Speaker 1: Pushkin Pushkin from Pushkin Industries. This is Deep Background, the
Speaker 1: show where we explore the stories behind the stories in
Speaker 1: the news. I'm Noah Feldman. Before we start today, I
Speaker 1: want to let you know that this is the last
Speaker 1: episode in our season about power. After this, we're going
Speaker 1: on a hiatus for the next few months to work
Speaker 1: on our next season. If you have thoughts or suggestions,
Speaker 1: please let me know. You can find me on Twitter
Speaker 1: at Noah R. Feldman, or you can reach me on
Speaker 1: my website Noah Dashfeldman dot com, where I also have
Speaker 1: a newsletter which you can use so that we can
Speaker 1: keep in touch while I'm off the air. It's been
Speaker 1: a joy to explore behind the headlines with you all
Speaker 1: these last two seasons, and I want to take a
Speaker 1: moment to thank you for joining us on this journey
Speaker 1: over the years. Okay, on with the show. For our
Speaker 1: last episode of the season, we're returning once more to
Speaker 1: the biggest story of them all, the global pandemic. Joining
Speaker 1: us once again on just about the exact second anniversary
Speaker 1: of his first time on the show, we have Mark Lipsich,
Speaker 1: the brilliant and influential epidemiologist from Harvard University's School of
Speaker 1: Public Health. Mark is a professor of epidemiology and he
Speaker 1: directs the Center for Communicable Disease Dynamics. It's no exaggeration
Speaker 1: to say that Mark has been the go to person
Speaker 1: for interpreting the trajectory of the COVID nineteen pandemic and
Speaker 1: indeed for trying to make sense of its future. Mark,
Speaker 1: thank you so much for joining me. It's almost exactly
Speaker 1: two years since we first had a conversation in the
Speaker 1: very early days of realization of what was having with COVID,
Speaker 1: and we've checked in periodically since. And I would like
Speaker 1: nothing better than for this to be a valedictory conversation
Speaker 1: on the topic, so that next time we could talk
Speaker 1: about some other aspect of disease dynamics. But somehow it
Speaker 1: won't quite go away. So how many more times are
Speaker 1: you and I are going to do this? I mean,
Speaker 1: but put another way, how many more letters of the
Speaker 1: Greek alphabet are we going to need to learn? Is
Speaker 1: this is the variant process, one that is probabilistically likely
Speaker 1: to just come back again and again and again. Well,
Speaker 1: until we see a protracted period without new variants, we
Speaker 1: have to assume they will keep coming. What their characteristics
Speaker 1: will be we can make some speculations about but those
Speaker 1: speculations would not have probably included omicron in the form
Speaker 1: that it had, so we should be humble about our
Speaker 1: speculations as well. I mean, I think when you have
Speaker 1: tens to hundreds of millions of people infected in any
Speaker 1: given a short period of time around the globe with
Speaker 1: a virus, there is an opportunity for natural selection and
Speaker 1: genetic drift to play their tricks and for new variants
Speaker 1: to evolve, and our immune systems impose selective pressure. Our
Speaker 1: transmission behavior impose a selective pressure. So the ingredients are there.
Speaker 1: We all knew sort of intellectually that variants were a possibility.
Speaker 1: There was some hope that maybe the evolutionary rates were
Speaker 1: a little bit lower in coronaviruses, but that has not
Speaker 1: turned up to be true. And in fact, the big
Speaker 1: puzzle in some of my friends minds right now is
Speaker 1: why is omicron so different from from the last one.
Speaker 1: So I think we're going to be at this COVID
Speaker 1: game for a long time and the real question what
Speaker 1: the impact of that on health is and what the
Speaker 1: properties of these variants are, which is I think the
Speaker 1: hardest thing to predict other than likely being more and
Speaker 1: more transmissible, and the easier thing to predict but still
Speaker 1: not certain, is what is the state of us in
Speaker 1: terms of our immunity and the level to which vaccine
Speaker 1: and prior infection confer on us lasting immunity. I would
Speaker 1: love to learn more in our conversation Mark about what
Speaker 1: are the kinds of logics that you and your colleagues
Speaker 1: use when trying to talk about what those properties might be,
Speaker 1: understanding that they're not perfectly predictable. So you mentioned transmissibility,
Speaker 1: that seems like the obvious one. What are other criteria
Speaker 1: of fitness that you usually ascribe to viruses that would
Speaker 1: lead one to make any kind of speculations? And it
Speaker 1: might be interesting just to hear some examples of what
Speaker 1: you expected to happen how omicron differs from those. Yeah. Well,
Speaker 1: so transmission for the virus is sort of, roughly speaking,
Speaker 1: a two part job. It has to find new naive hosts,
Speaker 1: and as those become less and less common because more
Speaker 1: people are immune from prior infection or vaccination or both,
Speaker 1: it also needs to transmit to immune hosts. So one
Speaker 1: sort of generalization is that initially the selection is for
Speaker 1: more transmissibility. When almost everyone as naive, and as more
Speaker 1: people are immune, it's always good to be more transmissible.
