In this episode of Rule Breaker Investing: Authors in August, Motley Fool co-founder David Gardner chats with Dr. Jeremy Brown about his book Influenza: The Hundred-Year Hunt to Cure the 1918 Spanish Flu Pandemic. Brown is director, Office of Emergency Care Research, NIH, and is one of the people who is at the forefront in the fight against COVID-19. He talks about the spread and extent of the 1918 virus and the many similarities between then and now, what has changed, what's next, and much more.

Also get a sneak peak of what's coming up next on Authors in August.

To catch full episodes of all The Motley Fool's free podcasts, check out our podcast center. To get started investing, check out our quick-start guide to investing in stocks. A full transcript follows the video.

This video was recorded on August 11, 2020.

David Gardner: My brother-in-law spoke truth when, at a recent family barbecue, he pointed out that seemingly every conversation these days, seemingly, somehow ends up getting back to COVID. He was getting tired of it. It just has such a strong gravitational attraction; we can't get away from it. It reminds me of Godwin's law, which I've mentioned before in this podcast, maybe you know it, the old internet law that states, "As an online discussion grows longer, the probability of a comparison involving Nazis or Hitler approaches 1." Well, these days, as any discussion grows longer, the chances that it'll arrive back at COVID approaches 1. You could call it my brother-in-law's law.

So just as my brother-in-law challenges all of us to consider specifically not mentioning COVID in a given conversation or a period of hours or a day, if you like, try it. Just as that challenge is issued, [laughs] here I am with this week's entire podcast focused on influenza and, to a lesser but inevitable extent, COVID.

It's Authors in August, and my guest this week is the splendid Dr. Jeremy Brown, who will be talking about his book Influenza: The Hundred-Year Hunt to Cure the 1918 Spanish Flu Pandemic. And that talk about what happened 100 years ago would be interesting enough on its own, fascinating and full of lessons, but of course, it seems even more pertinent in light of what we are all living through in 2020. So 1918-2019, right here now, Jeremy Brown, Influenza, only on this week's Rule Breaker Investing.

Welcome back to this week's Rule Breaker Investing. I have a real treat in store for you. We'll get to that very shortly. As I mentioned at the top, Influenza: The Hundred-Year Hunt to Cure the 1918 Spanish Flu Pandemic with author Dr. Jeremy Brown, who also happens to work in the Office of Emergency Care here at the National Institutes of Health in Greater Washington, DC. So of course, we'll be talking about the very far away and the very here and now.

I do want to mention, you've joined me during Authors in August, that's a Rule Breaker Investing tradition every August on this podcast. We just celebrate one book after another book that I find fascinating, that I've read in full, that I encourage you to read in full. Whether you do so ahead of the podcast or afterward, that's your call, but I know you're going to enjoy Jeremy's book.

I want to mention again, last week Jay Jakub, Completing Capitalism, I've heard back from a lot of you on that about how you enjoy being reminded of the power of conscious capitalism, business done well. And, yeah, it works both for us as investors, these are the stocks that we pick. After all, when you're investing in businesses that solve the whole problem, not just for one group of people, those are usually going to be the best stocks of our time, but we also try to do this as businesspeople. And So Jay Jakub and what he's working on at Mars, and now outside Mars, exciting. I know you're going to enjoy that if you didn't have a chance to hear it.

I do want to flag next week's author, and it's going to be Amy Castoro. Now, Amy has written, with her co-author, Roy Williams, a book called Bridging Generations: Transitioning Family Wealth and Values for a Sustainable Legacy. You can order this one on Amazon, it's in a Kindle edition; very quick, very readable, and boy! Very relevant for Rule Breaker Investing. It's something I've tried to think about some. I'm still in the early stages myself. Many of you will already have done this, in some cases, well; in some cases, not. And many have not even really thought about it. After all, many people don't even fill out their will, which is a big mistake. If you have something to give away, you should have a will.

But beyond that, thinking about what succeeds, and when you leave something to others, will it work or not. The troubling statistic that Amy is targeting is that 70% of all inheritances, all transitions of wealth from one generation to another -- this is true in America, it's true globally -- 70% fail. They end up not really taking, for really important reasons that you're going to learn next week, or if you just read the book, you can learn ahead of next week, but we're going to be talking about that.

Because I know so many of us, regardless of how much or how little you have to leave others. And I hope it's as much as possible; we're all about abundance here at The Motley Fool and on the Rule Breaker Investing podcast. But there are ways to make it work and then there are ways that if you don't know the ways to make it work that you will fail at it or not do it as well as you wanted. You can end up messing up lives that aren't your own as well as disappointing yourself. So this is a great topic. I'm looking forward to sharing that with you.

I will mention, that book is the second edition, Bridging Generations, that's the newer 2017 edition. I myself read the first edition, which is only in hardback these days, and it's called Preparing Heirs. So in a sense we're talking about that book, because that's the one I've read, but you can read the more recent version that Amy co-authored. So she'll be with us next week.

And now, without further ado, my conversation with Dr. Jeremy Brown.

Dr. Jeremy Brown is director of the Office of Emergency Care Research, where he leads efforts to coordinate Emergency Care Research funding opportunities across the National Institutes of Health. He also serves as NIH's representative in governmentwide efforts to improve emergency care throughout our country. Prior to joining NIH in 2013, Jeremy served as research director in the George Washington University's Department of Emergency Medicine, where he founded an HIV screening program and received three NIH grants focused on a new therapy for renal colic. He is a veteran of emergency care rooms, but most important and relevant to this week's podcast, Jeremy is the author of the wonderful 2018 book Influenza: The Hundred-Year Hunt to Cure the 1918 Spanish Flu Pandemic.

