Speaker 1: Pushkin from Pushkin Industries. This is deep background to show
Speaker 1: where we explore the stories behind the stories in the news.
Speaker 1: I'm Noah Feldman. As states begin to reopen, we're all
Speaker 1: desperately trying to figure out what is going to happen next.
Speaker 1: What are the possible courses of COVID nineteen, what are
Speaker 1: the possible outcomes if there is a vaccine, and what
Speaker 1: are the possibilities if indeed we don't get a vaccine
Speaker 1: or a therapeutic treatment that actually changes things. Joining me
Speaker 1: to discuss these issues is doctor Jonatan grad. He's an
Speaker 1: assistant professor in the Department of Immunology and Infectious Diseases
Speaker 1: at the Harvard chan School of Public Health. He's also
Speaker 1: an attending physician in the Division of Infectious Diseases at
Speaker 1: Brigham and Women's Hospital and Harvard Medical School. You know, Tom,
Speaker 1: thank you so much for being here. I really hugely
Speaker 1: appreciate it. And the first topic I want to ask
Speaker 1: you about is a paper on which you're one of
Speaker 1: the co authors, that was published in Science magazine. That
Speaker 1: is a model or a series of models, among other things,
Speaker 1: of what could happen under conditions of reopening if a
Speaker 1: vaccine is not yet available or potentially not available at all.
Speaker 1: Would you start by just describing at the core what
Speaker 1: predictions you and your co authors were able to make
Speaker 1: about the patterns of covid resurgence that are potentially out there. Sure,
Speaker 1: there really seems to be only a couple of ways
Speaker 1: in which a pandemic ends. One of them is elimination
Speaker 1: of the virus. If you're able to control the spread
Speaker 1: sufficiently towards the beginning of the virus emergence, you can
Speaker 1: perhaps contain it to the extent that you can eliminate
Speaker 1: its ongoing transmission. That I think is what happened with
Speaker 1: the experience of stars in two thousand to three. I
Speaker 1: think that this possibility for ending the pandemic now is
Speaker 1: extremely unlikely, given how globally we've seen the spread of
Speaker 1: SARS CoV two. The second way to end a pandemic
Speaker 1: is through population immunity or herd immunity, when enough of
Speaker 1: the population has acquired immunity to the pathogen that you
Speaker 1: don't see ongoing epidemic spread. This can happen either with
Speaker 1: a vaccine that can confer sufficient immune production or through
Speaker 1: natural infection, where that infection elicits immunity. A key to
Speaker 1: thinking about HERD immunity, then, is understanding what fraction of
Speaker 1: the population would have to be infected and recovered from
Speaker 1: infection with immunity in order for the pandemic to end.
Speaker 1: That gets to the notion of the basic reproductive number,
Speaker 1: a sense of just how transmissible the virus is. Estimates
Speaker 1: of this number for Sarryscoop two place it around three,
Speaker 1: although there have recently been some estimates that are considerably higher.
Speaker 1: There was one published last week at five point seven.
Speaker 1: But let's start with just the notion of this are
Speaker 1: not or the basic reproductive number of three. What this
Speaker 1: means is that on average, an infectious person will infect
Speaker 1: three other people. To prevent these ongoing transmission chains, then
Speaker 1: two out of three people would have to have immunity, right,
Speaker 1: so we would have to get to a point in
Speaker 1: which roughly sixty six percent of the population was immune
Speaker 1: in order to see that transmission would diminish. We then
Speaker 1: became interested in asking, given the broad based quarantine for
Speaker 1: communities that had been introduced through these social distancing measures
Speaker 1: and lockdowns, both in China and in elsewhere, what the
Speaker 1: impact would be of these social distancing measure of different
Speaker 1: durations and different effectiveness. We wanted to know if we
Speaker 1: were to have lockdowns or social distancing with effectiveness of
Speaker 1: say twenty percent so mildly effective, forty percent more effective,
Speaker 1: or sixty percent on the order of what was seen
Speaker 1: in China, what would happen and what would happen if
Speaker 1: it were four weeks, eight weeks, twelve weeks, twenty weeks,
Speaker 1: or for a long period. The key intuition here gets
Speaker 1: back to what I was describing about the fraction of
Speaker 1: the population that would have to be immune the extent
Speaker 1: to which we are successful in preventing spread. So that's
Speaker 1: the intervention. These lockdowns really diminished transmission, would maintain a
Speaker 1: susceptible population in the community, so that when you stop
Speaker 1: that intervention, when you lift the restrictions, now the virus
Speaker 1: would have the opportunity to spread again through the susceptible population.
