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Speaker 1: Pushkin from Pushkin Industries. This is deep background to show

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Speaker 1: where we explore the stories behind the stories in the news.

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Speaker 1: I'm Noah Feldman. As states begin to reopen, we're all

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Speaker 1: desperately trying to figure out what is going to happen next.

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Speaker 1: What are the possible courses of COVID nineteen, what are

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Speaker 1: the possible outcomes if there is a vaccine, and what

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Speaker 1: are the possibilities if indeed we don't get a vaccine

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Speaker 1: or a therapeutic treatment that actually changes things. Joining me

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Speaker 1: to discuss these issues is doctor Jonatan grad. He's an

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Speaker 1: assistant professor in the Department of Immunology and Infectious Diseases

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Speaker 1: at the Harvard chan School of Public Health. He's also

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Speaker 1: an attending physician in the Division of Infectious Diseases at

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Speaker 1: Brigham and Women's Hospital and Harvard Medical School. You know, Tom,

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Speaker 1: thank you so much for being here. I really hugely

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Speaker 1: appreciate it. And the first topic I want to ask

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Speaker 1: you about is a paper on which you're one of

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Speaker 1: the co authors, that was published in Science magazine. That

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Speaker 1: is a model or a series of models, among other things,

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Speaker 1: of what could happen under conditions of reopening if a

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Speaker 1: vaccine is not yet available or potentially not available at all.

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Speaker 1: Would you start by just describing at the core what

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Speaker 1: predictions you and your co authors were able to make

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Speaker 1: about the patterns of covid resurgence that are potentially out there. Sure,

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Speaker 1: there really seems to be only a couple of ways

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Speaker 1: in which a pandemic ends. One of them is elimination

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Speaker 1: of the virus. If you're able to control the spread

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Speaker 1: sufficiently towards the beginning of the virus emergence, you can

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Speaker 1: perhaps contain it to the extent that you can eliminate

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Speaker 1: its ongoing transmission. That I think is what happened with

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Speaker 1: the experience of stars in two thousand to three. I

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Speaker 1: think that this possibility for ending the pandemic now is

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Speaker 1: extremely unlikely, given how globally we've seen the spread of

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Speaker 1: SARS CoV two. The second way to end a pandemic

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Speaker 1: is through population immunity or herd immunity, when enough of

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Speaker 1: the population has acquired immunity to the pathogen that you

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Speaker 1: don't see ongoing epidemic spread. This can happen either with

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Speaker 1: a vaccine that can confer sufficient immune production or through

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Speaker 1: natural infection, where that infection elicits immunity. A key to

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Speaker 1: thinking about HERD immunity, then, is understanding what fraction of

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Speaker 1: the population would have to be infected and recovered from

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Speaker 1: infection with immunity in order for the pandemic to end.

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Speaker 1: That gets to the notion of the basic reproductive number,

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Speaker 1: a sense of just how transmissible the virus is. Estimates

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Speaker 1: of this number for Sarryscoop two place it around three,

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Speaker 1: although there have recently been some estimates that are considerably higher.

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Speaker 1: There was one published last week at five point seven.

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Speaker 1: But let's start with just the notion of this are

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Speaker 1: not or the basic reproductive number of three. What this

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Speaker 1: means is that on average, an infectious person will infect

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Speaker 1: three other people. To prevent these ongoing transmission chains, then

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Speaker 1: two out of three people would have to have immunity, right,

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Speaker 1: so we would have to get to a point in

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Speaker 1: which roughly sixty six percent of the population was immune

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Speaker 1: in order to see that transmission would diminish. We then

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Speaker 1: became interested in asking, given the broad based quarantine for

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Speaker 1: communities that had been introduced through these social distancing measures

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Speaker 1: and lockdowns, both in China and in elsewhere, what the

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Speaker 1: impact would be of these social distancing measure of different

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Speaker 1: durations and different effectiveness. We wanted to know if we

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Speaker 1: were to have lockdowns or social distancing with effectiveness of

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Speaker 1: say twenty percent so mildly effective, forty percent more effective,

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Speaker 1: or sixty percent on the order of what was seen

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Speaker 1: in China, what would happen and what would happen if

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Speaker 1: it were four weeks, eight weeks, twelve weeks, twenty weeks,

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Speaker 1: or for a long period. The key intuition here gets

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Speaker 1: back to what I was describing about the fraction of

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Speaker 1: the population that would have to be immune the extent

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Speaker 1: to which we are successful in preventing spread. So that's

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Speaker 1: the intervention. These lockdowns really diminished transmission, would maintain a

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Speaker 1: susceptible population in the community, so that when you stop

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Speaker 1: that intervention, when you lift the restrictions, now the virus

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Speaker 1: would have the opportunity to spread again through the susceptible population.

