COVID-19: Origins, Spread, and Impacts

June 17, 2020

[Title card with image of COVID-19 model and text reading, “COVID-19: Origins, Spread, and Impacts. Panelists: Nancy Simmons, Joshua Sharfstein, and Lisa Cooper. Moderated by Apoorva Mandavilli. Livestream will start at Noon ET.]

[Museum curator Rob DeSalle speaks via webcam.]

ROB DESALLE (Curator, Molecular Systematics, American Museum of Natural History): Good afternoon, and welcome to the first of two American Museum of Natural History web panel discussions.

The discussion today is on COVID-19: Origins, Spread, and Impacts. My name is Rob DeSalle, and I a curator here at the Museum in the Institute for Comparative Genomics.

Before starting I would like to thank Mike Novacek, Provost of the Museum, and Lisa Guggenheim, Vice President of the Education Department for their strong and rapid support for these events.

And a big thanks goes to Ruth Cohen and especially Bella Desai for their amazing work in organizing the events.

The AMNH is proud to present two events—one today and one on July 8th, called COVID-19: Vaccines, Testing, and a Science Behind a Cure. We're excited about these panel discussions to educate the public here in New York City and across the nation.

You all may know that our doors have been closed to visitors for four long months due to the pandemic. But we hope these web panels fill a gap and are informative and helpful in navigating the next months.

The AMNH has twin directives in education and science. You can visit our web page at www.amnh.org to view the ways our scientists and educators have responded to the pandemic.

The AMNH has, for over a century, focused its exhibitions and science on public health, and has been involved in educating the public about infectious disease and its impact. The best attended exhibition ever mounted at the AMNH was on a health issue—the scourge of tuberculosis.

Over the past two decades, a dozen exhibitions have been mounted focused on public health and infectious disease. We extend that commitment and tradition to the current pandemic, in the hopes that knowledge of the science of this disease will give you answers and advance us closer to the end of this pandemic.

Today's event will be moderated by Apoorva Mandavilli. Apoorva is a reporter who was awarded the 2019 Victor Cohen Prize for Excellence in Medical Science Reporting. She was an editor-in-chief of Spectrum, an autism news site for 12 years. She has contributed to The Atlantic, Slate, the New Yorker, Scientific American, and several scientific journals.

Apoorva is currently writing for the New York Times, reporting on the pandemic. And I'm sure many of you have encountered her amazing work in the Times on this subject. I've read some of the questions she intends to pose to our panel and I simply can't wait to get the panel rolling. So, now, Apoorva, I will hand things over to you.

[Science journalist Apoorva Mandavilli speaks via webcam.]

APOORVA MANDAVILLI (science journalist, New York Times): Hi everybody. Thank you so much for having me. This is going to be a really great event and I'm looking forward to learning a lot. So, today, we're going to be talking about how and why does a virus jump from animals to humans, how do we model the spread of infection, and how do racial inequities in health and health care affect how a pandemic unfolds.

We're joined today by evolutionary biologist Nancy Simmons, public health and policy expert Joshua Sharfstein, and social epidemiologist Lisa Cooper. We're going to be talking about the basic biology and social context of COVID-19, and what these mean for how we anticipate and mitigate the spread of the virus.

I'll start out by asking them some questions, but there will also be plenty of time after that for your questions.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Let me begin by introducing the panelists.

[Lisa Cooper appears via webcam.]

MANDAVILLI: Dr. Lisa Cooper is the James F. Fries Professor of Medicine at Johns Hopkins University Bloomberg School of Public Health. An international thought leader on health disparities, a 2007 MacArthur Fellow, and Founding Director of the Johns Hopkins Center for Health Equity, she studies how race and socioeconomic factors shape patient care, and how patients and health systems with communities can help at-risk populations.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Next, we have Joshua Sharfstein. Dr. Sharfstein is the Vice Dean for Public Health Practice and Community Engagement for the Bloomberg School of Public Health.

[Joshua Sharfstein appears via webcam.]

MANDAVILLI: He's also the Director of the Bloomberg American Health Initiative. Previously, he served as the Secretary of the Maryland Department of Health and Mental Hygiene, the Principal Deputy Commissioner of the U.S. Food and Drug Administration, and Commissioner of Health for Baltimore City.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: And finally, we have Nancy Simmons. Dr. Nancy Simmons is Curator-In-Charge of the Department of Mammalogy at the American Museum of Natural History.

[Nancy Simmons appears via webcam.]

MANDAVILLI: She specializes in the morphology and evolutionary biology of bats. Recently, she's been studying bat ecology, bat parasites, and disease dynamics, including the connection between human-bat interactions and zoonotic diseases.

We're lucky to have her here because, as I think some of you know, that's where all of this began.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: So, let's actually begin there and ask—Dr. Simmons, can you tell us- We've all heard that the coronavirus jumped from bats and then bats got some very bad press. Can you tell us what that even means for a virus to "jump" from another species? How should we be thinking about this kind of movement of viruses?

[Simmons appears via webcam.]

NANCY SIMMONS (Curator-in-Charge, Department of Mammalogy, American Museum of Natural History): Well, let's start by talking about SARS CoV-2, the virus that causes COVID-19 and where we think it came from. Very soon after the initial outbreak of COVID-19, scientists sequenced its DNA and compared it to the genomes of other known viruses.

They found that SARS CoV-2 belongs to an evolutionary radiation of coronaviruses whose natural hosts are bats. Its closest relative is a virus found in a horseshoe bat in China in 2013. That bat virus has a genome that's 96 percent similar to the human virus.

[Image of flying bat]

SIMMONS: Now, that number sounds very high, but for context, humans and chimpanzees have genomes that are 95 percent similar.

[Simmons appears via webcam.]

SIMMONS: So, the human virus and bat virus are not the same. Indeed, they're no more similar than humans are to chimpanzees.

In fact, there are no known cases of a bat having SARS CoV-2. It's a human virus. However, because SARS CoV-2 belongs to a group of viruses that are mostly hosted by bats, and because its closest relative—closest relative we know of—is a bat virus, we have to conclude that it originated at some point in the past from bats. And somehow got into the human population.

So, based on how fast coronaviruses are thought to mutate, it's been estimated that the human virus, which emerged in 2019, and the bat virus, collected in 2013, actually separated somewhere between 40 and 70 years ago.