Speaker 1: To the extent that we are successful, we will then
Speaker 1: see the resurgence of the virus. And that was really
Speaker 1: one of the main findings in this paper for that
Speaker 1: one time social distancing interventions. As there are susceptible people,
Speaker 1: the virus has no memory, it doesn't care what we've done.
Speaker 1: It just carries if there are susceptible people around that
Speaker 1: it can infect, and so we would expect to see
Speaker 1: a resurgence of the virus. So that resurgence is a
Speaker 1: version of what people call the second wave, and I
Speaker 1: take it the way you're saying is that that second
Speaker 1: wave is going to be a lot bigger than perhaps
Speaker 1: people might assume, given the success of social distancing measures
Speaker 1: that reduce the number of people who are exposed. So
Speaker 1: this is sort of the downside of flattening the curve
Speaker 1: is that fewer people have been exposed, and so when
Speaker 1: the time comes that they are exposed, potentially a lot
Speaker 1: of them could be exposed. Imagine a scenario and I
Speaker 1: think you do imagine this in the paper where then
Speaker 1: the government responds to that by saying, Okay, we have
Speaker 1: a second wave coming. We see it rising, we see
Speaker 1: the number of cases going up, in the number of
Speaker 1: deaths going up, and so now we're going to reimpose
Speaker 1: social distancing. Any reason to think that you wouldn't get
Speaker 1: similar effect of that social distancing in the second time
Speaker 1: as you did the first time, and then similarly the
Speaker 1: third and the fourth, and however many times you need
Speaker 1: to do this, that's right. So it gets to the
Speaker 1: question of why are we doing social distancing in the
Speaker 1: first place. If this virus were benign, we would just
Speaker 1: let it run through the population, right because there wouldn't
Speaker 1: really be a downside to that. But because this virus
Speaker 1: causes the extent of disease that it does, we worry
Speaker 1: about the impact it has on the healthcare infrastructure. So
Speaker 1: the reason for enacting social distancing and putting communities in
Speaker 1: lockdown is to not only try to save lives directly,
Speaker 1: try to diminish the spread so that fewer people are
Speaker 1: getting infected and dying from the disease, but also from
Speaker 1: the effect it would have on our healthcare infrastructure. What
Speaker 1: was seen in Uhan and then replicated in northern Italy
Speaker 1: and more recently in New York is that when we
Speaker 1: see this large fraction of the population infected all at once,
Speaker 1: it overwhelms the healthcare system, and then we see things
Speaker 1: like rationing ventilators, and also that people who would normally
Speaker 1: be able to come into hospitals to get care for
Speaker 1: their heart attacks or strokes were not coming in, so
Speaker 1: there would not only be death from the virus itself,
Speaker 1: but from our inability to properly care for people who
Speaker 1: have the virus and the inability to care for people
Speaker 1: who have other conditions, we would see extensive excess mortality.
Speaker 1: That led to this effort to flatten the curve. Once
Speaker 1: we stop and see a resurgence of virus, as you say,
Speaker 1: we would expect that if we are still being guided
Speaker 1: by that principle of trying to maintain the healthcare infrastructure,
Speaker 1: then to the extent that it threatened by this resurgence,
Speaker 1: we would imagine reinstituting social distancing measures. This led to
Speaker 1: our consideration of, well, for how long would we have
Speaker 1: to do that? Assuming no other intervention, And that's the
Speaker 1: question I think everybody is so focused on. You know, again,
Speaker 1: assuming no other magic bullet solution, how many times are
Speaker 1: we going to have to run this same cycle of
Speaker 1: up and down and up and down. It looks like
Speaker 1: from our models that this could take a couple of
Speaker 1: years of cycles, and that may be influenced by a
Speaker 1: variety of factors. Those factors include whether we can expand
Speaker 1: our critical care capacity. So really what we were thinking
Speaker 1: about in this paper was can we titrate to some
Speaker 1: extent the turning on and off of social distancing to
Speaker 1: optimize the number of people were caring for in hospitals
Speaker 1: or in the healthcare infrastructure, and that really seems keyed
Speaker 1: to our critical care capacity. So the goal, then, from
Speaker 1: a intervention perspective, would be to try to find the line,
Speaker 1: which is how many cases we can handle in our
Speaker 1: critical care facilities in the hospitals, and then to just
Speaker 1: bring the number of infections up to that line as
Speaker 1: close to that line as possible, and then back down again,
Speaker 1: and to do that as long as it takes, And
Speaker 1: of course how long it will take depends on how
Speaker 1: high you can make that line, because that's the question
Speaker 1: of how many people you can manage to infect. But
Speaker 1: it sounds like making fairly reasonable assumptions about how high
Speaker 1: that line could be set. You're suggesting that we could
Speaker 1: end up having to do this again and again into
Speaker 1: twenty twenty two. That's right, And it could be that
Speaker 1: those numbers are adjusted by a variety of different factors.
