this start to reach a peak. Peter, do we have a sense of what the excess capacity is in the ICU
00:42:10.520
and where the, where's the bottleneck going to be in the supply chain? Is it the number of ventilators,
00:42:15.760
the number of ICU beds or beds that could be repurposed for ICU? Is it going to be the number
00:42:19.940
of anesthesiologists, respiratory therapists, nurses? There are so many things here.
00:42:23.860
Yeah, I think, I think only now we're really starting to look at this. And if you've ever listened
00:42:28.260
to Zeke Emanuel, he's been commenting a lot about this. We don't have a great capacity. Hospitals
00:42:35.760
for cost-saving measures and everything else have operated at slim margins. So it's not like we have
00:42:42.640
a lot of excess capacity laying around. And does this mean we're going to have to build
00:42:48.140
tent city hospitals? Will we have to bring in the National Guard? I think all of that, you know,
00:42:54.240
it's a big unknown. I mean, the only good thing that we have going for us is we did make that
00:43:01.540
sacrifice of shutting down things we love, like the National Basketball Association, the NBA and
00:43:07.820
the rodeo and that sort of thing. And that's a good thing about America. We did this to protect
00:43:12.780
our most vulnerable or older citizens, a lot of them veterans of foreign wars. And
00:43:18.300
I think that that's important. And maybe if there is a seasonality to this virus, maybe we're just
00:43:25.760
hitting it right in terms of moving into warmer weather, but we have no evidence for that.
00:43:30.580
That certainly was not the case with the first SARS, right? I mean, it didn't seem to stop when
00:43:34.900
the summer came, did it? Well, you know, if you look at the curves, the peaks that I saw looked like
00:43:39.860
more around the springtime, but who knows? I mean, we certainly can't count on it. You know,
00:43:45.480
there's some people who feel that it may start to go down in the summer, but not disappear entirely
00:43:50.180
and then come back in the fall. So we just don't know. As I've also been saying is confronting a
00:43:56.380
new serious virus pathogen is one of the hardest things our country faces, has faced the last 20
00:44:02.700
years. And it always starts out pretty bumpy and pretty rocky, I think in part because it takes the
00:44:08.600
CDC a while to figure out how the federal government and the CDC, how to work with state and local
00:44:13.600
health authorities. This one has been rockier than most because of the inability to do the testing
00:44:20.020
and other factors. But the problem is unlike Ebola, which was never going to be transmitted
00:44:25.840
widely across the country because that very low reproductive number, unless you're taking care of
00:44:30.880
a dead or dying Ebola patient, you're not going to get Ebola. This one is pretty transmissible. So
00:44:36.100
our margin for error is much smaller as the studies in China have pointed out. So we could be in for
00:44:44.420
some very serious times. Mark Lipsitch has stated that he believes we could be entering kind of a new
00:44:51.660
world where two years from now, half the world's population or thereabouts has been infected by this
00:44:58.480
virus. And even if you use the absolute lowest estimate of mortality that's being provided,
00:45:04.760
which is 0.5% or 1 in 200 people dying, the impact of what I just reiterated as his estimate is
00:45:13.340
staggering. Do you share that view or do you at least think that that is a plausible scenario?
00:45:19.500
Yeah, it's absolutely plausible. And Mark's an outstanding epidemiologist. And a lot of these estimates are
00:45:25.400
based on models. I would say the only thing about models, and I'm not a modeler, but I've collaborated
00:45:31.180
with modelers to look at projections of our different vaccines and to give us a sense of what level of
00:45:38.640
protection we would need to have a significant impact on a population and how wide a coverage
00:45:46.600
we would need. And one of the things that always impresses me working with modelers is that a modest
00:45:52.660
change in assumptions of what goes into the model can often have huge differences. So the only
00:45:59.040
comfort I take in that is to say, well, maybe if those models are like the ones I've worked with,
00:46:06.000
a few tweaks to the model can result in two or three log reductions in deaths and cases and that
00:46:13.360
sort of thing. So models are useful exercises to help you think through problems, but how predictive
00:46:21.040
they are is only as good as the assumptions with the new virus agent, where we don't even know all the
00:46:26.100
modes of transmission and everything else, don't fully understand reproductive number, that might
00:46:31.720
help us. Yeah. As a physicist, a very famous physicist once said, all models are wrong, some are useful.