Where has the virus been in all that time? And how did it get into people? The scientists simply don't know yet. Most bat viruses, or basically all viruses, are very particular about what hosts they infect. They've evolved to infect and replicate in cells of one species or one group of animals and they cannot easily do so in others- do the details of the machinery of how they infect cells and replicate.

When a virus jumps or spills over into a new host species, a whole slew of factors have to align to make that possible. First, the machinery of virus infection and replication—things that are very specific to that particular virus have to be compatible with the physiology and the cell biology of the potential new host, or nothing will happen.

Then there has to be a contact of some kind between infected host animals and a new host animal, or humans. This can be very direct contact—one animal eating another, for example—but it can also be indirect since viruses can be transferred through droppings or aerosols—coughing, for example.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVALLI: Can I ask you a quick question? Is there a role for pangolins in this? Because we've heard a little bit about how pangolins were intermediate hosts. Do you know if we know that for sure yet?

[Simmons appears via webcam.]

SIMMONS: We do not know that for sure yet. So, there are pangolin viruses, which are also similar to the coronaviruses that include SARS CoV-2, but they're not as similar as some of the bat viruses are. So, it seems coronaviruses can infect a wide variety of different mammals, but the ones that seem most closely related to SARS CoV-2 are the bat ones.

But all of these viruses are different in different ways and recombination can take place. Where genomes from part of one virus can combine with a virus if they're mixed in the same animal host and new viruses can develop that way, evolve that way.

And this is where human behavior comes into the story. If I had one takeaway for you from all this, it would be that humans are to blame for this pandemic, not animals. In most cases of animal to human virus spillover, it's human activities that start it. Activities that involve or increase human-wildlife interaction like habitat destruction, urbanization, bring people and the domestic animals that live with people into closer contact with wildlife all the time.

And activities that facilitate close proximity and mixing of different kinds of animals that don't normally live together can make it easy for pathogens to move between species. These sorts of things include intensive animal farming, keeping exotic animals as pets, hunting wildlife for food, and live [unintell]

MANDAVALLI: The food markets?

SIMMONS: Yes, live wildlife markets are one of the places that are highly implicated in the crossing of viruses and other pathogens from one species to another.

[Screen split between Mandavilli and Simmons]

SIMMONS: We've all seen pictures of live wildlife markets where cages of animals are stacked up, one on top of another, with the potential for droppings from one species to rain down on others. With people moving the cages around and cleaning up and, well, it's the perfect scenario for virus transfer from one species to another.

Another factor in these situations is stress. Just as in people, stressed animals can cause changes in their immune systems that make it easier for them to get sick and more easily spread viruses.

So, stress can be caused by being put in a cage, you know, captured in a trap and put in a cage and hauled into a market, or kept in overcrowded conditions, but it can also be caused by habitat destruction, fragmentation. So, squeezing wildlife into smaller and smaller areas and reducing the resources available to them and increasing competition.

Basically, whenever wildlife, including bats, are left alone by people there's very little risk of virus spillover. It's the human activities that cause the risk. So, it's humans that are the cause of the spillover in emerging infectious diseases, not the animals.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Thank you so much for that answer. I want to mention to our listeners that we do have a Facebook chat and there are people monitoring the Facebook chat. So, the question about pangolins, for example, that I inserted came from that. So, if you have questions while one of our experts is answering my question, feel free to add that in and maybe we'll get to it.

Thank you so much, Nancy, for that answer.

Josh, it's now several months into this pandemic. What do we know now about how the virus spreads in people? And what have we learned about all of the models that we saw in the beginning? There were so many. How accurate or off-base did they turn out to be?

[Sharfstein appears via webcam.]

JOSHUA SHARFSTEIN (Vice Dean for Public Health Practice and Community Engagement, Johns Hopkins Bloomberg School of Public Health): Sure. Well, when this all started, there were so many questions that people had about this new virus that was emerging from China. And we only had limited bits of information and we had so many urgent needs to plan. And so, people jumped out with a whole different, you know, different sets of models.

And each of the models was for different purposes, had different assumptions, and so, it's not surprising that you had all kinds of different projections. I think I do have a slide somewhere of a great graphic the New York Times did at one point, which just showed the different models—that some were quite different from others, in terms of just how serious it would be.

[Graph titled “U.S. coronavirus deaths in five different forecasts.” Y-axis is “deaths per day” from 0 to 4,000. X-axis is from approximately mid-March to mid-June. April 1 and May 1 are labelled points. Text in graph reads, “Reported U.S. Deaths,” and “Five models of future U.S. deaths.” The five models are: (1) Imperial, which begins at about 2,500 deaths in early April and rises sharply up over the course of a few days to about 3,800, (2) Columbia, which begins in mid-April with about 3,300 deaths and falls to less than 1,000 by early June, (3) MIT, which begins in mid-April with about 2,300 deaths and falls to less than 1,000 by early June, (4) Northeastern, which begins with about 1,400 deaths in mid-April and falls to about 1,200 by late-April, and (5) IHME, which begins with about 2,100 deaths in mid-April and slopes off to 0 by early June. Two plots also represent reported deaths from JHU and NYT. Text to the side reads, “Reported deaths are rolling 7-day averages. Lines differ on whether to include roughly 5,000 probably deaths in New York City.”]

SHARFSTEIN: Among the different questions that we didn't know was the- how quickly the virus reproduces without intervention, how you can bring that reproduction rate down with intervention. This- I did a very early interview with an epidemiologist at the School of Public Health who said that the most important question he had was whether there was asymptomatic spread.

We didn't really know that at the beginning. And of course, it's become clear that there is before people get symptoms, particularly, they can be quite infectious.

The fatality rate for the number of cases and the number of infections was not well-known. So, all those things were put into models with, basically, just guesses. And then the models differ in terms of whether they are based on a mathematical kind of set of assumptions about infectious disease, or whether they're trying to model what happened in other countries for the United States.

And so you just had- just like this graphic shows, just all over the map, different kinds of projections. You notice, we're not using models quite as much, and that's partly because we understand a lot more.

And, you know, we've learned a few really important things. And I'll just say a couple of them. I mentioned the fact that people can spread without symptoms. We've also learned about the cycles that happen. It's about five days between one group of people with symptoms and then the next group of people with symptoms, on average.

And that it takes several cycles to really see the effect of changes. So, we're starting to see the effect of the opening on Memorial Day six weeks later. So, that's a really important thing. It's like a delayed effect.