Speaker 1: If we find an effective therapeutic that diminishes the need
Speaker 1: for hospitalization, or if a person is hospitalized that diminishes
Speaker 1: the need for critical care, that effectively increases our critical
Speaker 1: care capacity, right, So it's mathematically the same essentially as
Speaker 1: increasing our capacity, so that can help shorten the duration
Speaker 1: with which we'd have to go through these cycles. It
Speaker 1: could also be impacted by seasonality, which is another aspect
Speaker 1: of the projections that we evaluate in this paper. We
Speaker 1: don't really know yet whether there is seasonality in transmission
Speaker 1: of SARS CoV two. For some other respiratory viruses, we know, like,
Speaker 1: for example, for influenza, that seasonality influences transmission such that
Speaker 1: it is more transmissible in the winter than it is
Speaker 1: in the summer. We see as well for a couple
Speaker 1: of the other human coronaviruses that circulate in the US
Speaker 1: and cause common cold type symptoms, that it appears they
Speaker 1: also have seasonality. Using those as a basis for seasonality
Speaker 1: for SARS CoV two, assuming that whatever factors influence the
Speaker 1: other coronaviruses would also influence this one, we would see
Speaker 1: that there would be less transmission in the summer, and
Speaker 1: then transmission would pick up in the fall and peek
Speaker 1: in the winter. That could also influence the deboration of
Speaker 1: lockdown and release from social distancing interventions. So if COVID
Speaker 1: nineteen does turn out to be seasonal in similarity to
Speaker 1: these other viruses. That would suggest that we ought to
Speaker 1: try to reopen going into the summer rather than going
Speaker 1: into the winter. And that part sounds like good news
Speaker 1: insofar as most of the openings up that are happening
Speaker 1: now are going into summer months. That's right, And I
Speaker 1: think it does raise further concern for the possibility of
Speaker 1: augmented transmission in the fall and the winter. And I
Speaker 1: think it's of concern for two reasons. One, it overlaps
Speaker 1: with the increase in transmission of influenza, which we already
Speaker 1: know creates stress on our healthcare infrastructure. So to see
Speaker 1: both flu and COVID nineteen coupled together increasing together, I
Speaker 1: think that is something that we all worry about. The
Speaker 1: second reason is actually just one of domestic politics, right.
Speaker 1: The importance of this election in November is one where
Speaker 1: seeing a rise in cases and a second wave that
Speaker 1: overlaps with the election, I think is something that people
Speaker 1: have to be aware of and be concerned about. So,
Speaker 1: just to understand what you're saying, what you're saying very politely,
Speaker 1: but it sounds like what you're saying is you could
Speaker 1: see a moment where over the summer, as reopenings occur,
Speaker 1: we actually don't get a huge spike because the virus
Speaker 1: is more seasonal. But then starts getting colder, people start
Speaker 1: going inside. It's October, and the case rate might actually
Speaker 1: begin to go up pretty rapidly, and then boom. We
Speaker 1: have an election in the first week of November, as
Speaker 1: mandated by federal statute, and the president may think he
Speaker 1: can change that, but he can't. So it's going to
Speaker 1: happen in early November one way or the other. Is
Speaker 1: it cold enough in October to have this seasonal impact
Speaker 1: before the election? I mean, I hate to ask such
Speaker 1: a crudely political question, but it seems relevant. How does
Speaker 1: flu do or how do these other coronaviruses do in October?