Now, I want to say, before welcoming Jeremy, he will only be speaking for himself in this week's interview. He's not in any capacity speaking as an employee of NIH. Jeremy, welcome.

Dr. Jeremy Brown: Thank you. What a pleasure to be back talking to you.

Gardner: Thank you. Yes, you and I first met because I'm part of a wonderful book club here in Washington, DC, which somehow manages to get authors to come and join us in our book club talks, and you graciously volunteered to do so. We had such a great time talking about your book Influenza last year, pre-COVID. And so here we are now, Jeremy, in a much different environment that no doubt will color aspects of this interview, but I'm certainly going to stay focused initially on the book.

So let's go right there. At the beginning of your book Influenza, you say something to this effect, "Be glad you weren't born in the 1900s." [laughs] Setting the stage for telling the story of the 1918 flu epidemic, you remind us that the following were all state-of-the-art therapies for treating the flu, prescribed by doctors a century ago: enemas, mercury, tree bark, and my favorite, venesection, the age-old unsuccessful, persistently crazy notion of bloodletting.

Dr. Brown: That's right. A century ago seems like a long time ago, but that's the lifetime of our grandparents, great-grandparents. And it's really remarkable to see some of these therapies that were given to all kinds of patients who had fevers and infectious diseases, as we call them today. It's really fascinating to see that they are the same therapies that were used for, in some cases more than 2,000 years, that's how far back bloodletting goes. And it's both sad and important for us to remember that we have come a long way since then. There are still some therapies which, even though they were tried a century ago, have come up again, and they turned out to be not terribly good therapies or actually useless therapies; and we can perhaps talk about that.

But it was really an era in which medicine was just coming out of the Dark Ages. In fact, one historian has said that, from the time of Hippocrates until the 1860s, medicine had not advanced at all. So you know, over 2,000 years. And only in the 1860s, when the whole idea of antisepsis came in, only then did medicine really make its first real step into what we would call the modern age. So for over 2,000 years, we were doing the same as we had always done, more or less.

Gardner: And was it Louis Pasteur who discovered bacteria, and was it somewhere around -- yeah, I think it was the 1850s?

Dr. Brown: It was really the development of the microscope in the late-1600s that really got us on the way to seeing these very small living things in droplets. And from there, it took a little while for the notion that there were bacteria under the microscope, but it was soon developed. And those famous bacteriologists -- Koch working, I believe, in Germany, who did a great deal to advance our understanding of bacteria.

But remember, when we're talking about influenza and also about COVID, remember that those two diseases are not caused by bacteria, they're caused by viruses. And viruses were, kind of, imagined in the mind, because people said, hmm, there must be a very small thing that's causing this, and we can get to reasons, but they figured out that it must be something smaller than the bacteria, but they couldn't see it.

And it was only in the 1930s, almost 18 years after the great influenza pandemic, it was only around then that viruses were really isolated and a little bit later, the electron microscope managed to capture a picture of one. So when we talk about bacteria, they were, sort of, beginning to be understood, but viruses were a long way off from having any kind of medical understanding, let alone identification.

Gardner: And picking it up right there with viruses, Jeremy, you spent chapter 2, well, you titled it "A Jolly Rant: A History of the Virus," and I'm going to read the first two paragraphs of that chapter right now, so that anyone who is not yet read Influenza can see, not only is it a fascinating history of an event that seems so relevant to 2020, but it's such a well-written book as well.

So here's the start of chapter 2.

Viruses were here long before us. They were here before intelligent life, before apes and chimpanzees, before reptiles, before anything crawled out of the slime of creation. Viruses are ubiquitous, but their mystery is inherent in their origin. We don't know exactly how they developed, but we do know they've been around for millions of years. They exist on the edge of life and they challenge our definitions of what it means to be a living thing. A rock is not alive, but a bacterium is; a virus lies somewhere between the two.

And just continuing a little bit more.

A virus is a box of chemicals without the structures of a basic cell it cannot metabolize or replicate on its own. In order to reproduce, it must invade living cells. Viruses infect bacteria and plants, reptiles, fish, birds and mammals. They've been so intertwined with our own evolution that over millennia, some became incorporated into our own genetic code. Nestled into the long strands of our DNA are sequences that originated from ancient viruses. Their genetic code was so bound with ours that the virus became a harmless part of us, freeloading off human cells as they reproduced.

So my question, Jeremy -- this one is from a different angle, maybe it'll catch you off guard a bit just for a second -- where or how did you learn to write so well?

Dr. Brown: Oh, you are too kind. Well, I suppose some people have fishing as a hobby and others like to watch sports. Unfortunately, I was never terribly good at catching fish and never developed much of an appetite for sports, neither in England, where I grew up, nor in the U.S., much to my children's disappointment. And So the natural way for me to spend some of my time is writing. I was always interested in the history of science. I had written a previous book on a particular aspect of the development of Copernican theory, the theory that the earth is not at the center of the universe. And this was the next book that I tackled. And so I'm grateful for the accolade, and I hope others find it as entertaining and as useful as you did.

Gardner: And so viruses, as you pointed out, are just different creatures altogether. Antibiotics don't fight viruses, they're completely ineffective against the flu; you remind us in the book. You talked a little bit about how, with your own medical practice, your patients will sometimes walk away disappointed when Jeremy refuses to prescribe them an antibiotic for their virus.

Dr. Brown: Yes, it's a very, what do I say, I'm often successful, and I'm sure I'm not the only one who has this challenge. The thousands of emergency physicians working on the front lines every day, with the nurses and the techs and everybody who makes the emergency department run as efficiently as possible, and I realize that though it doesn't always seem to be efficient, all of us struggle. And indeed, primary care doctors struggle with giving the patient what she might want, what he might want, and doing the right thing by the patient.