And so, it's very important to take some time to see what's happening, rather than make a judgment just based on a few days.

We have a good sense of how the virus spreads through respiratory transmission and that there are certain scenarios and locations—indoors, people singing, exercising—which are a risk for a huge amount of spread. Many people getting sick.

And so, the importance of people keeping their distance, and particularly keeping their distance from those types of situations has become extremely clear. We have a much better sense that masks are helpful because of this importance of respiratory transmission and that even cloth masks can prevent droplets from spreading and putting other people at risk.

We certainly have learned a lot because—and I know Dr. Cooper's going to speak about this—because we see that infections are concentrated in areas where people cannot isolate or quarantine effectively. Where people can't just have food for two weeks because they don't have the resources to do that or they have to leave for their jobs or they're stuck in crowded public transportation.

And so, that has helped us understand, you know, certainly it has revealed some inequalities that have existed for quite a while, but it also illustrates the importance of in those areas providing the same opportunity to be able to distance and do things that reduce the spread of the virus.

And I think the biggest thing--maybe I'll end my initial thoughts here—is that those initial models and our current sense, there's one commonality, which is it's very hard to predict what human beings will do. It's hard to predict whether we will be able to take those steps, whether we will invest the resources in the areas that are seeing the hardest hit for COVID.

Whether we can continue to keep our distance from each other. There were some models initially that assumed that it would be just amazing how we would just shut everything down and just end the transmission of the virus. Well, those didn't work in the United States.

There are other models now that assume that, well, if we just relax, it's just going to go back to complete free transmission between people, which of course will have an enormous spike that would probably swamp our health care system's ability to take care of patients.

We don't know. That's up to us. There's no model that's going to predict that. And I think, ultimately, what we've learned enough about the virus to know what to do. And it's really a question of whether we can, you know, carefully, slowly follow that advice as we're opening, in order to substantially reduce the spread of transmission and even, you know, put in place public health measures like contact tracing that could really drive down the infection rate overall.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Can I ask you a quick follow-up question to that? I was really struck that you said it takes about six weeks, that it’s taken us six weeks to see the effects of all of the reopening, you know, on Memorial Day. Is there anything- That seems like a very long time for people to wait and see what the impact is. And it seems almost understandable that people would assume because they haven’t seen any immediate effects that everything is fine, and continue to congregate.

Are there signals that we could pick up on earlier than that period—within a week, say—that would give us any indication that the numbers might come back up?

SHARFSTEIN: So, I think the signals there are not just- are not going to be immediately obvious in the cases because- because of the potential for exponential spread, it’s a few cycles and then you start to really see the problem. But you could look at- at different measures to see whether people are able to keep their distance from each other, whether they’re wearing masks.

Which we think is helpful. Whether they’re, you know, basically staying close to home or not overly going to locations that are indoors in high numbers. So, those would be, like, predictors. You’d be a little bit more nervous if you saw that, you know, people were going and congregating indoors and, you know, things like that, or they, you know, their travel patterns look similar to similar when- before the pandemic hit. That would make you nervous.

But then you would still have to look for the data. And probably you’d start to see the data in the percentage of tests coming back positive. That would start to go up, and then that would then, as we’re seeing now in Arizona, Texas, some other places—we’d then start to see that in emergency room visits, hospitalizations, ICU admissions, and deaths.

MANDAVILLI: Okay, okay. Thank you for that. Now, Lisa, one of the most striking aspects of the pandemic’s effect has been the really strong racial disparities in whom it affects and- How have those patterns really manifested themselves, but also as Representative Katherine Clark said in a recent House hearing, shouldn’t these disparities have been eminently predictable?

[Cooper appears via webcam.]

LISA COOPER (Bloomberg Distinguished Professor, Equity in Health and Healthcare, Johns Hopkins University School of Medicine and Bloomberg School of Public Health): Yeah, I would agree with what she said. I mean, I think what we’ve seen—and Josh alluded to this, as well—is that this virus has claimed the lives of African Americans and American Indians, in particular, at very, very high rates and, you know. We- we see right now that, you know, we have sort of over 115,000 Americas who have died from this infection.

And we’ve been collecting information on race and ethnicity at increasing rates. So, now we have information for about 93% of these deaths. And what we’ve seen- I believe I have a graphic on this, as well—is that the deaths per 100,000 for people in each racial and ethnic group are completely different.

[Bar graph titled “COVID-19 Deaths Per 100,000 People of Each Group, Through June 9, 2020.” Bars represent Indigenous, Asian, Black, Latino, White, and All deaths with known race. X-axis runs from 0-70. Bar for Indigenous group shows about 35 deaths, per 100,000. Bar for Asian group shows about 26 deaths, per 100,000. Bar for Black group shows more than 60 deaths, per 100,000. Bar for Latino group shows about 28 deaths, per 100,000. Bar for white group shows about 25 deaths, per 100,000. Bar for “all deaths with known race” shows about 32, per 100,000.” Asterisked footnote reads, “Includes all available data from Washington, D.C., and the 50 states. Users are cautioned that the Indigenous rate is calculated from just 21 reporting states. States employ varying collection methods regarding ethnicity data. Denominator is built from data aggregated from each state, aligned with their method.”]

So, you can see in green that the death rate for African Americans is about 2.5 times, almost, the rate that it is for whites. The death rates for American Indians also much higher.

And, you know, so why are we not surprised? Well, we know that, you know, these inequities in health have been- have existed for a long time and they really are a result of social inequities in our society. We have an overrepresentation of frontline workers among ethnic minorities. And so-

I think I even have a graphic on this that basically shows that frontline workers are- are, you know, more likely to have to work outside of the home.

[Bar graph titled “Higher-wage workers are six times as likely to be able to work from home as lower-wage workers. Share of workers who can telework, by wage level, 2017-2018.” Arrayed down the Y-axis: 61.5% of workers with earnings greater than the 75th percentile can telework, 37.3% of workers with earnings from the 50th to 75th percentiles can telework, 20.1% of workers with earnings from the 25th to 50th percentiles can telework, and 9.2% of workers with earnings less than or equal to the 25th percentile can telework. Text reads, “Source: U.S. Bureau of Labor Statistics, Job Flexibilities and Work Schedules – 2017-2018 Data from the American Time Use Survey. Economic Policy Institute.”]