Speaker 1: That's really the key timing. By the time you get
Speaker 1: to November, the election will have happened, right. I expect
Speaker 1: there to be an increase in transmission. The seasonality is
Speaker 1: not an on off process. It's one that fluctuates with
Speaker 1: the season. So as we start to move into the
Speaker 1: fall and winter, I do worry that there will be
Speaker 1: increased transmissibility and arise in cases. And I think even
Speaker 1: as this is an issue that we can't know for
Speaker 1: sure at this point, it is nonetheless one worth preparing for,
Speaker 1: just in case. It's concerning enough that being able to
Speaker 1: have the option to vote by mail seems critical for
Speaker 1: an election where there may be risks as we've seen
Speaker 1: in Wisconsin and the primaries to standing in line when
Speaker 1: there are serious respiratory viruses in circulation. There's a fascinating
Speaker 1: counterintuitive result of this, which is there's been a lot
Speaker 1: of talk about what Donald Trump tried to delay the elections.
Speaker 1: If Donald Trump were to listen to this podcast and
Speaker 1: read your paper, he ought to not, under any circumstances
Speaker 1: even think about delaying the elections, because if you delay
Speaker 1: the elections, there might be a lot more COVID nineteen
Speaker 1: cases as the weather gets colder, Whereas in the first
Speaker 1: week of November it's entirely possible that that might be
Speaker 1: going on, but we wouldn't have seen it yet. I
Speaker 1: think it's so tough to speculate even months out at
Speaker 1: this point. Frankly, I think with all of the variation
Speaker 1: in social distancing interventions across the United States, it's very
Speaker 1: hard to predict what the prevalence will be, and with
Speaker 1: the risks for recurrence will be by community. Different states
Speaker 1: and different regions have taken very different approaches to how
Speaker 1: to manage the response to COVID nineteen. Some seem to
Speaker 1: have adopted the Boris Johnson phrase take it on the chin.
Speaker 1: Others are trying to flatten the curve, and yet others
Speaker 1: are trying to crush the curve. And by crush the curve,
Speaker 1: what I mean is really prevent any transmission through a
Speaker 1: combination of social distancing interventions, contact tracing, and other means.
Speaker 1: So it's hard for me to say exactly what the
Speaker 1: dynamics will be come September, October, and November, because those
Speaker 1: in part depend on the fraction of the population that
Speaker 1: remains susceptible, and that right now is just so hard
Speaker 1: to predict. We'll be back in a moment you're not on.
Speaker 1: One of the findings that really struck me in your
Speaker 1: paper was the finding that if immunity two stars COVID
Speaker 1: two is not permanent, is likely to enter into regular circulation,
Speaker 1: sort of like the flu comes around every year. There's
Speaker 1: something a little terrifying about that because the idea that
Speaker 1: we'll have stars CoV two with us in this form
Speaker 1: for a long time is kind of world changing. But
Speaker 1: hidden in there is a fascinating assumption that I think
Speaker 1: opened something that I did not understand at all, and
Speaker 1: I wonder if you would share with us, And that
Speaker 1: is what does it mean to say that if the
Speaker 1: immunity is not permanent? I tend to think I think
Speaker 1: a lot of non physicians tend to think that either
Speaker 1: you do become immune after you're exposed to something I
Speaker 1: have antibodies, or you don't become immune. But I'm sensing
Speaker 1: that that's not the right way to think about it. Immunity,
Speaker 1: we like to think of, is something that is lifelong,
Speaker 1: sterilizing protection that you get infected with something, you develop
Speaker 1: immunity to it, and you are protected against infection with
Speaker 1: that particular pathogen for the rest of your life. This
Speaker 1: is one of the concepts we think about for vaccines generally,
Speaker 1: and it's in some ways how they're pitched. Although you
Speaker 1: know from your own experience, if you go in for
Speaker 1: all of your recommended vaccines, as one should, you might
Speaker 1: have wondered why it is that for some vaccines you
Speaker 1: get several doses. Right, So every ten years, for example,
Speaker 1: you're supposed to get an updated tetanus shot right, So
Speaker 1: it gives a sense even just the fact that that happens,
Speaker 1: that immunity is not an all or nothing, It is
Speaker 1: not a one or zero. It is something that can
Speaker 1: change over time. And also that it is not necessarily
Speaker 1: as if you have some kind of invincibility shield. We
Speaker 1: can think of immunity as being in a few different
Speaker 1: categories of things. And does immunity prevent you from getting infected?