So as you mentioned, and it's worth mentioning again, antibiotics work against bacteria. They have no effect against viruses, although, they do work against the bacteria that sometimes settle in our bodies after a viral infection. So you could get a bacterial pneumonia after a viral infection like influenza. And similarly with COVID, and in those instances, of course, you're now dealing with a bacterial infection, and the antibiotics are game changers, absolute game changers.

But in the emergency department, if a patient has been waiting two or three hours and they've come with an expectation that I can do something for their cold symptoms, it's very challenging to appear to be sympathetic, which we always are, and also to do the right thing. In fact, it's so much easier, it's so much easier to give the patient a prescription to leave the office or the emergency department, because they have something solid in their hand and they feel, oh, my time was well spent, I got something. If you tell the patient, "Look, you're going to get better with antibiotics or without antibiotics. I think the best thing for you, just to go home, go to bed and drink some soup and have some hot tea or fluids." Well, the patient is often disappointed with that.

And it's fascinating. Sometimes I would, kind of, gauge what the patient wanted by talking to them and I would say something, like, well, the good news is, you're going to get better without antibiotics. And the patient would look at me and smile and say, oh, great, I just wanted to get checked out for that. I can say the exact same line to another patient thinking I've got it right, and they would say something like, what do you mean you're not going to give me antibiotics? My husband sent me here because he told me I need antibiotics, or I called my doctor's office and he said you need to go to the emergency department to get antibiotics.

So as many times as one can try and get it right, there's always the challenge of fulfilling a patient's, perhaps, reasonable expectations without going into the whole history of antibiotic resistance. And so fulfilling the patient's expectations in a gracious way, but also pointing them in the right medical direction.

Gardner: Let's stay focused a little bit more now on viruses and the specific one that you've written a lot about, and that's influenza. So in your book, Jeremy, you write that influenza throws

a wrench into our elegant system of defenses, because it is a shape shifter. It frequently changes the proteins on its surface, makes it harder for our body to recognize them. Think of a criminal...

you write,

...who makes convincing disguises, who can easily disappear in a crowd. These alterations provide the virus with an invisibility cloak, making it unrecognizable by existing antibodies. This is why you catch the flu more than once during the season, your body produces antibodies to the first virus, but is infected by a second that it did not recognize."

Again, it's so much fun to quote you from the book and some of your analogies.

Jeremy, can you remind us of the scale of the 1918 influenza, how long it lasted, how much damage it did? America was fighting two wars in 1918, as one historian said, you wrote: germs and Germans.

Dr. Brown: That's right. America had come into the war in 1917, dragged into this war, was shipping vast numbers of troops across the ocean to fight on the European front, and at the same time, you know, sort of a year into this war, it was actually, sort of, in the months before the armistice was finally signed, in 1918, we had this fire that swept through all of humanity, taking with it somewhere between 50 million and 100 million people. No one is ever going to know the exact number, but these are good guesses. Here in the United States, 675,000 people lost their lives. Which, if you were to do a calculation given today's population of the U.S., that's the equivalent today of 3 million deaths.

So you had this disease sweeping through the country, sweeping across Europe, into New Zealand and Australia, into South America, into India, and nobody knew what it was, this to me is a very, perhaps the most chilling aspect of the whole thing. Even though it had a name, we didn't know what it was that was killing us. And this disease swept across, in barely a year, there was an early wave in January-February of 1918, it died away in June-July. And everybody hoped that would be the end of it, but it came back with a vengeance in a much more serious second wave that lasted until winter of -- you know, end of 1918, early 1919. For reasons that are not really clear, it died back and returned to its baseline levels.

So the numbers here are absolutely staggering. It's very hard to get our head around that. I had written elsewhere that COVID is no 1918 pandemic. And so far, that is proven to be true. The deaths and the infection rates, so far, so far, thankfully, do not mean that this disease COVID-19 is coming close to being as terrible a disease as was the 1918 virus. But as we all know, we are not at the end of the story of COVID-19 just yet.

Gardner: That's right. And I was just googling it to make sure I understood. So the world population in the year 1917 was estimated at 1.9 billion people. So we'll just round that to 2 billion. Today, it's over 7 billion, and to think about losing 50 million to 100 million of 1.9 billion people is just staggering.

And part of the devastation of the influenza of 1918, as you point out in the book -- and it is in contrast to COVID-19 -- and that is how it devastated healthy, young adults. A lot of us take some comfort, some small comfort, if you're under the age of 70, that maybe you won't get hit as badly or as lethally, more importantly, as older people. That's not a comfort, really, for humanity. But if you're especially a young person thinking about going back to a college campus, you think, well, it's probably not a big deal for me, but, boy! Was that not the case in 1918.

Dr. Brown: Yes. As you point out, look, typically infectious diseases of all kinds take a much worse toll on the very young and the very elderly. And that's because in the very young, their immune system has simply not been exposed to as much of the environment as older people, they haven't developed antibodies, and their immune system is just young and, sort of, learning.

In the elderly, the opposite has happened. The immune system, for want of a better description, is tired, is not as nimble as it once was. The immune system, perhaps, is a mirror image of the body itself. As we age, our age-related ability to run a marathon generally decreases, and similarly our immune systems age with us.

So typically in any infectious diseases, it's the very young and the very old who are most at risk, and this remains true of influenza. COVID-19 is a little bit different because it doesn't seem to be as dangerous for children as it is for the elderly -- although, we have to put an asterisk by that and point out that now the new evidence seems to be that children can carry it in a much higher rate than we had suspected.