COOPER: So, that graphic basically showed that.

[Bar graph titled “Less than one in five black workers and roughly one in six Hispanic workers are able to work from home. Share of workers who can telework, by race and ethnicity, 2017-2018.” Arrayed along the X-axis: 29.9% of White workers can telework, 19.7% of Black or African Americans can telework, 37.0% of Asians, 16.2% of Hispanic or Latino, and 31.4% of Non-Hispanic or Latino. Text reads, “Source: U.S. Bureau of Labor Statistics, Job Flexibilities and Work Schedules – 2017-2018 Data from the American Time Use Survey. Economic Policy Institute.”]

COOPER: The more money you earn, you know, you are less likely to be able to work from home. And you can see that one in five Black workers, and only one in six Hispanic workers are actually able to work from home.

So, we’ve seen death rates that are much higher in African Americans and American Indians, and we’ve seen infection rates that are much higher in African Americans and Hispanics. Across the country.

And, you know, one of the statistics that comes from the American Public Media Research Lab is that if they had died from COVID-19 at the same rate as white Americans, at least 14,400 Black Americans, 1,200 Latino-Americans, and 200 American Indians or Native Americans would still be alive.

[Cooper appears via webcam.]

COOPER: So, you know, these communities have been really hard-hit. A lot of it is due to being overrepresented among frontline workers, living in neighborhoods that have not had the social investment that other neighborhoods have had. So, less- less safe housing, more crowded housing in those neighborhoods, less access to healthcare.

[Text on card reads, “Black Americans continue to experience the highest overall mortality rates and the most widespread occurrence of disproportionate deaths. The latest overall COVID-19 mortality rate for Black Americans is 2.3 times as high as the rate for Whites and Asians, and 2.2 times as high as the Latino rate. If they had died of COVID-19 at the same rate as White Americans, at least 14,400 Black Americans, 1,200 Latino Americans, and 200 Indigenous Americans would still be alive.”]

COOPER: Basically, needing to go out and buy food more often than other people because not being able to afford to stock up on food. And so, you know, people from those neighborhoods basically being exposed to the virus at much higher rates. Working in health care settings, taking care of older and disabled people, basically. Driving buses, driving subway trains. Doing a lot of the frontline work that we actually need. Working in grocery stores. Working in drugstores, things like that.

[Cooper appears via webcam.]

COOPER: So, people like that getting infected and not actually, you know, having access to testing, either. We’ve been looking at things like access to testing and seeing that the access to testing is not as high in communities of color. So, people maybe not even knowing that they might be infected and actually then going- spreading it to others or delaying seeking care because not having access to primary care.

So, you know, there are some short-term strategies that Josh and I have talked about with policy makers and I don’t know if we want to move into that discussion now or wait until later, but I’m happy to talk more about what we think some of the short-term and what some of the longer-term strategies might be to address this crisis that we’re facing.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Okay. So, you know, I would definitely like to talk about that, but I want to go back a really quick second to what Josh was saying and what I asked about with the six-week delay. People seem quite interested in that in the Facebook chat, as well.

Josh, does that mean that we also won’t see the impact of the protests for another six weeks?

SHARFSTEIN: Yeah. And, just to be clear, it’s not like you see nothing and then, boom, something happens at six weeks. The idea is that the impact of anything that is happening in terms of transmission, if it is increasing, it’s going to continue to snowball up over time.

I think it’s a little bit different to think about the- the just general opening and the protests, but I think, yes, it will take some time to really see the impact. The general opening, I think what’s happening is that people are perhaps putting the concept of the pandemic behind them. And so, when it opened in certain states, people were sort of headed back to their normal routines. And there’s some evidence that, you know, through cell phone data and other things they were really rejoining, you know, kind of going back out and gathering again.

And when that’s continuing to happen, that’ll increase the reproduction rate of the virus, and then you start to see these generations of cases and eventually now you’re seeing it in the hospital.

The protests are- It’s a little bit apples and oranges. Because that- Those are specific things that are happening. It doesn’t necessarily refer to the overall approach people are taking to their whole lives. We know a lot of protestors are protecting themselves with masks and other types of things.

So, I don’t think it’s necessarily the same. I think we’re going to have to see, though. I think, obviously, any time people are around each other, there’s the potential for viral transmission. Outdoors, you know, with distance, with masks, with hand sanitizer is going to be much less of a risk. But you know, when the police are arresting a lot of peaceful protestors and putting them in jail, much more of a risk.

So, it’s really going to depend. And, you know, I would- I would imagine that we’ll see a few different things that have happened, based in part on the overall attitude people have about reopening and the protests just being one part of that.

MANDAVILLI: Okay. And Lisa, we have a question here from a viewer who wants to know what’s the reason for this ethnic and racial susceptibility. I think you answered some of this, but he’s also asking if some of it is genetic.

COOPER: Yeah. I think we don’t have any- We don’t have really much evidence at all to suggest that this is genetic. You know, I think that we have a lot of evidence that it’s due to some of the social factors that I talk about—not being able to engage in social distancing, and not- because of that, also because of the exposure to negative social environments, being also at higher risk of having chronic illness and having diseases like diabetes and heart disease and lung disease, obesity—things that actually not only make people more likely to become infected, but also to be more sick once they do get infected with COVID-19.

So, I don’t think it’s genetic. I think that there are some biological factors. There- there’ve been a lot of studies looking at Vitamin D, for example, and the fact that people with darker skin complexions have lower levels of Vitamin D. Vitamin D is known to be an important factor in the immune system. And so that that could be a contributor. But I think there’s an overwhelming amount of evidence that suggests that most of this is due to our social and economic factors.

MANDAVILLI: Josh, do you have anything to add to that?

SHARFSTEIN: Yes, thanks. I did a great interview for a Public Health On Call Podcast with Eduardo Sanchez, who is one of the Chief Medical Officers of the American Heart Association. And we were talking about this issue that Lisa just mentioned, that for example, there are populations, including African Americans and Latinos, who may have higher rates of certain chronic illnesses, like diabetes and hypertension.

And the point that he made, from the American Heart Association, is well, why did they have that. We know those are very serious predisposing factors, for example, for severe illness and death from COVID. Why do we see those higher rates? Well, it has a lot to do with where they’re living, their access to food, their ability to exercise, the stress that’s in their job, the kind of jobs that they have.