00:46:38.040
So hopefully that model is woefully wrong. But I think part of that is, as you said, it's a little
00:46:45.080
bit in our hands how wrong that model is going to be, isn't it? I mean, it's still, we still have some say
00:46:50.880
over our response to this, both in terms at the federal level, but also at the local and state
00:46:56.860
level. And then at the individual level, we can all take steps to reduce our risk and buy more time.
00:47:02.900
How are you thinking about this? I don't want to say personally, because you're in a very unique
00:47:07.880
position where you have to be out there talking about this. You don't have the luxury of maybe being
00:47:13.760
a little bit more sequestered, but are there a certain subset of people that at this point,
00:47:19.140
Peter, you would say absolutely need to be self-quarantined, either the symptomatic folks,
00:47:24.740
obviously who run the risk of infecting others if they can't be tested, but also people who are
00:47:28.720
showing no signs or symptoms, but who are at high enough risk. How are you helping people create their
00:47:34.900
own sort of framework around that very difficult decision? Well, certainly older individuals where
00:47:41.680
they're clustering together, we've seen the devastation. So we can't repeat the debacle
00:47:47.360
that we had in that nursing home. And so it's all hands on deck with protecting those individuals.
00:47:53.340
Then you can say, okay, Peter, well, tell us what that means. Does that mean thinking of my 90 year
00:47:58.560
old mother in the Hebrew home in Brooklyn, outside of Brookline, Massachusetts, do we now tell her that
00:48:05.340
she has to stay in her room and can't go down to the cafeteria and sit with her friends? Is that what
00:48:10.800
you're telling us? And so these are going to be really tough decisions. We know how important
00:48:16.960
socialization is for older people, for anybody, right? But for older people in nursing facilities,
00:48:22.540
that's really heartbreaking. And so Dr. Hotez, is he telling us that the grandkids can't visit,
00:48:29.960
can't visit. So these are really tough decisions for us. Because at what point do you say,
00:48:36.120
we know older populations are so fragile in terms of suffering serious mental decline? And do you want
00:48:43.760
to do that just to protect them from this virus? And this is where I say, well, I'm a vaccine
00:48:50.260
scientist, pretty good at understanding infectious disease epidemiology, because I've had to really
00:48:59.020
understand how to make the best vaccine. But there's a certain point where the decisions become
00:49:04.500
so tricky that I have to say, no, I'm starting to exceed the limits of my comfort zone. And here's
00:49:11.380
where we start needing some federal guidance, state and federal guidance, people to really think about
00:49:16.480
this very deeply and bringing experts together that understand that. And I don't see that happening,
00:49:22.300
unfortunately. What I'd like to see are key task force created around, not in general, as has been done,
00:49:29.920
the president's created on sort of an overarching task force for this. But there are so many
00:49:35.520
specialized pieces to this that we have to focus on, like creating an antibody based technology,
00:49:42.480
bring those experts together, bring experts together around what nursing homes are like and
00:49:47.900
how they're structured, which would include experts in the mental health of older people,
00:49:53.580
those experts in diabetes and hypertension to understand what's going on. And I think
00:49:58.120
that's going to be really critical as well. Peter, what are you personally going to be paying
00:50:04.580
closest attention to in the next seven days besides the potential for using convalescent serum,
00:50:12.320
both from the sort of clinical trial standpoint and or utilization standpoint? And in terms of data
00:50:18.780
that are going to say, hey, are we heading towards the Italian path or are we heading towards sort of the
00:50:25.580
Singapore path? What data are you monitoring closely?