Speaker 1: But there's more and more of a premium on being
Speaker 1: able to escape immunity, particularly for infection and transmission, Meaning
Speaker 1: there's not direct selection to escape immunity against severe outcomes
Speaker 1: that may happen as a side effect of selection for
Speaker 1: immune escape. That's not the primary goal of the virus.
Speaker 1: So I mean market for one quick second, I mean
Speaker 1: it's never the primary goal of a virus to make
Speaker 1: you very sick. It's just that the virus will do
Speaker 1: whatever it takes to make more of the virus, and
Speaker 1: if it happens to be then making you very sick,
Speaker 1: does that the virus will do that at least in
Speaker 1: so far as it doesn't kill you and therefore make
Speaker 1: it harder to spread to more people. Right, That's right,
Speaker 1: And that's why everybody's watching very carefully to see whether
Speaker 1: the immune escape of omicron, for example, is to one
Speaker 1: extent it also escapes the immunity to severe disease that
Speaker 1: people have, and it's less but to some extent it
Speaker 1: does escape even that level that type of immunity. Okay,
Speaker 1: so sorry interrupted, but go go ahead back to what
Speaker 1: you're saying. So as you say, the virus wants to
Speaker 1: make more copies of itself once in an evolutionary sense,
Speaker 1: to make more copies of itself. There's been a long
Speaker 1: standing discussion in the evolutionary biology community and parallel, mostly
Speaker 1: separate discussion in the medical and public health community about
Speaker 1: what that does to the severity of viruses. And in fact,
Speaker 1: that was what I wrote my PhD thesis on long
Speaker 1: time ago, was making models of that interaction between the
Speaker 1: severity of the infection and the direct targets of selection,
Speaker 1: which are more transmission. So in the old days, people said,
Speaker 1: in a sort of hand wavy way, without much quantitative reasoning,
Speaker 1: that if you kill somebody that you in fact then
Speaker 1: you can't spread if you're a virus, And so viruses
Speaker 1: try to become over evolutionary time, less harmful to their hosts,
Speaker 1: and at the same time the hosts become immune. It
Speaker 1: was then, on sort of conceptual grounds, noted that that's
Speaker 1: true up to a point. But if a virus is
Speaker 1: trying to grow in a host and does so so
Speaker 1: weakly that it doesn't make more copies of itself, that's
Speaker 1: the other extreme. So killing the host is too much growth,
Speaker 1: and not even making many copies of itself to transmit
Speaker 1: is the other extreme. And so the notion of that
Speaker 1: viruses evolved to an intermediate level of virulence to their
Speaker 1: host was sort of what many models predict, and then
Speaker 1: factors that can modulate that include how it's transmitted and
Speaker 1: the relationship between how many copies of itself it makes
Speaker 1: and the transmission rate. So the old idea they always
Speaker 1: try to become more mild is not widely held by
Speaker 1: people who know what they're talking about, but is widely
Speaker 1: held by the general public. Right, yeah, So is it
Speaker 1: correct even to say that, as a probabilistic matter, of
Speaker 1: the viruses we know about, they are more likely to
Speaker 1: evolve to being less harmful over time, or is even
Speaker 1: that which I've sometimes heard as a fallback statement, Is
Speaker 1: even that not empirically observably true. I don't know if
Speaker 1: we have enough of the history of viral virulence to
Speaker 1: look back at and watch. The most famous experiment was
Speaker 1: the release of mixomatosis, a disease of rabbits caused by
Speaker 1: maxomavirus in Australia, which was done as an effort to
Speaker 1: kill off the Australian pest rabbit population, and indeed that
Speaker 1: started out as an exceedingly virulent virus and did evolve
Speaker 1: to become less harmful beautiful. Experiments done by Frank Fenner,
Speaker 1: who was better known for a smallpox eradication, he showed
Speaker 1: very conclusively that it did become milder. It didn't become mild,
Speaker 1: it became milder, and the counterbalancing problem was that if
Speaker 1: it became very, very mild, it just couldn't grow in
Speaker 1: the rabbits. So that's probably the best documented example of
Speaker 1: watching evolution in practice, because rabbits and that virus both
Speaker 1: reproduce quickly, so you had a lot of generations each year.