All the same things that are contributing separately to the risk for COVID. So, just to say, well, there are higher risks of chronic illness, that’s not really exactly a biological cause. Because those risks are, in fact, socially mediated also. And so, it’s like a double hit—they’re more likely to get severe illness because of the challenges in their social environment that lead to cardiovascular disease and diabetes, and then they’re more likely—because of those same underlying factors—to actually get COVID.

So, that’s I think- I thought it was a very interesting and persuasive explanation.

MANDAVILLI: Okay, thank you for that. I’d like to ask another question that we got ahead of time from one of our viewers. Gregg Grinspan would like to know, “How accurate are the PCR tests, versus clinical diagnosis, and what does this mean for confirmed vs. ‘suspected’ cases in terms of tracking the spread?”

Josh, I don’t know if you want to take that one?

SHARFSTEIN: Sure. Sounds like that might have been asked by a physician, I’m guessing. So, the PCR tests are measuring for the presence of the virus. And it is possible that the swab can’t find the virus, or the test won’t pick it up, but the person actually does have COVID and there are different stages of illness where they’re more likely to be detectable on the test.

So, you know, some people have given an estimate of the sensitivity of PCR at around 70%, meaning of 10 people with the disease, it’ll pick up seven of them.

So, for- That’s at any one time. Over time, some of those patients might turn to test positive. So, it depends, you know, how you’re looking at it. From a clinical perspective, clinicians may decide to treat someone like they have COVID just on the basis of the history and the symptoms, and the- perhaps the exam.

For example, the idea of losing smell and taste seems to be a quite specific symptom. But someone who just is a little bit achy, maybe, and has a negative test, there would be less of a suspicion to consider it like COVID if the test is negative. So, there’s some clinical judgement in there.

I think we have to separate out in terms of how to think about this and truly diagnose with a test, versus suspected. For clinical purposes, it’s really a clinical judgment that is based on, you know, all these different factors, including other information like other people with COVID in the household. Have you been- Is there a known exposure? Things like that.

But then from an epidemiological perspective, you would look at the same thing every time, so you would look at the confirmed cases by actual test result and assume that you’re basically seeing real trends and that if -the underlying biological characteristics aren’t changing, but you’re also going to measure other things.

If there were a really consistent definition of suspect cases, you could measure that, but certainly hospitalizations, ER visits, ICU admissions—all those things. And that paints the overall picture of how things are going and the trends.

MANDAVILLI: Nancy, we’ve been hearing a lot that we can expect to see more of these pandemics, that this isn’t going to be the last one that we deal with. And, you know, I was wondering what do we know about where those might come from?

You know, there’s been- You know, there’s been viruses that have jumped from birds and pigs and, you know, what should we be worrying about? And along those lines, actually, one of our viewers, Anna Shneidman, also has a question: Have any viruses jumped from standard pets—cats, dogs—to humans? And if not, why not? Why is it more common for exotic animals?

SIMMONS: Well, I’m not sure it’s more common for exotic animals. In this particular case, we know that other animals besides humans can get COVID-19. So, there are some well-publicized cases—the tigers at the Bronx Zoo got COVID-19 from the keepers. So, it was transferred from humans to tigers.

There have been some cases, not very many, of household pets getting COVID. Cats, primarily. I think there’s at least a couple cases of dogs. Dogs don’t seem to be nearly as susceptible. If they get it, they perhaps are not capable of transmitting it onward.

[Simmons appears via webcam.]

SIMMONS: We do know from the Netherlands very recently- They have mink farms in the Netherlands for fur. And there’s been a recent case where humans have given- the keepers of the mink have given COVID-19 to the farmed mink, and then at least one case where a worker at one of these places then subsequently got COVID from the mink.

So, we know that it can move back and forth in this way. In general, what we’re concerned about in thinking forward to the next pandemic is the more that humans interact with wildlife directly and in wildlife markets, in situations like this, the more likely it is for various viruses to potentially move into humans. Through these same ways.

So, there’ve been cases where pigs have become ill and passed the virus on to humans. Any place where we have basically close proximity of humans and animals, there’s potential for transfer of diseases.

Should you be afraid of your- of getting COVID from your pet? Actually, it’s much more likely that a pet is potentially going to get it from their- their people. Because in this case, SARS CoV-2 is really a human disease, and it’s the humans who are transmitting it back and forth and occasionally giving it to other animals.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Okay. As a follow-up question to that, just to stay on that for a minute… You know, there was a lot of anger directed at China and, unfortunately, by extension to Chinese people after we found out the origins of this virus. And, you know, some of that vitriol was outright racist. But China probably does have a role to play in controlling the spread, and I was wondering if you could talk a little bit about what some of the measures are that countries like China could take, where there are these wildlife markets, to minimize the chances that another virus might jump this way?

SIMMONS: Well, wildlife markets in general where you bring live animals together and you keep them in very close quarters are always going to be a problem.

[Simmons appears via webcam.]

SIMMONS: So, shutting down wildlife markets is probably the number one thing that we can do.

Viruses can also move be- in- and frequently do, in domestic animals, as well. There just has to be a lot more surveillance and a lot more care given to how we treat animals and how we treat the environment. Because, frankly, the more that we continue to degrade our environment, continue to cut down forests, continue to urbanize areas, the more pressure we’re going to be putting on wildlife populations, and the more people are going to be coming in contact with wildlife.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

SIMMONS: So, in essence, we’re our own worst enemy here. So, efforts to close wildlife markets, or to control them in some fashion that prevents mixing different species of animals, piling them on top of each other, is- is going to be a big step forward.

MANDAVILLI: Josh, do you have any thoughts about this?

SHARFSTEIN: Yes. As a former Food and Drug regulator, this is a really important question. And in many countries in the world informal food markets are extremely common and important to the economy and to culture. And so, you have this challenge of, well, we know this is a dangerous situation, what do we do about it. And just trying to shut it down, sometimes, doesn’t make it go away. It may make it, you know, actually more dangerous, less- fewer precautions taken.

So, this becomes, then, a real challenge in regulation. There’s a report from the National Academies of Sciences earlier this year where we, you know, tried to grapple with this. And the conclusion was that it’s probably better to try to come up with a way to regulate informal markets that- You know, put a lot of surveillance, safety measures, phase out the cages, do whatever you can so that it’s allowed to happen in a way that is as safe as possible and as closely monitored as possible.