But in any event, in 1918, it wasn't just the young and the elderly who were at risk, as usual. There was this middle group: the young, healthy workforce that was infected for reasons, again, that we do not understand, and we are trying to understand it, because it's terribly important to understand. But the young, healthy people were disproportionately affected. And you had this knock-on effect to the workforce where mines were closed, where police officers couldn't turn up to work, where telephone exchanges couldn't run because the telephone exchange operators were all sick, the young, healthy people who were running those.

So that is a specific feature of the 1918 influenza virus, and it doesn't appear to be a feature of COVID, thankfully.

Gardner: Now, speaking of bacteria, Jeremy, you wrote that we now think -- and this is ironic perhaps -- we now think that the majority of deaths in that pandemic resulted, and you hinted at this earlier, from secondary bacterial pneumonia infections, not influenza.

Dr. Brown: Yes, that's right. And think about influenza. Once it's inhaled, it goes straight for the lungs, where it latches into the lung cells and uses the cell machinery to reproduce itself and destroys the cells in the lung at the same time. That leaves the lung damaged. There was a battle fought there and the lung is weakened. And it's in that weakened state that secondary bacterial infections are able to sneak in and to blossom.

So thankfully now, we have antibiotics which we did not have at the time, and these can indeed save people's lives who get these secondary infections. But back in 1918, it was likely that rather than a primary viral infection that would kill somebody, it would more likely be the secondary bacterial infection, although this was by no means always the case. And there were many examples, we think, of young people who got sick and died so quickly from the viral pneumonia that it must've been the primary influenza infection that caused their death rather than a bacterial infection coming on a little bit later.

Gardner: And, Jeremy, before we go forward through history a little bit -- because part of what I learned from your book is, turns out it's not just about the pandemic of 1918 -- there have, in fact, been [laughs] a lot of important recurring flus over the last century. But I was just checking my friend Wikipedia for what was the worst pandemic of all time, and it's listing the Black Death; which I guess makes sense, mid-1300s in Europe. I am seeing here 75 million to 200 million people died. And we know that the world population was much smaller then --

Dr. Brown: That's right. I think the numbers are that a third of everybody in Europe died. So it certainly proportionally killed more people than any other -- the influenza of 1918, of course, the world was larger, so I think globally more people died; not that it's a competition that one would want to win [laughs] in any way.

Gardner: Do you want to flag any of the other influenza strains or events between 1918 and 2019 as worthy of some notice, and/or could you then put COVID-19 against the backdrop of pandemics and give us a sense of how big or not this is?

Dr. Brown: Well, we've had several rounds of influenza, going back, we believe, to 430 in the Peloponnesian War between Athens and Sparta. There is writing from the Greek historian Thucydides, who described what, to all intents and purposes, is an outbreak of influenza that ran through the city and killed perhaps a third of the 13,000 soldiers stationed there.

So we've certainly had that many, many years ago. We know that there were continuing influenza pandemics; in November of 1675 there was one in my hometown of London. And we had another one in the late 1890s. We had influenza in 1918. And then we had similar waves; it's sometimes difficult to determine whether they're technically a pandemic or not, but we had waves in the 1950s. In 1976, we had an outbreak of influenza that, in many ways, is worthy of discussion because of the way that vaccines were rolled out then. And that might be something we want to come back to talk about. And then, of course, we had the swine flu in 2009. And then more recently, of course, these have all been eclipsed by the COVID pandemic.

So there have been these recurrent waves, some to a worse degree, some to a less degree. The word "influenza" means under the influence, from the Italian influentia, meaning influence. And it's described as early as, I believe, 1670s. And the word means that the origin of the disease is, in fact, due to the misalignment of the planets, perhaps Saturn and Jupiter in conjunction. So people were calling this disease in front of them influentia. So it reminds us that the disease was identified, people could point to, and say "This one has this disease" way before, of course, the modern era.

And the responses to the influenza pandemic, as I have found in the last few months, really have pre-echoed the responses that we are seeing in COVID. So it's as if one would say, there's nothing new under the sun when it comes to pandemics. You could look at influenza and see examples of quack medicine, snake oil medicine, involving, incidentally, antimalarial drugs. And we've seen antimalarial drugs being touted as possible cures. Fortunately, the FDA has stopped all that.

We've seen, actually, in 1918-1919, there were marches and groups that were completely opposed to the wearing of masks as against their civil liberties. And so you think, well, the mask arguments that we've heard must be new that nobody else would have this, but actually it turns out that in late 1918 there was quite a movement against the wearing of masks that actually took place in San Francisco.

And we've had other examples. Unfortunately, there was a terrible race riot in 1918, and we've seen race riots in the beginning or in the middle of our own COVID pandemic.

So it's remarkable to me how some things that we consider to be quite new aspects of this pandemic have actually already been foreshadowed in prior epidemics, either influenza or from other organisms.

Gardner: Always love the study of history, historical backdrop. Thank you very much for that context, Jeremy. You know, the term "Spanish flu" has been bandied about for decades, you actually use it in your book subtitle. But you point out that Haskell County, Kansas, not only was that ground zero in the U.S. for the 1918 influenza, but it might have been ground zero for the world. Can you tell a bit of that story, reflect on the phrase "Spanish flu," to which some people take xenophobic offense today?

Dr. Brown: Let's take that last part first. So the disease, everybody agrees that the influenza virus did not, I repeat, did not originate in Spain. It was termed the Spanish flu because it was in Spain that the outbreaks were first described. Why were they only first described in Spain? Because, as you remember, we were at war, all of Europe was at war. And there was a tacit agreement, it would appear, between the newspaper editors and the Western governments to, as it were, keep the bad news of influenza at bay. And it wasn't censored, but it certainly didn't appear on the front pages as much as you would have thought.

It was in Spain, that was a neutral country, that the media could publish without any of these tacit agreements or censorship. So the first reports came from Spain. And then, from there, we got the moniker "the Spanish flu." But everybody is in agreement that it did not originate in Spain.