00:50:29.800
Well, certainly incidents and prevalence data is going to be really important because right now
00:50:34.860
there's none, right? We've done so little testing. So as we ramp up and also starting to see which new
00:50:42.320
communities are becoming infected, I think that's going to be absolutely critical. And seeing if the
00:50:48.560
situation that we've seen in the Pacific Northwest and New Rochelle is being replicated elsewhere,
00:50:54.400
or the demographics taking on a different characteristic, those are some of the big
00:51:00.520
things that I'll be looking for. And then also there are some vaccine trials that have started
00:51:05.240
in the Washington area. Interest in following those because my understanding is the one in Seattle
00:51:11.540
began with one of the vaccine trial evaluation units at the University of Washington, and it was
00:51:17.820
initiated at a time where there wasn't transmission of this virus. Now there is.
00:51:21.460
So you're doing something that is going to be very interesting, but also a little bit scary because
00:51:29.300
if there is immune enhancement, now we're going to start to see it among those volunteers who are
00:51:34.960
getting immunized. Peter, I want to be respectful of your time, and I promised you we would only take
00:51:39.640
an hour. We've now gone a little over an hour. So I want to let you go with the ask that either we can
00:51:46.300
speak again, either formally or informally, because again, I think it's probably less important to
00:51:50.560
spend hours at any one point in time and maybe more important to... And this is what I've been
00:51:55.720
saying, you know, on CNN and Fox and MSNBC, and it's not easy going from one network to the other,
00:52:01.760
right? Especially those networks. Yeah. Well, you know, one, you have to say something nice about
00:52:06.780
the president. The other one, you're not allowed to say anything nice about the president. It's also
00:52:10.580
polarizing threading that needle. It's interesting. But one of the things I always say is this is where
00:52:17.200
we are right now, and this virus is racing so quickly that new pathogens in general set you up
00:52:24.100
to look stupid because, you know, when you're trying to learn something about a new pathogen, but this
00:52:29.040
one especially because it's so fast-moving and transmissible, I would cringe if I were to look at my
00:52:35.020
interviews from two or three weeks ago in terms of the things I said, I think. And probably a month
00:52:41.780
from now, I would say, oh my God, I can't believe I said that at what we're talking about now. So I
00:52:47.000
think absolutely that's important to update this and to say, to take a step back and look to see what
00:52:52.240
have we learned in the last week? And because we're trying to make our best guesses, best estimates on
00:52:58.280
what we're seeing now. But this is, as I say, it's moving so quickly. We have to continually
00:53:04.040
reevaluate that. And that's why I'd like to see the White House out there every day because this
00:53:10.120
thing is moving so quickly. Yeah. Well, look, for those listening to this, probably on a Saturday,
00:53:15.040
it's now Friday night in real time, March 13th. Peter, let's let you get back to work. Let's touch base
00:53:22.100
next week and continue to look at the data and in real time, try to come up with the best
00:53:28.100
assessments of what we can. Thank you very much, Peter. Thanks for having me. Thanks for all your
00:53:32.300
great work. One of the things that I do when I give talks about confronting anti-science, and I do that
00:53:38.740
a lot standing up to the anti-vaccine movement, I say part of this is our fault because as physicians
00:53:44.660
and scientists, we're too inward looking. We've somehow decided that engaging public audiences is not
00:53:51.380
important. And so the kinds of things you're doing is really critical to break that. I think the best
00:53:58.700
weapon against ignorance and false information is the kinds of things that you're doing. So I just
00:54:04.180
want to congratulate you on what you're doing and there's nothing more important. Thank you, Peter.
00:54:08.520
We're greatly appreciated. And I hope you get some rest tonight and we'll be back in touch next week.
00:54:12.680
Thanks. Me too. I hope we get some rest. Thank you for listening to this week's episode of The Drive.
00:54:18.300
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