That may be a alternative approach to trying to do it just purely through outlawing it and then having the risk that it would continue.

SIMMONS: Yeah, outlawing it, I would say, is not the way to go because of the cultural concerns. And also, in many parts of the world, people depend for the protein in their diet from some of these sources. So, coming up with alternative ways of providing protein and more sa- in a more safe fashion to populations is a big part. And monitoring and controlling in some fashion to keep these various species separate, instead of just trying to shut it down so it all goes underground. And then you’re just making it even worse, in essence.

MANDAVILLI: Okay. Lisa, I have a question for you about, you know, what Josh was talking about earlier, that the states are opening back up and we’re seeing these clusters. What are you most worried about as states start to open back up? And where do you think we’ll see the clusters of disease? And also, what are some things that governments at every level—national, state, local level—do to help the communities that are hardest hit?

[Cooper appears via webcam.]

COOPER: Right. Well, you know, I think it depends on actually who starts going back to their normal activity, as to who we’re going to see hardest hit. But again, I think that people who are least able to stay at home and to safely engage in social distancing are probably going to continue to be hit harder.

So, I think we’re still going to see communities of color, African Americans, American Indians, Latinos, you know, having- getting COVID-19 at higher rates than others because they already are, and then with everybody opening up and there being more contact among people, we’re going to see these rates go up. And especially among, again, people who are already vulnerable—older individuals, people with chronic conditions, people living in institutions, institutionalized settings like nursing homes, prison populations.

You know, we’re going to be seeing a lot more infections in those groups. So, the real concern is what are we doing, first of all, to make sure that people understand when they are at risk and what they need to do to protect themselves. Are we communicating? Have we had experts who are communicating clearly what is people need to do to stay safe?

And part of the problem is that the public is getting mixed messages from leaders. And I think it’s really important for public health and health experts to be, you know, stepping forward and not giving people false reassurances about where we are, but really being very direct about what’s going on and what people need to do to stay safe.

I think what we’re going to have to do is to continue to expand our capacity for testing and contact tracing, as Josh mentioned. It’s really going to be important to try to have people tested and have the contact trace as quickly as we can so that we know who to tell that they need to quarantine themselves.

And also, you know, to ramp up capacity in the health care settings that deliver care that are being hardest hit. So, you know, I- that’s what I’m really concerned about, honestly. I think we’re going to need to continue to protect our frontline workers, to really make sure they have good Personal Protective Equipment they have. That the policies we have about the workplace will protect them so that they don’t have to work in very close proximity to one another. That they have adequate sick leave, so they don’t feel compelled to work when they’re sick. And that they have benefits.

You know, I think we’re going to need to really focus on that. And addressing these, like, very acute social needs. Things like food, housing, places that people can go to quarantine themselves without spreading the infection further to their family members. Really working on policies that will help to address these inequities that we have in our society. And that will focus on the most vulnerable.

But, we have a lot of work ahead of us. I think that there are certain states that have made more progress than others, and we can look to those for examples. And really just try to keep the lines of communication open and communicate in a trustworthy and respectful manner with people about what their real concerns and fears are, so that we can help to address those in a compassionate way.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Okay. Thank you for that. We have a follow-up question from an audience member. Rudy Lewis wants to know if the racial disparities are similarly found in minority populations in England and France and other countries.

COOPER: Yes. They actually are, which actually, you know, lends further support to the- the hypothesis that we have around social conditions. Because we know a lot of the communities of color in Western Europe are similarly socially disadvantaged.

We also know that the stresses of sort of racism contribute to poorer health and also sort of predispose people to getting sicker at higher rates. So, we are seeing similar rates of- similar disparities in other places in the world.

MANDAVILLI: Okay, thank you for that. And we also have another question that maybe, Josh, you could address. You know, we’ve seen a lot of misinformation and models that aren’t quite right and studies that aren’t quite fully baked and things like that. And one of the questions asks about a Belgian report based on a simulation about how the virus spreads when people are running or exercising outdoors. Annie de Flores would like to know, “What do models tell us about how the virus spreads when exercising outdoors?”

SHARFSTEIN: Sure, so I would just take a step back on the question and say we want to know more than what the models suggest. We want to know does the- how well does the virus spread when exercising outdoors. Not just what did the model say. Because you could put a model in and you could say, “I think it’s the following,” and then it’ll tell you, but you don’t know whether those assumptions are true.

So, the evidence right now—there’s not a lot. You know, there’s certainly with a lot of circulation and being outside, it’s way better to be outside than inside. Inside the droplets can hang around. You’re within a closed location, you move into somebody’s area and there’s- you know, it’s just- it’s just stuck there. People can be exposed. And if it’s an extended period of time, that’s particularly dangerous.

Outdoors is going to be much less. There have been different papers that have said, you know, don’t jog right behind someone so you’re inhaling exactly what they’re exhaling for a certain period of time, and based on our model that could be more dangerous.

I think the general principle is stay away from other people to the extent you can when you’re exercising outside.

[Sharfstein appears via webcam.]

One other thing about exercising—you know, we’ve been hearing about six feet, six feet, six feet. That’s about droplet distance, you know, in normal kind of breathing and conversation. It’s not about droplet distance when people are singing, shouting, or breathing really hard from exercise. And so, it’s probably- you want to give yourself a little bit of extra room in that situation.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: And is that because there are also smaller droplets or aerosols that can stay in the air longer and travel further?

SHARFSTEIN: I think it’s a little bit because of that. I think it’s a combination. I think just in general droplets can be propelled further if they’re just pushed out much harder.

MANDAVILLI: Okay, thank you for that. I have one more audience question here from Anne Canright—How is COVID-19 different from the flu? And, Nancy, I’d love it if you could explain, too, how some of the flu viruses that have jumped from other animals been different. And maybe Josh and Lisa, you could talk a little bit more about how the impact has been different with the coronavirus, compared to flu.

[Simmons appears via webcam.]

SIMMONS: Well, I can just say just to begin with that the coronavirus and the flu are completely different viruses. So, they have some of the same clinical symptoms, but from an evolutionary perspective, a biological perspective they’re different. And so, we shouldn’t necessarily expect them to behave in the same way.

And I think that I’m going to have to pass this off to Lisa or Josh to explain the clinical differences between how humans react to these two different viruses when we get sick.

MANDAVILLI: Lisa, do you want to take it?