Speaker 1: There is also a sort of mechanistic consideration that seems
Speaker 1: to be true in flu viruses and might be true
Speaker 1: also for omicron, which is that replicating deep in the
Speaker 1: lungs is a different property from replicating further up the
Speaker 1: respiratory tract. Replicating deep in the respiratory tract down in
Speaker 1: the lungs is more likely to cause severe disease, and
Speaker 1: replicating up at the top of the respiratory tract is
Speaker 1: more likely to spread. So to the extent that that's
Speaker 1: a tradeoff. There might be some selection for transmission that
Speaker 1: is indirectly selection for mildness. But you can imagine a
Speaker 1: situation where that's not true. Is it fair to say? Then?
Speaker 1: So I'm trying to get what one should say around
Speaker 1: educated people. Somebody says, well, you know, the great thing
Speaker 1: about omicron is that it shows you that, like all viruses,
Speaker 1: this is getting more mild. I mean, the first thing
Speaker 1: to say is that's an old view and it's not
Speaker 1: on conceptual grounds. Is not necessarily true. And then there
Speaker 1: are certainly counterexamples of viruses that have not evolved to
Speaker 1: be substantially less virulent. Are there any that come to mind?
Speaker 1: What happened with smallpox? By the way, which you mentioned,
Speaker 1: my layman senses that smallpox was still pretty virulent up
Speaker 1: to the time when it was eliminated. Yeah, that's right.
Speaker 1: What's difficult is that proving a negative is hard, and
Speaker 1: we didn't see the initial emergence of most viruses when
Speaker 1: they became human pathogens or pathogens of whatever organisms they
Speaker 1: In fact, that's why Maxsoma introduced into Australia was such
Speaker 1: a great example. You could watch the whole time course.
Speaker 1: But I think it's hard to settle the history, especially
Speaker 1: because we usually also can't separate the changes in the
Speaker 1: host from the changes in the virus. In other words,
Speaker 1: as we become more immune, even the same virus will
Speaker 1: cause less severe disease. Mark we want to warn readers
Speaker 1: not to generalize for the mixed homa case to thinking
Speaker 1: that's true of all viruses. Tell me again so that
Speaker 1: I understand it. The conceptual reason that we cannot assume
Speaker 1: the way people did in the old days through hand waving.
Speaker 1: As you said that overtime virulence would necessarily be reduced.
Speaker 1: In this kind of Dayton picture, virulence is selected along
Speaker 1: with transmissibility to maximize transmissibility. And so when there is
Speaker 1: a trade off between making more copies of the virus
Speaker 1: and harming the host, the virus will choose making more
Speaker 1: copies of itself. When there's a reinforcement between making more
Speaker 1: copies of itself and harming the host, the virus will
Speaker 1: choose making more copies of itself. So what it does
Speaker 1: to us, as you said at the beginning, it doesn't
Speaker 1: really care. It's trying to maximize its own function. It
Speaker 1: is true, I think where there have been observations of evolution.
Speaker 1: The virulence has gone down in several examples, and I
Speaker 1: can't think of an example where it started mild and
Speaker 1: became more virulent that we can really document, but that
Speaker 1: would be hard to see. If it did happen, we
Speaker 1: might just see when it jumped out. So I think
Speaker 1: the thing to say is that there are some examples
Speaker 1: where viruses have become more mild, and there are some
Speaker 1: reasons why that might happen, But more mild and completely
Speaker 1: harmless are very different things, and that really the part
Speaker 1: that we can control is our immunity. We can control
Speaker 1: to some extent, and that is almost always a beneficial
Speaker 1: thing in terms of virulence of the virus. So that's
Speaker 1: the part where at least we can do something about it.