There are three possible well-established theories about where it originated from, and very briefly, they are these. No. 1, it originated here in the United States, possibly in Haskell County, which is a perfect square piece of land in southwestern Kansas. And a doctor there called Loring Miner reported that one day, early in 1918, 18 of his patients fell ill with influenza and three of them died, which is a remarkable number given the small number of people who lived there. And Miner then wrote a description of this to a journal, and that may well have been the origin of the 1918 virus.

And the reason that it's plausible, is No. 1, there were a lot of farms there, and we know that the virus originated in birds and then made its way through possibly pigs, swine, or possibly another mammal and then into humans, that would certainly fit Haskell County. And then we know that, for example, soldiers who worked at military camps near Haskell County soon became ill, in February of 1918. And, of course, as they moved out eastwards and across the Atlantic, they would have brought the disease with them.

So it's a hunch, it's a possibility that the disease originated in the American heartland, in which case we should probably be calling the Spanish flu, we should you probably have called it the American flu. So that would upset a lot of people, though.

And there's two other possible places where ground zero could've been. Very briefly, they are in northern France, where there was an outbreak of influenza in 1916, a terrible outbreak, actually. And the theory there is, it began in a place where humans and swine and birds have a lot of overlap, a lot of intermingling, and from there spread out across the world and reared up its head again two years ago in 1918. That's a second possibility.

The third possibility is that actually the disease comes from China. And this is supported by the reports that came from China of a terrible disease of influenza that was sweeping through northern China. And that was actually reported in The New York Times. And at the time, Chinese laborers were recruited as supporting the war effort on the Western Front. So we know of at least 140,000 Chinese laborers who came to France from China. And the theory is that they brought this disease with them.

Now, each of these theories has a lot of interesting evidence to support it. Each of these theories has holes in it. Each of these theories leaves, in some ways, many more questions than it answers. But those are the three, I would say, most likely contenders.

But as I say, this was now over a century ago, and we're unlikely to all agree or to find the evidence that could pinpoint it to one specific place. And this is indeed an example of the difference between the Spanish influenza of 1918 and today, where we know more precisely where the COVID virus originated.

Gardner: And that was where I was headed next. There's obviously some politicization of this. And you're already pointing out historical antecedents that exist in 1918 that speak to us -- racial riots in 2020. So much has been made of the idea of whether we should be calling this the Wuhan flu. And I'm going to remind my listeners again, Jeremy, if he answers this question, speaking for himself, he's not speaking on behalf of NIH. But, Jeremy, what do you think of calling this flu the Wuhan flu?

Dr. Brown: Let me answer that question like this. It is not unusual for the scientific community to name a disease or a virus discovery after the place where it was discovered. So for example, Ebola is named after a river in Africa, because that's where it was discovered. And each year, when you get your influenza vaccine, it usually contains three or four strains of the influenza. And they are designated by what strain they are and the country or the place where they originated. So you might have an influenza virus that is known by, you know, A147 Phuket because it was discovered in Phuket. Indeed, West Nile Virus is named after the place where it originated. So that's one thing that we just have to be honest about.

But, of course, naming a virus, naming a disease, and perhaps projecting blame is a whole other story entirely. And I think none of us want to do that.

Gardner: Very well put. You know, it's sadly ironic, perhaps, that the country -- based on my memory of having read your book some months ago -- the country that was hit hardest in 1918 might have been India. I think you listed something like 20 million deaths in India. Now, maybe somebody else had more than that, but that is a huge hit. And we only -- and this is all horrific -- we "only" lost 675,000 Americans. So certainly [laughs] if it did originate here in America, it did gigantic damage worldwide and perhaps no place more than India.

Dr. Brown: Yeah, that's right. The mortality rate was very high there, probably around 20 million. Yes, many places had it a lot worse than we did in the U.S., [laughs] and we had it pretty bad.

Gardner: So a critical aspect of the 1918 pandemic was that it was bad, but then it seemed to get better over the summer, and then it got, as you mentioned earlier, a whole lot worse. Now, as the stock market fan, I'm kind of picturing a bad bear market. I'm looking at a stock graph. It's early 1918, the market is crashing, but then it's kind of perking back up, that stock graph starts coming back, and then it crashes to unthought-of lows by the end of that year. And you mentioned it, it went right into the spring of 1919.

So it has a lot of people wondering the same now, of course, about COVID-19. So Jeremy, from your own perch, and now thinking of our own time, how do you see the graph of what we've already seen from COVID-19, and then how do you think about this fall and this winter?

Dr. Brown: So I will preface my remarks by saying that I was wrong. I had hoped that we -- actually, I had hoped, and many people who study viruses and are far more knowledgeable about them than I am -- we, I think, had all hoped that COVID-19 would follow the regular path of winter viruses. So influenza is a classic example. You can get influenza in the summer, but it's extremely unusual, it's a winter virus. And so are the regular COVID viruses; just to remind people that the coronaviruses are, as a family, are responsible for generally for mild symptoms of a common cold, although they can certainly do a lot worse damage, as they did with SARS and MRSA and now with COVID-19. But the winter viruses come in the winter, and they generally do their damage in the winter. And as the weather gets warmer, they disappear only to flare up again the following fall and winter.

And I had hoped, as I was doing some interviews at the beginning of the pandemic, I had hoped that COVID-19 would just follow the regular pattern of all of the winter viruses. And, yes, we were being hit in that springtime of this year, but hopefully it would die down and go away. And then the big question would be, would there be a fall return and a second wave?

Despite what I had said, it appears that there was really never an end to this first wave. We're now in the middle of summer. Across the United States, we have seen incredible flare-ups in places that are certainly hot and one would have expected the disease to have been less likely to spread there.