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

COOPER: Sure, I mean, I think what I would say is what they have in common is that both of them have spread across the entire globe and are killing millions of people.

[Cooper appears via webcam.]

COOPER: That both of them have been very- viruses that have caused very severe human illness. That even back in 1918- And I’m just saying that- Not every influenza is the same, but the influenza virus of the- the strain that was in 1918, 1919 was particularly severe. So, that’s what I would say.

The current- the more recent influenza strains that we’ve seen have not caused as severe human illness and have not had as high a mortality rate as COVID-19. So, I think the difference is that we have- no one has immunity to this strain of the coronavirus. And we have no treatment for it. And we have no vaccine for it.

And so, that’s the- one big difference from what we see clinically. But I do think that, like the flu pandemic, for example, of 1918, 1919, had a similar impact on the population and showed similar patterns in terms of people who were living in poverty and people who were in socially crowded conditions and not able to engage in, you know, safe hygiene practices were definitely at higher risk of dying from influenza back then.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Okay. I think, you know, one of the things that seems to have surprised scientists from my conversations with them is that this virus behaves a lot more like the flu than like other coronaviruses. And Josh, you mentioned earlier that we- that people were a little surprised about the pre-symptomatic or asymptomatic transmission of the virus. Can I broaden that a little bit to ask, you know, what do you think are some aspects of the virus—and maybe that’s one them—that has made this particularly difficult to control?

[Sharfstein appears via webcam.]

SHARFSTEIN: Sure. So, that aspect—that people without symptoms can transmit it has made it particularly difficult to control. We should be clear—compared to the seasonal flu, this is very highly infectious and very highly lethal. So, it doesn’t behave like a typical flu virus at the level of the population.

You know, flu doesn’t bring the hospital system of New York to its knees or lead to these kinds of challenges that were in northern Italy. Flu isn’t- doesn’t force us to take all these extreme measures. And it’s because of the infectiousness, which is partly related to the virus, partly related to the fact that it’s a new virus—we don’t have any latent immunity for it—and there’s no vaccine.

And then on top of that, the pathology that it causes is very, very different than the flu. It’s not just that it causes pneumonia. It causes a very severe viral pneumonia, but then it also has this big impact on clotting. There are all kinds of different conditions that are now being associated with it.

So, the way it affects the body is different. So, I think that there are, you know, some similarities—mainly in the symptoms—but in the way that it’s actually affecting people, individually, and the population, it’s quite different.

And I think probably the touchpoint of the flu as a point of comparison has been one of the things that’s made it hard for people, I think, to recognize just how serious the threat is.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Okay. I do want to clarify, though—when I said that I didn’t mean that it’s just as trivial as the flu, and more that the coronaviruses that we’ve known before haven’t had this pre-symptomatic spread or, you know, have not been quite as- not been able to take hold as easily as this virus has seem to have taken hold.

SHARFSTEIN: Well, that’s totally, totally true. And if you think about SARS, SARS was very lethal. Even more lethal than this coronavirus. And- But not so easily spread. And so, this combines the, you know, easy spread of the flu—maybe it’s even a little easier in some respects—with the- much more lethality. So, that’s really what- that combination has really been what we hoped didn’t happen.

And, you know, so many times in the last 20 years we’ve had this challenge. It’s been the SARS, or with H1N1, the flu, where we’ve said, “Well, we’re lucky because of, you know- We’re lucky that SARS isn’t more transmissible. We’re lucky that H1N1 isn’t more lethal.” You know, and we were lucky then. Because we’re not so lucky now that it combines both.

MANDAVILLI: It seems like one of the things that’s made it very hard for people to acknowledge the seriousness of what we’re dealing with is the sort of really high level of sacrifice it has demanded of, you know, the lockdowns, the, you know, schools being shut down, kids having to do online education, the economy taking this massive hit, all the job losses. I think there are several people in our audience who want to know how do we balance between, you know, the relative needs of public health, versus education and economy and all of the other things that we need to worry about?

SHARFSTEIN: I’m happy to give a quick answer. I’m very interested in what Lisa thinks. If you want to jump in here, I’ll defer.

[Cooper appears via webcam.]

COOPER: Sure, I mean, I’ll say a few words and then defer to you as a former public health commissioner. I mean, I definitely think that we- these are things we do have to balance. I think people need to understand that it’s a- it’s a relatively shorter-term sacrifice, hopefully, for a longer-term benefit.

That it’s about if we had invested in our public health infrastructure, we might not have found ourselves in this predicament. And so, I think it’s really a lesson for the future in what we do, in terms of making sure that we have invested in our public health system, in its ability to be prepared for a pandemic like this, and to respond to it rapidly.

The fact that we didn’t invest in it and that we used a lot of our resources in other ways meant that we were not prepared for this at all. So, as a result, this is our most effective strategy at this moment in time to contain the spread is to basically, you know, make it- have everyone make these sacrifices.

But if people could understand that it’s for the- it’s a shorter-term sacrifice for a much longer-term benefit, I- hopefully that will bring about better understanding. And the fact that, you know, that this may be a back and forth thing, that if we reopen, we’re going to have to do so cautiously and we may need to keep a close eye on how things are going, and then backtrack, if necessary.

So, I’ll just stop there and let Josh, you know, take over.

[Sharfstein appears via webcam.]

SHARFSTEIN: Well, I think it’s useful to look around the world—places that were able to respond very seriously and have major public health responses, strong investments in contact tracing, a real commitment to follow-up public health guidance—they’re opening up now. And they’re able to do a lot more than we are without inhibition.

We’ve sort of picked a muddled path where we’re convinced that there’s this trade-off in the short term. I think, like Lisa said, a very strong public health response is what allows those other things to happen. And what we don’t want to be doing is just pushing forward on things while more and more people are dying. It’s better to- Ultimately, I don’t think that’s going to be successful.

I don’t think people are going to want to go out to eat if they’re at risk of catching a deadly illness. I think that we’re going to need to really have a serious plan and execute it to reduce the viral spread. And then that will allow these other things to happen. I think these other things are very important.

And it’s critical to have economic activity. It’s critical for kids to go back to school. Kids are losing a tremendous amount not being in schools. But the path to doing that safely is the path of really investing in public health. I’m just mystified where I hear people talking about how important it is to reopen and those people are not the ones who are, like, banging on the CDC’s door or the state Health Department’s door and say, “Help us control this virus. Tell us what we need to do to control the virus.”