Speaker 1: You mentioned that one thing that variance want to do
Speaker 1: is of course they want to find new naive hosts,
Speaker 1: but over time that gets harder and harder, and so
Speaker 1: then they want to be able to get around sound immunity.
Speaker 1: Omicron seems to be pretty good at getting around immunity.
Speaker 1: Is there a sense a clear sense now of how
Speaker 1: it does so? And if so, is that a strategy
Speaker 1: that is likely to be replicated in future variants. Yeah,
Speaker 1: I mean, I think what's striking about omicron is that
Speaker 1: it not only has some mutations in its spike protein,
Speaker 1: which is a major target of antibodies, but it has
Speaker 1: a lot of mutations, more than it should given the
Speaker 1: amount of time that's passed if it were a typical
Speaker 1: virus out there. So I think the mechanism is still
Speaker 1: being understood in detail. But pridly speaking, the shape of
Speaker 1: its protein is different from the shape that the antibodies
Speaker 1: recognized which we're generated to previous variants, and so those
Speaker 1: antibodies don't bind as well, they don't neutralize as well,
Speaker 1: and therefore don't work as well. Any sense, people must
Speaker 1: be theorizing about this. You must be theorizing about this
Speaker 1: out why the jump seems to be as big as
Speaker 1: it is from earlier variants. Yeah, the evolution was faster
Speaker 1: than is typical in typical humans, and so the two
Speaker 1: leading hypotheses are it happened in a not typical human,
Speaker 1: meaning a human who perhaps had an immune system that
Speaker 1: was just good enough to exert selection but not good
Speaker 1: enough to end the infection. Part of why evolution doesn't
Speaker 1: happen too much during a typical infection is that there's
Speaker 1: a lot of selection to escape it, but not much
Speaker 1: time before the virus is gone, and dead viruses don't mutate,
Speaker 1: so once you clear an infection, it doesn't have the
Speaker 1: chance to evolve further. Immuno Compromised people in various forms
Speaker 1: often have much longer infections. If they're deeply immunocompromised, then
Speaker 1: they they may not exert much selection on the virus,
Speaker 1: and they may not survive for very long because they
Speaker 1: won't be able to control the virus. But if they
Speaker 1: are then this is just speculation. I mean compromised in
Speaker 1: some particular way that allows the virus to persist, but
Speaker 1: maintains that selection pressure that could accelerate. The other class
Speaker 1: of explanations is that, as we've seen, the Saris Kobe
Speaker 1: two can infect other mammals. For example, there was a
Speaker 1: lot of interest in the white tailed deer being infected.
Speaker 1: They were minks in Denmark that were infected earlier in
Speaker 1: the pandemic. So entering a new host species is often
Speaker 1: a trigger for accelerated evolution because the virus has a
Speaker 1: lot of new problems to solve to get good at
Speaker 1: infecting that host and So those are the two major
Speaker 1: hypotheses that people have thought about. We'll be right back.
Speaker 1: Mark word that one hears more and more is COVID
Speaker 1: is on its way to being endemic. Sometimes you hear
Speaker 1: people getting fancy and talking about a state of endemicity.
Speaker 1: My question is, first of all, what's the working definition
Speaker 1: that epidemiologists use for that? So what does endemic actually
Speaker 1: mean to an epidemiologist? And the second is in practice,
Speaker 1: what does that mean if and when we are there?
Speaker 1: I think we're The dirty laundry of the epidemiology community
Speaker 1: continues to be aired, and different people use these words differently,
Speaker 1: but I think the core idea of endemicity is that
Speaker 1: an infection is present at some level, almost constantly in
Speaker 1: a population, and it may go through say seasonal swings,
Speaker 1: and sometimes you call that seasonal upturn an epidemic, and
Speaker 1: sometimes people call averaging over the whole year to be
Speaker 1: endemic an endemic state. But it's a situation in which
Speaker 1: most people, by the time they reach some reasonably young age,
Speaker 1: have been exposed to the infection. That's an important characteristic,
Speaker 1: and where the swings are either very small, as with
Speaker 1: some infections that are just sort of pretty similar all
Speaker 1: year round, like some respiratory bacterial infections that are a
Speaker 1: little bit seasonal but basically kind of always there at
Speaker 1: similar levels, or they're predictable swings that are every winter
Speaker 1: or every summer or something like that. So it has
Speaker 1: aspects of predictability of most people having prior exposure. And
Speaker 1: therefore the reason why it's sort of a comforting word
Speaker 1: is that the two things that have really been miserable
Speaker 1: about sarskovi two have been the very large and unpredictable
Speaker 1: swings in the number of people infected, and the fact
Speaker 1: that it's preying on a population of us that is
Speaker 1: mostly naive to it and therefore at greater risk of
Speaker 1: having bad outcomes then we will be when we've all
Speaker 1: had the infection and or vaccination. The upshot that if
Speaker 1: I understand you correctly, is that even though endemic and
Speaker 1: epidemic are obviously etymologically related in terms of their relationship
Speaker 1: to the public, they're not in any very very sharp
Speaker 1: relationship to each other. Because something can be endemic and
Speaker 1: yet there can be epidemics that are seasonal. Is that right?