So in terms of forecasting the future, this virus is not playing by the expected rule book that one would have hoped, and that's actually challenging, because we did have hopes that this would really be another winter virus, and that hasn't proven to be the case.

Gardner: Well, and of course, that then puts me in mind, since we're talking about the here and now, just playing things forward into the fall, Jeremy. I know that you're a father.

Dr. Brown: Yes, I'm actually a grandfather. [laughs]

Gardner: You are the youngest-looking grandfather I know. But, OK, so I'm thinking about many of us, who may have kids in school, going to school; might be college, might be elementary school. And I'm just wondering, what are your thoughts in terms of the decisions that we're making at both the elementary school level, whether we're talking about public schools or whether we're talking about private colleges, all of the difficult decisions that are being processed so rapidly now in mid-August?

Dr. Brown: Yes. So three of my four children have graduated college, but my youngest, my daughter, is due to start just in a couple of weeks. The college that she has chosen to go to is going to be completely online. It's a college in New York, it's going to be completely online until at least September and October, and then they're going to reassess and may invite the students to come back. There are other models, for example, many universities have brought their students back, quarantined them, and then they're going to start up, and they're going to go all the way through to Thanksgiving without a break. There'll be no usual Thanksgiving break. And then, at the end of the semester there, the idea being that we want to limit the amount of times people come on and off campus.

This is such a challenging question that the only real response of which I'm certain is that I am grateful that I don't have to make this decision. Because it is a decision that, while we can look at the history books, and the evidence is that places, in 1918, American citizens that were more aggressive about their social distancing and closing of schools and limiting public spaces, the number of people who can go to public spaces, there is very good evidence that they did better off than places that were not as careful. But to suggest that that completely translates to what is going on today is, I think, a little more challenging. And for every example that we can bring of school districts that closed down and did well, it is possible to bring counterexamples.

And this is just really a terribly challenging question. I think that one of the most important ways to stop the spread is indeed to prevent children from going to school, but that's not a decision that can be made in isolation. That is a decision that has ramifications for their caregivers, for the children's parents, it is a decision that has ramifications for the way in which their parents may be able to work. And it also has ramifications, of course, rippling throughout society in so far as, if children are in fact able to contract COVID at a much higher rate than we expected and be asymptomatic, then they will turn out to spread the disease in perhaps ways that are really unfathomable. So I think it's a terribly hard decision to make.

And I think that all of us, whichever side of the political spectrum we are on and whatever we think about the way that this has been handled, our understanding of why this is a difficult decision, why it's not a simple, oh, obviously, they should go back to school, or, oh, obviously, they should not go back to school. Why these are very, very difficult decisions to make. And the correct answer, by the way, may never be known to us or it may only be known in many years.

You know, taking examples from other countries that did it one way or the other is only as good as the example overlaps with the United States. Different countries have different healthcare systems, they have different average ages of the population, they have different numbers of the population that are elderly. And all of this, of course, has a knock-on effect on how the disease is spread. So even looking to other countries for an example is going to be very challenging.

I know I didn't answer your question, but it's a terribly difficult question to really give a good answer to.

Gardner: Well, you did occasion in me a hope for all of us that we'll think that our fellow Americans, in this case, and our fellow earthlings are each trying to do the best that they can. To make that as a default assumption, as opposed to thinking the opposite of them and people who don't agree. I know one thing: We will, at some point in history, have a more developed idea of what we should have done, but I sure hope we're not going to second-guess ourselves, because we can only live forward from where we are here. And as you pointed out, it is hard to figure out the right thing to do. And what works in one place may not be the right thing for another, and there's just too much complexity.

Dr. Brown: Yeah. And let me just give you an example. As I said, notwithstanding the point there, it's hard to translate from one era to another and one country to another. But there is an interesting example, I mentioned this in my book, of an experiment, a natural experiment that took place in Japan. From 1962 to 1987 in Japan, almost all the children were vaccinated against influenza, and it was actually mandatory for a while. The vaccination rate grew to be around 85% or higher. But that mandatory vaccination of school children against influenza ended around 1994. It actually ended as a result of some of the outcry and hysteria around vaccines and their possible link to other disorders.

So Japan, basically for two, three decades vaccinates all its children against flu, then they stop. And over the next several years, what we saw was not an increase in the number of deaths in children, we saw in Japan an increase in the number of deaths in the elderly, in the elderly. And if you look in the U.S. over the same period, where there was no change in our vaccination policy, the deaths of the elderly over the flu seasons remained unchanged.

So in other words, the disease -- either vaccinating one part of the population benefits another or the disease that is carried in one part of the population can spread to another. And this example that's now almost 50 years old from Japan reminds us that our decision about what we do with our children not only will have an effect on our children but also on the caregivers, the grandparents, and other members of society who perhaps are more at risk from these viral infections.

Gardner: I want to go back to just one of my favorite chapters in the book briefly, as we start to near the end of our time together, Jeremy. I was fascinated by the story of how present-day virologists and virus hunters actually went back, seemingly in time, to rediscover, so that we could map it, the 1918 strain. Now, the hunt took them to the far north, to Brevig Mission, a tiny village on the shore of the Bering Sea.

I know you can't do justice to that full story here -- it was a racy and adventurous chapter -- but can you recapture a bit of that story here for my Foolish listeners?

Dr. Brown: Sure. You know, it is one of my, I think, one of the most exciting aspects of the history of this disease. And just we'll start at the end. The actual influenza virus of 1918. We were able to extract the genetic material from that very virus, and we were able to publish a map of that virus, but it took until the late 1990s.