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Speaker 1: To the extent that we are successful, we will then

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Speaker 1: see the resurgence of the virus. And that was really

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Speaker 1: one of the main findings in this paper for that

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Speaker 1: one time social distancing interventions. As there are susceptible people,

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Speaker 1: the virus has no memory, it doesn't care what we've done.

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Speaker 1: It just carries if there are susceptible people around that

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Speaker 1: it can infect, and so we would expect to see

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Speaker 1: a resurgence of the virus. So that resurgence is a

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Speaker 1: version of what people call the second wave, and I

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Speaker 1: take it the way you're saying is that that second

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Speaker 1: wave is going to be a lot bigger than perhaps

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Speaker 1: people might assume, given the success of social distancing measures

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Speaker 1: that reduce the number of people who are exposed. So

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Speaker 1: this is sort of the downside of flattening the curve

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Speaker 1: is that fewer people have been exposed, and so when

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Speaker 1: the time comes that they are exposed, potentially a lot

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Speaker 1: of them could be exposed. Imagine a scenario and I

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Speaker 1: think you do imagine this in the paper where then

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Speaker 1: the government responds to that by saying, Okay, we have

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Speaker 1: a second wave coming. We see it rising, we see

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Speaker 1: the number of cases going up, in the number of

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Speaker 1: deaths going up, and so now we're going to reimpose

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Speaker 1: social distancing. Any reason to think that you wouldn't get

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Speaker 1: similar effect of that social distancing in the second time

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Speaker 1: as you did the first time, and then similarly the

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Speaker 1: third and the fourth, and however many times you need

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Speaker 1: to do this, that's right. So it gets to the

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Speaker 1: question of why are we doing social distancing in the

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Speaker 1: first place. If this virus were benign, we would just

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Speaker 1: let it run through the population, right because there wouldn't

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Speaker 1: really be a downside to that. But because this virus

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Speaker 1: causes the extent of disease that it does, we worry

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Speaker 1: about the impact it has on the healthcare infrastructure. So

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Speaker 1: the reason for enacting social distancing and putting communities in

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Speaker 1: lockdown is to not only try to save lives directly,

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Speaker 1: try to diminish the spread so that fewer people are

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Speaker 1: getting infected and dying from the disease, but also from

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Speaker 1: the effect it would have on our healthcare infrastructure. What

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Speaker 1: was seen in Uhan and then replicated in northern Italy

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Speaker 1: and more recently in New York is that when we

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Speaker 1: see this large fraction of the population infected all at once,

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Speaker 1: it overwhelms the healthcare system, and then we see things

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Speaker 1: like rationing ventilators, and also that people who would normally

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Speaker 1: be able to come into hospitals to get care for

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Speaker 1: their heart attacks or strokes were not coming in, so

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Speaker 1: there would not only be death from the virus itself,

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Speaker 1: but from our inability to properly care for people who

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Speaker 1: have the virus and the inability to care for people

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Speaker 1: who have other conditions, we would see extensive excess mortality.

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Speaker 1: That led to this effort to flatten the curve. Once

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Speaker 1: we stop and see a resurgence of virus, as you say,

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Speaker 1: we would expect that if we are still being guided

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Speaker 1: by that principle of trying to maintain the healthcare infrastructure,

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Speaker 1: then to the extent that it threatened by this resurgence,

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Speaker 1: we would imagine reinstituting social distancing measures. This led to

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Speaker 1: our consideration of, well, for how long would we have

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Speaker 1: to do that? Assuming no other intervention, And that's the

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Speaker 1: question I think everybody is so focused on. You know, again,

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Speaker 1: assuming no other magic bullet solution, how many times are

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Speaker 1: we going to have to run this same cycle of

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Speaker 1: up and down and up and down. It looks like

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Speaker 1: from our models that this could take a couple of

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Speaker 1: years of cycles, and that may be influenced by a

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Speaker 1: variety of factors. Those factors include whether we can expand

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Speaker 1: our critical care capacity. So really what we were thinking