Speaker 1: So that those two and yet or you can have
Speaker 1: an epidemic that is not endemic, or you can sending
Speaker 1: it is endemic and is not epidemics. So it seems
Speaker 1: to have almost all the possible logical relationships. But I
Speaker 1: think I think the more helpful contrast probably is pandemic
Speaker 1: versus endemic. So the signal features of pandemics, although these
Speaker 1: are also revised as we as we have more of them,
Speaker 1: because they're each one is special. But the signal features
Speaker 1: of pandemics are a very naive population that is experiencing
Speaker 1: something for the first time, and being very widespread and
Speaker 1: having large swings and incidents and prevalence because of those
Speaker 1: two things. Yeah, so that's super helpful. I mean, that's
Speaker 1: super helpful because one can sort of think a pandemic
Speaker 1: nobody has it at first, then lots of people get
Speaker 1: it in bunches, and that's the pandemic endemic. Everybody's been
Speaker 1: exposed to it from the time that they were pretty
Speaker 1: small children, but it's still out there in the population.
Speaker 1: That seems to be very, very helpful. The thing that
Speaker 1: is a bit confusing to me at least is if
Speaker 1: we think about the relationships, say of omicron, to the
Speaker 1: earlier versions of COVID, it seems like even though in
Speaker 1: principle we should be moving to a place where almost
Speaker 1: everybody has been exposed or vaccinated one of the two
Speaker 1: that lots of people who were previously exposed to those
Speaker 1: other things or were vaccinated are getting o macron because
Speaker 1: of its capacity to evade immunity. And if that's the case,
Speaker 1: do you guys start thinking of it as though it
Speaker 1: were a separate disease and so therefore it doesn't really
Speaker 1: matter if let's say it becomes endemic. Let's say omicron
Speaker 1: becomes endemic, but something a new variant comes along that
Speaker 1: evades immunity, then aren't people sort of a naive population
Speaker 1: again with respect to that new variant if they're evading immunity, Yeah,
Speaker 1: that is the big question. The reason why omicron has
Speaker 1: been bad but not worse than it was is that
Speaker 1: the combination of somewhat lower severity and growing amounts of
Speaker 1: population immunity to severe disease, which still to a large
Speaker 1: degree though not perfectly hold against omicron, has meant that
Speaker 1: there are enormous numbers of cases, but not correspondingly many
Speaker 1: deaths and hospitalizations. And that's a kind of new thing.
Speaker 1: We haven't had a flu experience that's quite like that,
Speaker 1: and we haven't had a far as Kobe two experience.
Speaker 1: It's quite like that. So this is a new combination
Speaker 1: of properties to deal with. One way that I find
Speaker 1: it helpful to think about what's ahead in the next
Speaker 1: few years is that, as you say, the bad option
Speaker 1: will be if new variants continued to come and they
Speaker 1: really are either so good at escaping immunity and transmitting
Speaker 1: that the cases go shooting up, as they have with Omicron,
Speaker 1: or they are really good at escaping our immunity to
Speaker 1: severe disease, which was not that high at the beginning
Speaker 1: of Omicron, should be higher after Omicron, we hope. But
Speaker 1: if they're good at escaping our immunity to severe disease,
Speaker 1: then even modest numbers of cases could be a problem,
Speaker 1: and that would be like almost like a new flu pandemic.
Speaker 1: It would be an evolutionary jump that is highly consequential
Speaker 1: and is what we used to talk about with flu pandemics. Right.