Speaker 1: Does immunity prevent you from developing severe manifestations of infection
Speaker 1: should you happen to get infected, And could immunity or
Speaker 1: different elements of immunity help prevent ongoing transmission so make
Speaker 1: you less infectious to others? These are also the different
Speaker 1: ways in which we think about the potential outcomes of vaccination.
Speaker 1: So for SARS CoV two, what we wondered about was
Speaker 1: whether immunity might wane over time. There was a study
Speaker 1: with one of the common cold type coronaviruses where military
Speaker 1: recruits were exposed to one of these viruses and then
Speaker 1: a year later exposed again, and they could still become infected,
Speaker 1: although they had less symptoms. So it seemed as though
Speaker 1: even if they were able to recover and develop an
Speaker 1: immune response to the initial infection that let them clear
Speaker 1: it That immune response was not of sufficient strength and
Speaker 1: duration that they could not a year later again become infected,
Speaker 1: although it was for many of them enough to limit
Speaker 1: the end of symptoms. We see this with many pathogens.
Speaker 1: One of the reasons why influenza is such the challenge
Speaker 1: that it is is in part because immunity to flu
Speaker 1: seems to change. Flu itself seems to change, so the
Speaker 1: pathogens themselves may evolve in response to the immune pressure
Speaker 1: from the human populations. We don't know whether this will
Speaker 1: be the case with sarscoby two. That is yet to
Speaker 1: be determined as well. So there are a variety of
Speaker 1: factors at play, both in the dynamics of the human
Speaker 1: population and individual level immune response, and in the evolution
Speaker 1: of the pathogen as well. So the takeaway then is
Speaker 1: that if exposure to the virus creates an immunity that
Speaker 1: is time bound or that is not capable of completely
Speaker 1: eliminating the chances that you get the disease later on,
Speaker 1: but just weakens the case that you get, or if
Speaker 1: a vaccine does either of those same sorts of things,
Speaker 1: then we're going to get very possibly an annual COVID
Speaker 1: scare and that could last. I take it indefinitely, because
Speaker 1: if we're not talking about total immunity, then herd immunity
Speaker 1: is in a sense a misnomer. The herd will never
Speaker 1: be completely immune because no one is, on this theory
Speaker 1: completely immune. They're just partially or immune in some time
Speaker 1: bound way. And then it will have to become something
Speaker 1: that we're going to have to manage going forward without
Speaker 1: particular end, even if there is a vaccine, again, depending
Speaker 1: on how the vaccine operates. Yes, so if we get
Speaker 1: a vaccine, and I want to add a note of
Speaker 1: caution here that it is not a given. Even with
Speaker 1: the recent positive news from the phase one of the
Speaker 1: Maderna trial, it does not seem to me a given
Speaker 1: that we will have an effective vaccine for sure. I
Speaker 1: just point out using the example of HIV, a very
Speaker 1: different virus to be sure, but nonetheless a cautionary tale.
Speaker 1: We have been trying to get a vaccine for HIV
Speaker 1: for thirty years and we still don't have one. So
Speaker 1: just to keep that in mind, I hope we get
Speaker 1: one for SARS CoV two, and get one quickly. That
Speaker 1: is highly effective and that does induce long lasting sterilizing immunity.
Speaker 1: But if we don't, then you're absolutely right. We are
Speaker 1: going to be looking at dealing with SARS CoV two
Speaker 1: as another of the seasonal respiratory viruses. It will join
Speaker 1: the ranks of influenza para influenzas once or for respiratories,
Speaker 1: and sitial virus, man aneuma virus, the other coronaviruses, rhinovirus.
Speaker 1: They're a whole panoply of respiratory viruses that cause everything
Speaker 1: from common cold to very severe outcomes including death, that
Speaker 1: come through the human population regularly, and it may be
Speaker 1: that SARS CoV two will join that group. Is there
Speaker 1: any way to know whether a particular type of community,
Speaker 1: whether it's naturally occurring or whether it's vaccine induced, will
Speaker 1: last over time other than waiting over time to see
Speaker 1: what happens? I mean, is there any way to prefigure
Speaker 1: that out? Yeah? No, not that I know of. I
Speaker 1: think it is something where it really takes time to
Speaker 1: figure it out. Part of it is, you know, what
Speaker 1: is the robustness of the immune response, and then watching
Speaker 1: what happens even over short periods of time to see
Speaker 1: whether antibody levels rapidly decay or are maintained. What am
Speaker 1: I not asking you? What are major points that you
Speaker 1: think are not being sufficiently discussed in public right now?