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Speaker 1: about in this paper was can we titrate to some

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Speaker 1: extent the turning on and off of social distancing to

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Speaker 1: optimize the number of people were caring for in hospitals

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Speaker 1: or in the healthcare infrastructure, and that really seems keyed

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Speaker 1: to our critical care capacity. So the goal, then, from

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Speaker 1: a intervention perspective, would be to try to find the line,

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Speaker 1: which is how many cases we can handle in our

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Speaker 1: critical care facilities in the hospitals, and then to just

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Speaker 1: bring the number of infections up to that line as

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Speaker 1: close to that line as possible, and then back down again,

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Speaker 1: and to do that as long as it takes, And

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Speaker 1: of course how long it will take depends on how

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Speaker 1: high you can make that line, because that's the question

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Speaker 1: of how many people you can manage to infect. But

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Speaker 1: it sounds like making fairly reasonable assumptions about how high

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Speaker 1: that line could be set. You're suggesting that we could

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Speaker 1: end up having to do this again and again into

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Speaker 1: twenty twenty two. That's right, And it could be that

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Speaker 1: those numbers are adjusted by a variety of different factors.

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Speaker 1: If we find an effective therapeutic that diminishes the need

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Speaker 1: for hospitalization, or if a person is hospitalized that diminishes

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Speaker 1: the need for critical care, that effectively increases our critical

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Speaker 1: care capacity, right, So it's mathematically the same essentially as

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Speaker 1: increasing our capacity, so that can help shorten the duration

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Speaker 1: with which we'd have to go through these cycles. It

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Speaker 1: could also be impacted by seasonality, which is another aspect

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Speaker 1: of the projections that we evaluate in this paper. We

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Speaker 1: don't really know yet whether there is seasonality in transmission

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Speaker 1: of SARS CoV two. For some other respiratory viruses, we know, like,

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Speaker 1: for example, for influenza, that seasonality influences transmission such that

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Speaker 1: it is more transmissible in the winter than it is

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Speaker 1: in the summer. We see as well for a couple

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Speaker 1: of the other human coronaviruses that circulate in the US

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Speaker 1: and cause common cold type symptoms, that it appears they

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Speaker 1: also have seasonality. Using those as a basis for seasonality

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Speaker 1: for SARS CoV two, assuming that whatever factors influence the

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Speaker 1: other coronaviruses would also influence this one, we would see

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Speaker 1: that there would be less transmission in the summer, and

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Speaker 1: then transmission would pick up in the fall and peek

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Speaker 1: in the winter. That could also influence the deboration of

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Speaker 1: lockdown and release from social distancing interventions. So if COVID

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Speaker 1: nineteen does turn out to be seasonal in similarity to

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Speaker 1: these other viruses. That would suggest that we ought to

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Speaker 1: try to reopen going into the summer rather than going

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Speaker 1: into the winter. And that part sounds like good news

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Speaker 1: insofar as most of the openings up that are happening

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Speaker 1: now are going into summer months. That's right, And I

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Speaker 1: think it does raise further concern for the possibility of

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Speaker 1: augmented transmission in the fall and the winter. And I

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Speaker 1: think it's of concern for two reasons. One, it overlaps

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Speaker 1: with the increase in transmission of influenza, which we already

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Speaker 1: know creates stress on our healthcare infrastructure. So to see

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Speaker 1: both flu and COVID nineteen coupled together increasing together, I

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Speaker 1: think that is something that we all worry about. The

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Speaker 1: second reason is actually just one of domestic politics, right.

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Speaker 1: The importance of this election in November is one where

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Speaker 1: seeing a rise in cases and a second wave that

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Speaker 1: overlaps with the election, I think is something that people

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Speaker 1: have to be aware of and be concerned about. So,

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Speaker 1: just to understand what you're saying, what you're saying very politely,

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Speaker 1: but it sounds like what you're saying is you could

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Speaker 1: see a moment where over the summer, as reopenings occur,

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Speaker 1: we actually don't get a huge spike because the virus

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Speaker 1: is more seasonal. But then starts getting colder, people start

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Speaker 1: going inside. It's October, and the case rate might actually

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Speaker 1: begin to go up pretty rapidly, and then boom. We

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Speaker 1: have an election in the first week of November, as

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Speaker 1: mandated by federal statute, and the president may think he

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Speaker 1: can change that, but he can't. So it's going to

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Speaker 1: happen in early November one way or the other. Is

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Speaker 1: it cold enough in October to have this seasonal impact

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Speaker 1: before the election? I mean, I hate to ask such

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Speaker 1: a crudely political question, but it seems relevant. How does

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Speaker 1: flu do or how do these other coronaviruses do in October?