Speaker 1: It's the reason that the flu vaccine, it's a good
Speaker 1: thing to get it, but it doesn't guarantee that you
Speaker 1: won't get the flu, right because the variants comes so fast. Right,
Speaker 1: partly and partly because they just aren't fully protective even
Speaker 1: against what they're supposed to talk and nearly as good
Speaker 1: as these these vaccines that I say, I kind of
Speaker 1: categorize like the two possible futures are that we have
Speaker 1: changes like the usual changes between years of flu, or
Speaker 1: we have changes like new flu pandemics that just are
Speaker 1: more frequent, And those are the two broad categories that
Speaker 1: we really really hope the first happens, but we have
Speaker 1: to consider the possibility in the second. Mark I'm trying
Speaker 1: to figure out what the right kinds of policy responses
Speaker 1: are at this moment, partly in order to get sense
Speaker 1: of what they're going to look like going forward if
Speaker 1: we have more variants. So, for example, at our mutual employer,
Speaker 1: Harvard University, on the one hand, we have classes at
Speaker 1: least at the law school in person, but we are
Speaker 1: all told not just to wear masks, but to wear
Speaker 1: a ninety five masks and possibly to wear two masks.
Speaker 1: And there seems to be a heightening of concern about
Speaker 1: transmission because I guess of the great transmissibility of omicron.
Speaker 1: On the other hand, we're in person, which we weren't
Speaker 1: obviously at an earlier stage, and What's more, everyone is
Speaker 1: mandatorily vaccinated and boostered, So what's the policy logic if
Speaker 1: you can reconstruct it behind that kind of heightened prevention
Speaker 1: coupled with diving right in and having classes. Well, another
Speaker 1: part of it, at least at our school public health,
Speaker 1: is that contact tracing is basically now left to the individual.
Speaker 1: There's no centralized contact tracing. So putting that together with
Speaker 1: what you just described, my interpretation is that people are
Speaker 1: trying to do the things that are efficient and relatively
Speaker 1: low impact that reduced transmission, while reallocating resources from very
Speaker 1: very costly in terms of time efforts like contact tracing,
Speaker 1: and trying to return to doing as much of what
Speaker 1: we're supposed to be doing as a university as possible.
Speaker 1: So that's my interpretation. And an environment where let's say
Speaker 1: almost everybody or everybody has been vaccinated and boosted, then
Speaker 1: the goal would be try to avoid too many people
Speaker 1: getting omicron so that they have to miss class and
Speaker 1: stay home and give more people omicron, but nevertheless still
Speaker 1: try to push forward with as much normalcy as can
Speaker 1: be mustered under these circumstances. And I guess the question
Speaker 1: that leads me to is and It's not that I
Speaker 1: think either has the answer to it, but I want
Speaker 1: to talk about it. Is this the new normal? Right?
Speaker 1: I mean, is there any reason if people can bear
Speaker 1: going to class in masks or teaching in masks? Will
Speaker 1: there be a policy argument to you me going forward
Speaker 1: that even if as the omicron surge continues to decline,
Speaker 1: as it's doing in Massachusetts, we should just stick with
Speaker 1: this because it's a good preventive measure. To get people
Speaker 1: to comply with something like that, there would have to
Speaker 1: be a continuing real threat of severe outcomes in large
Speaker 1: numbers in the populations doing those behaviors, and or of
Speaker 1: overwhelming healthcare, which are closely related, of course, although not
Speaker 1: perfectly correlated. Because the burden on hospitals from omeocron has
Speaker 1: been enormous, the severity has been less, and that's because
Speaker 1: so many people were getting it at the same time.