And what happened was basically this: that in 1950 a young medical student who was visiting the U.S. had, for various reasons, become fascinated with the idea of finding an old sample of the influenza virus. So this Swedish man, called Johan Hultin, basically goes off on an expedition by himself to try and dig up some of the bodies that had died from the 1918 virus. The idea being that the frost, the permafrost, would preserve the lung tissue and that it was, perhaps, possible to extract the virus from that lung tissue that had been frozen in time.

To make a very interesting, fascinating story short. Though he did some digging, he was unable to send that virus, anything back of use, and he forgot about this for the next 46 years until he read some reports about the hunt for the 1918 flu virus that was taking place actually in Washington, DC, looking for the virus in some old sites buried in the Armed Forces Institute of Pathology. But anyway, Hultin hears about this and he says, you know, I'm going to give it one more go. So he flies out, once again, and he gets permission from the village elders and he digs and digs and digs, and this time he was successful. He was able to come across some lung tissue that had not decomposed and had been preserved by the permafrost.

And in 1997, August of '97, after digging by hand with the help of some villagers, he finds a body, and he basically extracts the 1918 virus and mails it to an important microbiologist/virologist called Jeffrey Taubenberger in Washington, DC, who can then extract and rebuild the entire genetic code of the 1918 virus.

And that is how, essentially, we got to first understand the actual genetic makeup of this disease. It was a result of this man, Johan Hultin's perseverance over 50 years and two separate expeditions to go and find these samples, together with some other samples that were found in storage in Washington, DC. And of course, the new technology that enabled us to resurrect these viruses, that was absolutely, of course, unimaginable even 40 or 50 years ago, unimaginable. But those three parts came together and allowed us to actually, as I said, completely understand and type out on a page the virus and its genetic code.

Gardner: And you told it well. And it is amazing to think that it was 1953 when Crick and Watson discovered DNA. I mean, to think about those 50 years and the progression that occurred is truly remarkable. Great story right in the middle of your book.

Just a few more questions for you, Jeremy. So one of the early lines that you'd hear about COVID from some prominent and educated people is that, "Hey, the flu, you know the normal one, kills or has killed many more people than COVID, so this is all overhyped." What did you think when you heard people saying, look, how many people have died of the flu every year, and then, what about COVID? And then, does any aspect of you think that now?

Dr. Brown: Let me start with a little confession. I was one of those people, and I'm in good company, by the way, [laughs] but I was one of those people who thought, at least in the very early stages of COVID, that we have more to worry about from the flu than from COVID. And the reason that I thought that is that in the very early stages, there were a handful of descriptions of this COVID pandemic in Wuhan in China. And for anybody who follows the patterns of viral infections that break out across the world, there are often flare-ups of weird viruses that kill 18, 20, and 50 people and then seem to disappear.

And so at the time, I think many of us, but certainly including myself, thought that this would likely be another example. And of course, we were mistaken. I would say, we were possibly mistaken. This disease turned out to be far more lethal and far more infectious than we had thought about at the beginning and the middle of, let's say, January, February of this year.

Now, the question is, do we still have to fear more from influenza than from the flu? Unfortunately, we don't know the answer to that. There are currently, as we make this recording, about 163,000 deaths from COVID in the United States. Each year, there are somewhere between, and the data is not terribly good, but somewhere between 20,000 to 60,000 deaths in the United States from influenza. Sometimes it can be worse than that, but that's generally the order of magnitude, between 20,000 and 60,000 deaths.

So we have already almost, that we've doubled it and we've almost tripled that number. But -- and this is the important second part -- the denominator of this question is, what's the total number of cases? And So you have to remember that the total number of cases, the mortality rate is the -- you can either do it by in the population per million or you can look at the rate of deaths compared to the rate of cases. And there, we've got over 5 million cases in the U.S. of COVID, and as we increase testing, both here and around the world, the number of cases of asymptomatic carriage will continue to increase, which means that the proportion of people who die from COVID will decrease, simply because while there are still people dying, there are many more people who turned out to have the disease but were asymptomatic.

So what this means is that we don't know the answer until this disease is behind us. My rough calculation is that the disease in the United States has an approximately -- I think I'm right -- an approximately 3% mortality rate, which is terribly high, considering that the usual rate of death from influenza is about 1 in 1,000 or 0.01%.

So what I'm saying here is that we don't know yet what the end story will be. We don't know how many asymptomatic cases there will be of COVID. And so not yet possible to say, was this disease really as bad as influenza or was it worse? We don't know yet. But I will finish with this: I think the numbers are certainly heading in the wrong direction. So we may end up with the contender that this disease, even at the end, is far, far worse than anything the influenza could throw at us, even when we take into account all the asymptomatic carriers.

Gardner: Thank you for that. All right, two final questions for you, Jeremy; one about your book and one about life. The one about your book, the inevitable question. If you could write an extra chapter today -- you did finish that book and published it in 2018. I'm pretty sure your publisher, if not you, thought it would be a great idea to publish the 1918 Influenza book for 2018; makes a lot of sense to me. So if you could write that extra chapter now, or maybe it's your introduction to the second edition of your book some years hence, what would you be writing?

Dr. Brown: Well, hopefully, in a couple of years' time, the dust will have settled on COVID-19 and we will have completed the data, if you like, about how severe this disease was. It was certainly much worse than any of us could have predicted. And I would, I think, at that time, really want to point out, I think, some more of the similarities between events that took place in influenza of '18 and show that they foreshadowed COVID-19.

It's terribly easy, of course, to have, with hindsight, to look back and say, this should have happened and that should have happened and you missed this. And in many respects, and this is not a discussion for now, but in many respects we should have been more on the ball about suspecting a COVID virus rather than influenza virus as being the next cause of a global pandemic.