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Speaker 1: That's really the key timing. By the time you get

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Speaker 1: to November, the election will have happened, right. I expect

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Speaker 1: there to be an increase in transmission. The seasonality is

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Speaker 1: not an on off process. It's one that fluctuates with

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Speaker 1: the season. So as we start to move into the

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Speaker 1: fall and winter, I do worry that there will be

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Speaker 1: increased transmissibility and arise in cases. And I think even

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Speaker 1: as this is an issue that we can't know for

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Speaker 1: sure at this point, it is nonetheless one worth preparing for,

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Speaker 1: just in case. It's concerning enough that being able to

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Speaker 1: have the option to vote by mail seems critical for

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Speaker 1: an election where there may be risks as we've seen

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Speaker 1: in Wisconsin and the primaries to standing in line when

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Speaker 1: there are serious respiratory viruses in circulation. There's a fascinating

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Speaker 1: counterintuitive result of this, which is there's been a lot

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Speaker 1: of talk about what Donald Trump tried to delay the elections.

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Speaker 1: If Donald Trump were to listen to this podcast and

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Speaker 1: read your paper, he ought to not, under any circumstances

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Speaker 1: even think about delaying the elections, because if you delay

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Speaker 1: the elections, there might be a lot more COVID nineteen

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Speaker 1: cases as the weather gets colder, Whereas in the first

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Speaker 1: week of November it's entirely possible that that might be

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Speaker 1: going on, but we wouldn't have seen it yet. I

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Speaker 1: think it's so tough to speculate even months out at

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Speaker 1: this point. Frankly, I think with all of the variation

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Speaker 1: in social distancing interventions across the United States, it's very

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Speaker 1: hard to predict what the prevalence will be, and with

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Speaker 1: the risks for recurrence will be by community. Different states

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Speaker 1: and different regions have taken very different approaches to how

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Speaker 1: to manage the response to COVID nineteen. Some seem to

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Speaker 1: have adopted the Boris Johnson phrase take it on the chin.

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Speaker 1: Others are trying to flatten the curve, and yet others

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Speaker 1: are trying to crush the curve. And by crush the curve,

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Speaker 1: what I mean is really prevent any transmission through a

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Speaker 1: combination of social distancing interventions, contact tracing, and other means.

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Speaker 1: So it's hard for me to say exactly what the

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Speaker 1: dynamics will be come September, October, and November, because those

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Speaker 1: in part depend on the fraction of the population that

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Speaker 1: remains susceptible, and that right now is just so hard

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Speaker 1: to predict. We'll be back in a moment you're not on.

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Speaker 1: One of the findings that really struck me in your

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Speaker 1: paper was the finding that if immunity two stars COVID

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Speaker 1: two is not permanent, is likely to enter into regular circulation,

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Speaker 1: sort of like the flu comes around every year. There's

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Speaker 1: something a little terrifying about that because the idea that

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Speaker 1: we'll have stars CoV two with us in this form

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Speaker 1: for a long time is kind of world changing. But

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Speaker 1: hidden in there is a fascinating assumption that I think

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Speaker 1: opened something that I did not understand at all, and

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Speaker 1: I wonder if you would share with us, And that

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Speaker 1: is what does it mean to say that if the

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Speaker 1: immunity is not permanent? I tend to think I think

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Speaker 1: a lot of non physicians tend to think that either

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Speaker 1: you do become immune after you're exposed to something I

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Speaker 1: have antibodies, or you don't become immune. But I'm sensing

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Speaker 1: that that's not the right way to think about it. Immunity,

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Speaker 1: we like to think of, is something that is lifelong,

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Speaker 1: sterilizing protection that you get infected with something, you develop

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Speaker 1: immunity to it, and you are protected against infection with

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Speaker 1: that particular pathogen for the rest of your life. This

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Speaker 1: is one of the concepts we think about for vaccines generally,

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Speaker 1: and it's in some ways how they're pitched. Although you

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Speaker 1: know from your own experience, if you go in for

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Speaker 1: all of your recommended vaccines, as one should, you might

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Speaker 1: have wondered why it is that for some vaccines you

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Speaker 1: get several doses. Right, So every ten years, for example,

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Speaker 1: you're supposed to get an updated tetanus shot right, So

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Speaker 1: it gives a sense even just the fact that that happens,

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Speaker 1: that immunity is not an all or nothing, It is

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Speaker 1: not a one or zero. It is something that can

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Speaker 1: change over time. And also that it is not necessarily

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Speaker 1: as if you have some kind of invincibility shield. We

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Speaker 1: can think of immunity as being in a few different

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Speaker 1: categories of things. And does immunity prevent you from getting infected?