Speaker 1: About broadly speaking, the issues that we've been talking about.
Speaker 1: I think that there are a few key points that
Speaker 1: we haven't discussed that we should be thinking about. One,
Speaker 1: we've talked about vaccines, but we have not talked about therapeutics.
Speaker 1: I think therapeutics really give us the best and probably
Speaker 1: closest off ramp. If we had effective drugs that could
Speaker 1: diminish the possibility of severe disease, that could really treat
Speaker 1: and cure infection with stars CoV two, the need for
Speaker 1: a vaccine would go down tremendously. We could manufacture these drugs,
Speaker 1: especially if they were oral drugs. Of course, there are
Speaker 1: all the issues with resistance, and I'll just say the
Speaker 1: reason that I haven't asked you about that is that
Speaker 1: we've talked about this extensively on the show on other occasions.
Speaker 1: Remdesivir does seem to be producing some appealing results, but
Speaker 1: the numbers that are reported thus far, at least in
Speaker 1: the NIH study, were not world transforming. It was mortality
Speaker 1: from eleven point six percent to eight percent, which is
Speaker 1: meaningful but is not fundamentally transformative. And reduction of time
Speaker 1: and hospital by some number of days also great, but
Speaker 1: not formed of an I understand that this could be
Speaker 1: combined with other anti virals and potentially something could be
Speaker 1: cobbled together. So or not ruling it out in any way,
Speaker 1: but it seems as though some of the initial enthusiasm
Speaker 1: that we would find a therapeutic that would be the
Speaker 1: magic solution has waned in recent weeks. I think that
Speaker 1: enthusiasm should needs. It's too easily swayed and endurance and
Speaker 1: a continued investment is required. We should not expect that
Speaker 1: our first shot on goal will go in. We will
Speaker 1: need to continue that investment. If anything, I would say,
Speaker 1: there's encouragement that we were able to take a drug
Speaker 1: off the shelf and show that it has some anti
Speaker 1: viral activity that is clinically meaningful. Investing further in finding
Speaker 1: other drugs that have more specific activity or that are
Speaker 1: more clinically effective, I think is hugely important. What about
Speaker 1: monoclonal antibodies. We had a Kiko Iwasaki from now on
Speaker 1: the program and she said, you know, no one is
Speaker 1: paying sufficient attention to this, and she even expressed some
Speaker 1: puzzlement about why more people aren't focused on monoclonal antibodies. Yeah,
Speaker 1: I think monoclonal antibodies most likely given in combination, So
Speaker 1: not just one anti saris COB two antibody, but several
Speaker 1: that you could administer as a cocktail or in combination
Speaker 1: with desevere for example. That I think is a super
Speaker 1: interesting therapeutic angle. I think one challenge with monoclonal antibodies
Speaker 1: is that they're very expensive right now, and another challenge
Speaker 1: is that they are hard it seems to manufacture at
Speaker 1: large scale. So I think that it's an extremely exciting
Speaker 1: and important therapeutic direction, but I'm not sure that it's
Speaker 1: the answer for the broadly available therapeutic that would really
Speaker 1: give us an off ramp. So we should be talking
Speaker 1: a little bit more about therapies. What else should we
Speaker 1: be talking about. We should all to be talking about
Speaker 1: or really trying to get a better handle on the
Speaker 1: age distribution of infectiousness and susceptibility. How much of a
Speaker 1: role our kids really playing. I think this remains an
Speaker 1: open question. We've gotten some data, but we need a
Speaker 1: lot more. Our kids getting infected to the same extent
Speaker 1: as the rest of the population. Are they as infectious
Speaker 1: once infected as the rest of the population. This has
Speaker 1: big implications for going back to school and how we
Speaker 1: want our population to re engage and emerge from the
Speaker 1: hibernation we're in now. Do we try to restructure our
Speaker 1: communities in significant ways or are we able to let
Speaker 1: kids go back to school without concern because they don't
Speaker 1: play a big role in transmission right. I think this
Speaker 1: is from a variety of perspectives of real important question Clinically,
Speaker 1: I think there are still questions that are coming up.