But I think that that's the way I would go. But I also want to really remind your intelligent and thoughtful audience that, as we mentioned earlier, the people who are making the decisions, the scientists who are providing the data, are all doing the very, very best that they can, with one hand tied behind their back and half a blindfold on, simply because this is so new, this is so rapidly changing, the science is continually evolving. That rather than being critical of them, we should really be thankful to them, to them and the people who are treating the patients, because much of this has been a surprise for everybody, and there will be, I'm sure, many inquiries in different countries as to what could have happened and what should have happened.

The people who are on the front lines of this, the scientists, the physicians, the nurses, they are all doing their very best to bring comfort, to bring scientific evidence, to study new possible drugs that can limit the disease and cure it, they're all doing their very best. And it's very easy to be cynical in the United States and, depending where you are on the political spectrum, to blame one person or another or one system or another. But all of us, I think, owe it to those people on the front lines. We owe them our gratitude and we owe them our respect. And of course, we owe them our prayers that they will indeed not only be able to treat the people who're coming down with this terrible disease in improved ways but also hopefully, to both be able to treat it and to prevent it with a vaccine. But unfortunately, vaccines do take a long time to be properly vetted and developed.

Gardner: Well said. Last question for you, Jeremy. So my friend Stephen Murphy the other day was talking about balancing the wealth of knowledge with the weight of knowledge. So I think of you, Dr. Brown, as having a huge wealth of knowledge, but how much do you let that knowledge weigh on your own habits and your own walk through life? We're all humans. That means a lot of us are waking up earlier than we may have previously, and all of a sudden, we're on Zoom with each [laughs] other, and we have all these new habits that we're trying to form. I'm just curious: How are you living your life right now?

Dr. Brown: You know, I heard on a podcast, I think it was a podcast of This American Life, I heard somebody being interviewed who said, we shouldn't call it working from home, we should call it living at work. And I thought this was a fascinating and insightful explanation of what's going on. I, like many people, I'm working from home, I've been -- we at the NIH, those of us who were not taking care of patients directly, we were sent home to work from home remotely. I believe it was the middle of March and have been there ever since. And there is no immediate prospect of our returning to our offices, although plenty of people have gone back to work at the NIH, who take part in patient care and run labs.

So my daily routine has been working from home. At the very beginning of the outbreak and just as the closures were being announced, my daughter, who is a pediatrics resident, and her husband and young baby came to stay with us, because they had lost their childcare. The childcare that they had closed down. And my daughter, as I said, is a busy pediatrics resident, her husband works in another section of the government. And they needed help watching our grandson, their baby. So like many people, we rolled our sleeves up and we just did it. And they ended up staying with us for several weeks.

So I consider myself lucky that I've been able to continue my job from home. That doesn't mean it's been easy, that doesn't mean I haven't felt sorry for myself. But I've actually been amazed at the stories that I've read of people who managed to do this in far more trying circumstances. I think the hard time that I'm having, while thinking of a family, perhaps, living in an apartment with three children under the age of 10, perhaps it's a single-parent family, and perhaps with one computer between them.

And while, as I said, we are blessed to live a comfortable life, it's not the same for everybody. This is not, as we have heard many times, is just a great leveler, everybody is being infected. One thing we know for sure is that people are not infected at the same rate, that this is a disease that is claiming more victims in the African American community, in the Latino community, in those who are less wealthy, as all diseases tend to do, they tend to affect the less wealthy.

So the one thing for sure is that we're all experiencing this in quite different ways. And it's a testament to the people who can keep it all together, I think, whatever their particular challenge is, to be able to keep it all together. And it's not been easy for anybody.

Gardner: Well, Dr. Jeremy Brown, thank you very much for spending this generous time with so many Fools worldwide, not just here in the U.S., many people affected in so many different ways by what has become truly a pandemic. And we didn't really know that at the start of it. I remember that debate too.

Anyway, you've been very gracious, and it was fun to go into your book, which I enjoyed so much. The book, again, Influenza: The Hundred-Year Hunt to Cure the 1918 Spanish Flu Pandemic, beautifully written by Jeremy in 2018. And yet, here we are talking about 2020, something that I know you and I didn't think about when we saw each other in the fall of last year. We didn't have much conversation around the table about the idea that something like this would hit.

Jeremy, thank you again so much. One of my watchwords these last few months has been "Wash your darn hands!" So I know you're doing that, and that's good advice, right?

Dr. Brown: That's certainly good advice. Washing our hands, wearing face masks, keeping a distance from one another, it should be a habit. Although, it's surprising to me how often I will get out of the car to walk to buy groceries and, oh, I forgot my mask! It's something that is so easy to do even though it has now become fairly routine. So let's bear it in mind. Thank you to you for your time. Thank you to the audience for listening. And I hope that everybody stays both healthy and sane.

Gardner: Well, I sure hope you enjoyed that conversation half as much as I did, because if you did, you had a great time and learned a lot. Thank you again to Jeremy, who mentioned modestly after the interview we did together that he was in fact doing it from Israel. He was there, he had taken a risk and time to fly across the Atlantic Ocean to be with an ailing father. And he said he was very graciously treated by Israeli officials who did allow him in, but with very stern protocols, as you would expect.

But that question of, how much should we risk ourselves? And when it's for family, we're often willing to do quite a lot. And so I thank Jeremy, especially, under somewhat trying circumstances that he broke out that time for you and for me this week.

All right. Again, Authors in August continues next week. Our final book for the month of August: Bridging Generations by Roy Williams and Amy Castoro. Amy will be joining you and me for next week's podcast. I will mention, of course, there's a Mailbag coming after that. So any reflections you had on my conversations with Jay Jakub last week, Dr. Jeremy Brown this week, or Amy Castoro next week are heartily encouraged, and we'll feature those in two weeks.

In the meantime, stay safe out there. Yeah, wash your darn hands! And Fool on!