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Speaker 1: Does immunity prevent you from developing severe manifestations of infection

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Speaker 1: should you happen to get infected, And could immunity or

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Speaker 1: different elements of immunity help prevent ongoing transmission so make

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Speaker 1: you less infectious to others? These are also the different

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Speaker 1: ways in which we think about the potential outcomes of vaccination.

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Speaker 1: So for SARS CoV two, what we wondered about was

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Speaker 1: whether immunity might wane over time. There was a study

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Speaker 1: with one of the common cold type coronaviruses where military

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Speaker 1: recruits were exposed to one of these viruses and then

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Speaker 1: a year later exposed again, and they could still become infected,

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Speaker 1: although they had less symptoms. So it seemed as though

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Speaker 1: even if they were able to recover and develop an

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Speaker 1: immune response to the initial infection that let them clear

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Speaker 1: it That immune response was not of sufficient strength and

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Speaker 1: duration that they could not a year later again become infected,

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Speaker 1: although it was for many of them enough to limit

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Speaker 1: the end of symptoms. We see this with many pathogens.

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Speaker 1: One of the reasons why influenza is such the challenge

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Speaker 1: that it is is in part because immunity to flu

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Speaker 1: seems to change. Flu itself seems to change, so the

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Speaker 1: pathogens themselves may evolve in response to the immune pressure

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Speaker 1: from the human populations. We don't know whether this will

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Speaker 1: be the case with sarscoby two. That is yet to

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Speaker 1: be determined as well. So there are a variety of

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Speaker 1: factors at play, both in the dynamics of the human

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Speaker 1: population and individual level immune response, and in the evolution

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Speaker 1: of the pathogen as well. So the takeaway then is

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Speaker 1: that if exposure to the virus creates an immunity that

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Speaker 1: is time bound or that is not capable of completely

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Speaker 1: eliminating the chances that you get the disease later on,

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Speaker 1: but just weakens the case that you get, or if

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Speaker 1: a vaccine does either of those same sorts of things,

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Speaker 1: then we're going to get very possibly an annual COVID

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Speaker 1: scare and that could last. I take it indefinitely, because

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Speaker 1: if we're not talking about total immunity, then herd immunity

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Speaker 1: is in a sense a misnomer. The herd will never

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Speaker 1: be completely immune because no one is, on this theory

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Speaker 1: completely immune. They're just partially or immune in some time

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Speaker 1: bound way. And then it will have to become something

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Speaker 1: that we're going to have to manage going forward without

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Speaker 1: particular end, even if there is a vaccine, again, depending

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Speaker 1: on how the vaccine operates. Yes, so if we get

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Speaker 1: a vaccine, and I want to add a note of

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Speaker 1: caution here that it is not a given. Even with

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Speaker 1: the recent positive news from the phase one of the

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Speaker 1: Maderna trial, it does not seem to me a given

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Speaker 1: that we will have an effective vaccine for sure. I

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Speaker 1: just point out using the example of HIV, a very

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Speaker 1: different virus to be sure, but nonetheless a cautionary tale.

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Speaker 1: We have been trying to get a vaccine for HIV

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Speaker 1: for thirty years and we still don't have one. So

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Speaker 1: just to keep that in mind, I hope we get

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Speaker 1: one for SARS CoV two, and get one quickly. That

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Speaker 1: is highly effective and that does induce long lasting sterilizing immunity.

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Speaker 1: But if we don't, then you're absolutely right. We are

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Speaker 1: going to be looking at dealing with SARS CoV two

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Speaker 1: as another of the seasonal respiratory viruses. It will join

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Speaker 1: the ranks of influenza para influenzas once or for respiratories,

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Speaker 1: and sitial virus, man aneuma virus, the other coronaviruses, rhinovirus.