Speaker 1: Why is it that this pathogen is causing hypercoagulable state
Speaker 1: where we're seeing clocks form both in the venus and
Speaker 1: arterial circulations. Why is it that we're seeing these unusual
Speaker 1: inflammatory conditions in some children. There are a variety of
Speaker 1: clinical questions that we're just really starting to pick up
Speaker 1: on and engage with. I think those are also going
Speaker 1: to be hugely important to understand. So there's the pathogenicity
Speaker 1: of the virus, the biology of the interaction between the
Speaker 1: host and pathogen, where I think we still have quite
Speaker 1: a bit to learn, and by understanding those features perhaps
Speaker 1: develop better interventions to prevent the severe sequila of COVID nineteen.
Speaker 1: Thank you for those steers. Those are all good stories
Speaker 1: for us. Continue to watch. Thank you for your clear analysis,
Speaker 1: and thank you for the work that you're continuing to
Speaker 1: do in this crisis. Thank you very much, Jonatan, Thank
Speaker 1: you for the conversation. It's been very fun. So many
Speaker 1: fascinating things came out of this interview with Yonatan that
Speaker 1: I tried to keep a running tally, and now looking
Speaker 1: at my notes, let me try to capture what I
Speaker 1: walked away with. First, in the absence of a vaccine
Speaker 1: becoming available very very soon, we're likely to see a
Speaker 1: recurring pattern of up and down, up and down of
Speaker 1: COVID nineteen. As the disease recurs, we respond with social distancing,
Speaker 1: and we lift the social distancing that could last at
Speaker 1: least into twenty twenty two. Second, COVID nineteen may well
Speaker 1: turn out to be seasonal, And if it does turn
Speaker 1: out to be seasonal, that will have a big impact
Speaker 1: on how the disease comes back and when. In particular,
Speaker 1: it's likely to recur in the fall, as it begins
Speaker 1: to get colder. That might turn out to be good
Speaker 1: news for Donald Trump. Third, depend on how immunity works,
Speaker 1: whether it's conferred by nature or conferred by a vaccine.
Speaker 1: It's entirely possible that we may see stars CoV two
Speaker 1: as actually turning into a permanently recurring disease that comes
Speaker 1: back again and again and again. Fourth, and perhaps I
Speaker 1: should have known this already, but I certainly did not.
Speaker 1: Immunity is not an on off switch. You're not either
Speaker 1: entirely immune to a disease or entirely not immune to it. Instead,
Speaker 1: it's a continuum operating on multiple different dimensions. How long
Speaker 1: it lasts can vary whether it's lifelong or partial. It
Speaker 1: can affect whether you transmit the virus more easily to
Speaker 1: another person. It could affect whether you get the disease
Speaker 1: to a lesser degree than you otherwise would. All of
Speaker 1: these factors turn out to vary from virus to virus,
Speaker 1: and from antibody reaction to antibody reaction. Last, but certainly
Speaker 1: not least, we're not going to know right away whether
Speaker 1: immunity that is conferred lasts or doesn't, and that will
Speaker 1: be true whether it's natural immunity or vaccine immunity. The
Speaker 1: only way to find out how well lasts will be
Speaker 1: to wait and to see. That's a lot to process
Speaker 1: and I'm still trying to process it. But as you know,
Speaker 1: here on Deep Background throughout the Corona Crisis, our goal
Speaker 1: is to bring you unvarnished the opinions of experts so
Speaker 1: that our learning process can be shared with you as well.
Speaker 1: Until the next time we speak, Be careful, be safe,
Speaker 1: and be well. Deep Background is brought to you by
Speaker 1: Pushkin Industries. Our producer is Lydia Jane Cott, with research
Speaker 1: help from zooe Win and mastering by Jason Gambrel and
Speaker 1: Martin Gonzalez. Our showrunner is Sophie mckibbon. Our theme music
Speaker 1: is composed by Luis Garat special thanks to the Pushkin Brass,
Speaker 1: Malcolm Gladwell, Jacob Weisberg, and Mia Lobel. I'm Noah Feldman.
Speaker 1: I also write a regular column for Bloomberg Opinion, which
Speaker 1: you can find at Bloomberg dot com slash Feldman. To
Speaker 1: discover bloomberg original slate of podcasts, go to Bloomberg dot
Speaker 1: com slash Podcasts. And one last thing. I just wrote
Speaker 1: a book called The Hour of Winter, a Tragedy. I
Speaker 1: would be delighted if you checked it out. You can
Speaker 1: always let me know what you think on Twitter about
Speaker 1: this episode, or the book or anything else. My handle
Speaker 1: is Noah R. Feldman. This is deep background