Because it is through a strong public health approach that we actually get to the other side of being able to do those other things with confidence.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: Thanks, Josh. Actually, you know, we are starting to run out of time here by a little bit, but I do want to ask very quickly, because a bunch of our audience members have questions about herd immunity, when we might expect to reach that and, you know, what do you expect to happen until that point? I don’t know if one of you can answer that briefly.

SHARFSTEIN: Herd immunity is not on the horizon, really, until we have a vaccine. I mean, and I call it population immunity. Population immunity will happen when enough people are not susceptible to the virus and, you know, hopefully that will happen because of a vaccine. And then the virus won’t be able to spread that easily.

If we’re going to wait for enough people to get sick from the virus to really have a major, major impact on transmission, so many more people are going to die in the interim. And so, it’s not- that’s the scenario we want to avoid.

MANDAVILLI: So, I’m going to take the moderator’s prerogative here and ask the last question. And I’d like to ask each of you the same thing, which is what are some lessons we can take from this pandemic to prepare for the next one? Because it seems like there will be a next one. Nancy, do you want to go first?

[Simmons appears via webcam.]

SIMMONS: Sure. I think the biggest lesson that we can take is that continued destruction of habitats by humans, misuse of the natural resources of the world, it’s- this is how this pandemic came to pass, and this is how the next one is going to start, too. So, we have to start taking a much more proactive role in protecting the environment because that’s what protects us from events like this in the long run.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: And that has to happen at a global scale, correct? Not just-

SIMMONS: It has to happen at a global scale, yes. But it starts at home. It starts on a very small scale, but it has to happen everywhere to protect us from the next pandemic.

MANDAVILLI: And are those conversations happening, you know, led by the WHO or anybody else to make sure that countries understand the importance of this and that they are starting to adopt regulations?

SIMMONS: One would hope. But it has to be more than discussions amongst academics. This has to be something that people understand at a grassroots level. Because everybody has to get on board or it’s not going to make a difference.

MANDAVILLI: Okay. Lisa, what about you? What do you think we can take from this pandemic?

[Cooper appears via webcam.]

COOPER: I think what I would say is we need to think of a different type of herd immunity. I’ve been going around saying this lately. If we thought of- If we really want to have herd immunity from this virus or any other negative impacts on the health of our population, then we really need to invest in improving the conditions in which people live, and in getting rid of the inequities in our society. We really need to address the things that we know as public health professionals that will work to improve the opportunities for people to be healthy.

So, things like addressing childhood poverty, you know, creating safer neighborhoods and affordable housing, and addressing income inequality and improving employment opportunities for people, including access to primary care and preventive care.

I think those are the things that are going to create herd immunity to poor health, and also herd immunity- In a way, they’re like a vaccine against poor health. And so, that is going to bolster us up, along with our investment in our public health infrastructure.

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: And I’ll ask you the same thing that I asked Nancy—are those conversations happening?

COOPER: They are. They are starting to happen with policy makers, local and federal. I think we have to create political will for this. I think our society needs to understand more about the connections between our social factors and health. And how investing in those things is going to enable people to be healthier and more productive, and therefore we will have a stronger economy.

I think oftentimes, people don’t see the connections between our living conditions and our social conditions and our health. And therefore, they don’t advocate for those. But if we can get that sort of education and understanding out to the public, and create political will for that change, I think it can happen.

And so, I’m seeing some glimmers of hope now.

MANDAVILLI: That’s good to hear. Josh, what about you?

[Sharfstein appears via webcam.]

SHARFSTEIN: So, after a crisis, there’s different kinds of learning that can happen. Some people call it first-order learning, versus second-order learning. And first-order learning is you just respond to the very specific things that you’d see. So, like, “Oh, we do need one of those machines that makes a whole lot of N95 masks really quickly.” You know, a very, very literal kind of learning.

And I think it’s pretty likely that we’ll have that kind of learning. But it’s the second-order learning that Lisa Cooper is talking about, which I think is essential. It’s not just those specific things, it’s the fact that there are aspects of our society and our approach to health that leave us fundamentally exposed to different kinds of threats.

And it’s both infectious threats and threats like chronic disease that really rob a lot of people of, you know, years of life and opportunity for their children. And if we can have some of that deeper learning, it’s really helpful.

The challenge is after a crisis people tend to want to do the first order learning and then move on to the next thing, or get back to their daily lives. It’s a very typical thing. It takes a lot of leadership to be able to say, “Hold on. Just having a few more machines that pump out N95s is not going to be enough.”

And so, I think it’s a very, you know, serious question at the state, and local, and of course the federal level—you know, will we have the kind of leadership to learn some of these key lessons? Will we have the kind of 9/11 report that we had after 9/11 that gets to some of the, you know, more of the core issues. And are we going to be able to listen to people like Lisa Cooper and her perspective on what it will take?

[Screen split into four quarters, each featuring the moderator or a panelist via webcam.]

MANDAVILLI: And the same question to you—are enough of those conversations happening for that deeper kind of learning?

SHARFSTEIN: So, I’m particularly interested in, as this starts to fade, what we see. And I think it’s going to depend on leadership. I don’t- I don’t know whether that’s going to happen. I- It- Pick- You know, on a Monday I might be feeling a little bit more cynical and say we’re just going to get the first order. And then, you know, on a Tuesday, I’ll talk to a mayor or a governor who is really thinking, you know, in a big picture.

And so it really- it depends. And I think it- you know, it may be spotty around the country, how we get to that. But I think that there is a potential. You know, things happen as a result of crisis that are never otherwise possible. I teach a course about that, wrote a book about that. And it’s like, you know, crisis creates a moment in time for people to look at things with a different, you know, perspective.

And if we can capitalize on that from the coronavirus, there are many, many lives to be saved, even if we don’t have another pandemic.

MANDAVILLI: It seems like you actually did on a somewhat hopeful note. So, thank you for that. I think we all need that right now.

Well, that actually brings us to the end of the program. Thank you all so much for all of your answers. I learned so much, and I’m sure our audience did, as well. I just want to remind everybody that there is a survey that you can fill out to tell us- well, to tell the American Museum of Natural History what you thought of this program.

[Card appears with text reading, “Survey: https://bit.ly/AMNHcovid19”]

MANDAVILLI: And thank you again for participating.