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Speaker 1: They're a whole panoply of respiratory viruses that cause everything

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Speaker 1: from common cold to very severe outcomes including death, that

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Speaker 1: come through the human population regularly, and it may be

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Speaker 1: that SARS CoV two will join that group. Is there

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Speaker 1: any way to know whether a particular type of community,

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Speaker 1: whether it's naturally occurring or whether it's vaccine induced, will

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Speaker 1: last over time other than waiting over time to see

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Speaker 1: what happens? I mean, is there any way to prefigure

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Speaker 1: that out? Yeah? No, not that I know of. I

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Speaker 1: think it is something where it really takes time to

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Speaker 1: figure it out. Part of it is, you know, what

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Speaker 1: is the robustness of the immune response, and then watching

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Speaker 1: what happens even over short periods of time to see

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Speaker 1: whether antibody levels rapidly decay or are maintained. What am

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Speaker 1: I not asking you? What are major points that you

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Speaker 1: think are not being sufficiently discussed in public right now?

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Speaker 1: About broadly speaking, the issues that we've been talking about.

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Speaker 1: I think that there are a few key points that

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Speaker 1: we haven't discussed that we should be thinking about. One,

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Speaker 1: we've talked about vaccines, but we have not talked about therapeutics.

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Speaker 1: I think therapeutics really give us the best and probably

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Speaker 1: closest off ramp. If we had effective drugs that could

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Speaker 1: diminish the possibility of severe disease, that could really treat

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Speaker 1: and cure infection with stars CoV two, the need for

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Speaker 1: a vaccine would go down tremendously. We could manufacture these drugs,

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Speaker 1: especially if they were oral drugs. Of course, there are

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Speaker 1: all the issues with resistance, and I'll just say the

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Speaker 1: reason that I haven't asked you about that is that

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Speaker 1: we've talked about this extensively on the show on other occasions.

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Speaker 1: Remdesivir does seem to be producing some appealing results, but

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Speaker 1: the numbers that are reported thus far, at least in

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Speaker 1: the NIH study, were not world transforming. It was mortality

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Speaker 1: from eleven point six percent to eight percent, which is

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Speaker 1: meaningful but is not fundamentally transformative. And reduction of time

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Speaker 1: and hospital by some number of days also great, but

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Speaker 1: not formed of an I understand that this could be

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Speaker 1: combined with other anti virals and potentially something could be

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Speaker 1: cobbled together. So or not ruling it out in any way,

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Speaker 1: but it seems as though some of the initial enthusiasm

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Speaker 1: that we would find a therapeutic that would be the

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Speaker 1: magic solution has waned in recent weeks. I think that

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Speaker 1: enthusiasm should needs. It's too easily swayed and endurance and

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Speaker 1: a continued investment is required. We should not expect that

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Speaker 1: our first shot on goal will go in. We will

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Speaker 1: need to continue that investment. If anything, I would say,

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Speaker 1: there's encouragement that we were able to take a drug

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Speaker 1: off the shelf and show that it has some anti

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Speaker 1: viral activity that is clinically meaningful. Investing further in finding

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Speaker 1: other drugs that have more specific activity or that are

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Speaker 1: more clinically effective, I think is hugely important. What about

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Speaker 1: monoclonal antibodies. We had a Kiko Iwasaki from now on

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Speaker 1: the program and she said, you know, no one is

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Speaker 1: paying sufficient attention to this, and she even expressed some

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Speaker 1: puzzlement about why more people aren't focused on monoclonal antibodies. Yeah,

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Speaker 1: I think monoclonal antibodies most likely given in combination, So

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Speaker 1: not just one anti saris COB two antibody, but several

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Speaker 1: that you could administer as a cocktail or in combination

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Speaker 1: with desevere for example. That I think is a super

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Speaker 1: interesting therapeutic angle. I think one challenge with monoclonal antibodies

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Speaker 1: is that they're very expensive right now, and another challenge

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Speaker 1: is that they are hard it seems to manufacture at

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Speaker 1: large scale. So I think that it's an extremely exciting

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Speaker 1: and important therapeutic direction, but I'm not sure that it's

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Speaker 1: the answer for the broadly available therapeutic that would really

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Speaker 1: give us an off ramp. So we should be talking

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Speaker 1: a little bit more about therapies. What else should we

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Speaker 1: be talking about. We should all to be talking about

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Speaker 1: or really trying to get a better handle on the

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Speaker 1: age distribution of infectiousness and susceptibility. How much of a

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Speaker 1: role our kids really playing. I think this remains an

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Speaker 1: open question. We've gotten some data, but we need a

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Speaker 1: lot more. Our kids getting infected to the same extent

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Speaker 1: as the rest of the population. Are they as infectious

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Speaker 1: once infected as the rest of the population. This has

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Speaker 1: big implications for going back to school and how we

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Speaker 1: want our population to re engage and emerge from the

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Speaker 1: hibernation we're in now. Do we try to restructure our

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Speaker 1: communities in significant ways or are we able to let

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Speaker 1: kids go back to school without concern because they don't

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Speaker 1: play a big role in transmission right. I think this

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Speaker 1: is from a variety of perspectives of real important question Clinically,

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Speaker 1: I think there are still questions that are coming up.

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Speaker 1: Why is it that this pathogen is causing hypercoagulable state

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Speaker 1: where we're seeing clocks form both in the venus and

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Speaker 1: arterial circulations. Why is it that we're seeing these unusual

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Speaker 1: inflammatory conditions in some children. There are a variety of

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Speaker 1: clinical questions that we're just really starting to pick up

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Speaker 1: on and engage with. I think those are also going

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00:27:47,196 --> 00:27:50,756
Speaker 1: to be hugely important to understand. So there's the pathogenicity

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00:27:50,916 --> 00:27:54,276
Speaker 1: of the virus, the biology of the interaction between the

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00:27:54,276 --> 00:27:57,076
Speaker 1: host and pathogen, where I think we still have quite

436
00:27:57,076 --> 00:28:00,956
Speaker 1: a bit to learn, and by understanding those features perhaps

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00:28:01,356 --> 00:28:05,836
Speaker 1: develop better interventions to prevent the severe sequila of COVID nineteen.

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00:28:06,316 --> 00:28:08,796
Speaker 1: Thank you for those steers. Those are all good stories

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00:28:08,796 --> 00:28:12,156
Speaker 1: for us. Continue to watch. Thank you for your clear analysis,

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00:28:12,196 --> 00:28:14,396
Speaker 1: and thank you for the work that you're continuing to

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00:28:14,436 --> 00:28:16,636
Speaker 1: do in this crisis. Thank you very much, Jonatan, Thank

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00:28:16,636 --> 00:28:19,276
Speaker 1: you for the conversation. It's been very fun. So many

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00:28:19,316 --> 00:28:22,756
Speaker 1: fascinating things came out of this interview with Yonatan that

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00:28:22,836 --> 00:28:25,796
Speaker 1: I tried to keep a running tally, and now looking

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00:28:25,836 --> 00:28:27,956
Speaker 1: at my notes, let me try to capture what I

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00:28:28,036 --> 00:28:31,476
Speaker 1: walked away with. First, in the absence of a vaccine

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00:28:31,476 --> 00:28:34,996
Speaker 1: becoming available very very soon, we're likely to see a

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00:28:35,036 --> 00:28:38,756
Speaker 1: recurring pattern of up and down, up and down of

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00:28:38,836 --> 00:28:43,996
Speaker 1: COVID nineteen. As the disease recurs, we respond with social distancing,

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00:28:44,116 --> 00:28:47,436
Speaker 1: and we lift the social distancing that could last at

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00:28:47,476 --> 00:28:52,476
Speaker 1: least into twenty twenty two. Second, COVID nineteen may well

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00:28:52,516 --> 00:28:54,716
Speaker 1: turn out to be seasonal, And if it does turn

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00:28:54,716 --> 00:28:57,276
Speaker 1: out to be seasonal, that will have a big impact

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00:28:57,556 --> 00:29:00,996
Speaker 1: on how the disease comes back and when. In particular,

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00:29:01,316 --> 00:29:03,796
Speaker 1: it's likely to recur in the fall, as it begins

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00:29:03,796 --> 00:29:06,076
Speaker 1: to get colder. That might turn out to be good

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00:29:06,116 --> 00:29:10,276
Speaker 1: news for Donald Trump. Third, depend on how immunity works,

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00:29:10,476 --> 00:29:13,956
Speaker 1: whether it's conferred by nature or conferred by a vaccine.

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00:29:14,476 --> 00:29:17,476
Speaker 1: It's entirely possible that we may see stars CoV two

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00:29:17,916 --> 00:29:22,716
Speaker 1: as actually turning into a permanently recurring disease that comes

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00:29:22,756 --> 00:29:27,676
Speaker 1: back again and again and again. Fourth, and perhaps I

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00:29:27,676 --> 00:29:29,716
Speaker 1: should have known this already, but I certainly did not.

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00:29:30,356 --> 00:29:33,516
Speaker 1: Immunity is not an on off switch. You're not either

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00:29:33,716 --> 00:29:37,876
Speaker 1: entirely immune to a disease or entirely not immune to it. Instead,

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00:29:38,036 --> 00:29:42,436
Speaker 1: it's a continuum operating on multiple different dimensions. How long

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00:29:42,476 --> 00:29:46,556
Speaker 1: it lasts can vary whether it's lifelong or partial. It

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00:29:46,556 --> 00:29:49,316
Speaker 1: can affect whether you transmit the virus more easily to

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00:29:49,316 --> 00:29:52,236
Speaker 1: another person. It could affect whether you get the disease

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00:29:52,356 --> 00:29:55,636
Speaker 1: to a lesser degree than you otherwise would. All of

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00:29:55,676 --> 00:29:58,516
Speaker 1: these factors turn out to vary from virus to virus,

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00:29:58,676 --> 00:30:02,676
Speaker 1: and from antibody reaction to antibody reaction. Last, but certainly

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00:30:02,756 --> 00:30:05,836
Speaker 1: not least, we're not going to know right away whether

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00:30:05,916 --> 00:30:09,516
Speaker 1: immunity that is conferred lasts or doesn't, and that will

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00:30:09,556 --> 00:30:12,596
Speaker 1: be true whether it's natural immunity or vaccine immunity. The

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00:30:12,636 --> 00:30:14,756
Speaker 1: only way to find out how well lasts will be

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00:30:14,836 --> 00:30:18,836
Speaker 1: to wait and to see. That's a lot to process

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00:30:18,876 --> 00:30:22,076
Speaker 1: and I'm still trying to process it. But as you know,

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00:30:22,316 --> 00:30:25,436
Speaker 1: here on Deep Background throughout the Corona Crisis, our goal

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00:30:25,596 --> 00:30:29,636
Speaker 1: is to bring you unvarnished the opinions of experts so

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00:30:29,676 --> 00:30:33,796
Speaker 1: that our learning process can be shared with you as well.

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00:30:33,836 --> 00:30:36,996
Speaker 1: Until the next time we speak, Be careful, be safe,

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00:30:37,236 --> 00:30:41,236
Speaker 1: and be well. Deep Background is brought to you by

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00:30:41,276 --> 00:30:45,236
Speaker 1: Pushkin Industries. Our producer is Lydia Jane Cott, with research

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00:30:45,276 --> 00:30:48,516
Speaker 1: help from zooe Win and mastering by Jason Gambrel and

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00:30:48,596 --> 00:30:53,076
Speaker 1: Martin Gonzalez. Our showrunner is Sophie mckibbon. Our theme music

486
00:30:53,156 --> 00:30:56,596
Speaker 1: is composed by Luis Garat special thanks to the Pushkin Brass,

487
00:30:56,836 --> 00:31:01,156
Speaker 1: Malcolm Gladwell, Jacob Weisberg, and Mia Lobel. I'm Noah Feldman.

488
00:31:01,516 --> 00:31:04,476
Speaker 1: I also write a regular column for Bloomberg Opinion, which

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00:31:04,516 --> 00:31:08,196
Speaker 1: you can find at Bloomberg dot com slash Feldman. To

490
00:31:08,276 --> 00:31:11,796
Speaker 1: discover bloomberg original slate of podcasts, go to Bloomberg dot

491
00:31:11,836 --> 00:31:16,116
Speaker 1: com slash Podcasts. And one last thing. I just wrote

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00:31:16,116 --> 00:31:19,196
Speaker 1: a book called The Hour of Winter, a Tragedy. I

493
00:31:19,196 --> 00:31:21,196
Speaker 1: would be delighted if you checked it out. You can

494
00:31:21,196 --> 00:31:23,276
Speaker 1: always let me know what you think on Twitter about

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00:31:23,276 --> 00:31:26,316
Speaker 1: this episode, or the book or anything else. My handle

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00:31:26,396 --> 00:31:29,636
Speaker 1: is Noah R. Feldman. This is deep background