Speaker 1: So I can't imagine that in a few years we
Speaker 1: will all be wearing masks for our daily life. I
Speaker 1: don't expect it, because I think, in my mind, the
Speaker 1: most likely scenario is that our immunity to severe disease
Speaker 1: continues to get ampleified by probably continued vaccination, and also
Speaker 1: continued circulation of the virus, and that this becomes a
Speaker 1: vaccine preventable disease, at least for the severe manifestations, and
Speaker 1: therefore we will start to dial back these control measures
Speaker 1: as they are dialing back. In fact, in many parts
Speaker 1: of the country already well in some parts of the country,
Speaker 1: they never really dialed up, right, They were dialed back
Speaker 1: from the very beginning, and they never stopped. I have
Speaker 1: a good friend in Oklahoma who this is long ago
Speaker 1: in this process. I asked him something about a public
Speaker 1: lecture and I said, he mentioned public and I said,
Speaker 1: there's going to be a public lecture, and he just
Speaker 1: laughed and he said, we have never stopped doing these things,
Speaker 1: he said, And by the way, my wife and I
Speaker 1: and all of our kids have had COVID, so's there's
Speaker 1: clearly a lot of local variation around the country. Yeah,
Speaker 1: But I mean, I think it's important to consider all
Speaker 1: the ways things could go bad, and it's really hard
Speaker 1: to do that at the saint and actually really put
Speaker 1: policy energy towards preparing for those and at the same
Speaker 1: time to have I think a reasonable level of optimism,
Speaker 1: like a realistic level of optimism that those things might
Speaker 1: well not happen, and we probably will not be wearing
Speaker 1: masks and a few hears, I think, and maybe even
Speaker 1: much sooner than that. So I mean, I think it's
Speaker 1: even possible that in say April, the amount of omicron
Speaker 1: immunity will be so great that will have a long
Speaker 1: rest from this. But it's also possible that we will
Speaker 1: have a new variant that creates bigger problems. Last question
Speaker 1: mark one of the optimistic thoughts. I don't want to
Speaker 1: say fantasies, but hopes that when sometimes hears about response
Speaker 1: to potential future variance, is one vaccine to rule them all,
Speaker 1: like some sort of a vaccine that is sufficiently protean
Speaker 1: and powerful that all it'll affect almost all coronaviruses, maybe
Speaker 1: all coronaviruses, such that you know, whatever these variants may be,
Speaker 1: they will probably be coronaviruses, and then we'll fall under
Speaker 1: that rubric. I guess what I'm wondering is, from the
Speaker 1: standpoint of epidemiology, do you have any thoughts on what
Speaker 1: are the probabilities of such a thing being possible? Are
Speaker 1: there other instances or areas where we've had effective vaccines
Speaker 1: that cover like a broad range of phenomena under some
Speaker 1: rubric like say coronavirus. Yeah, there have been. And the
Speaker 1: approach so far that has been the most effective with
Speaker 1: the vaccine that I used to study before COVID, which
Speaker 1: was the new Mecoco vaccine, and with the polio vaccine
Speaker 1: and with the flu vaccine is to just try to
Speaker 1: vaccinate people against everything that's around at once, and then
Speaker 1: with flu to change it over time. So those precedents exist,
Speaker 1: but other than flu, those are for things where there's
Speaker 1: a lot of variation and you need coverage of a
Speaker 1: whole bunch of different variants, but you have a list
Speaker 1: of them. It's not a changing list. It's just the list,
Speaker 1: or maybe a new one's discovered periodically, but it's kind
Speaker 1: of a fixed list, especially if they're ones that are worst.
Speaker 1: So that approach is well worn. There is a very
Speaker 1: strong effort right now underway in many quarters to create
Speaker 1: paying coronavirus vaccines. There will be different approaches of trying
Speaker 1: to put in a mix of different types, or of
Speaker 1: trying to find parts of the virus that are more
Speaker 1: conserved where immunity will be effective. And there's reason to
Speaker 1: be optimistic, but it still has to be proven. So
Speaker 1: I think it's a very worthwhile effort and we have
Speaker 1: to see if it works. Mark, thank you so much
Speaker 1: again for your insights. And I would say that I
Speaker 1: look forward to more conversations, and that would be true
Speaker 1: about this substance of the conversations, because a conversation with
Speaker 1: you is always illuminating. I hope we don't need too many, Moore,
Speaker 1: but my guess is we will be checking in in
Speaker 1: one form or another. Thank you so much for your time,
Speaker 1: look forward to talking about something else. Sometimes we'll be
Speaker 1: right back. As always, when talking to Mark Lipsitch, there
Speaker 1: are clear takeaways. First, as a probabilistic matter, it is
Speaker 1: overwhelmingly likely that variants are going to keep coming, possibly
Speaker 1: for a long time. The reason for that, Mark explains
Speaker 1: is that there is virus out there in the population,
Speaker 1: and while virus is out there among a large number
Speaker 1: of people, the probability that evolution will continue to do
Speaker 1: its work and develop new variants remains. Next, Mark points
Speaker 1: out that omicron has been a surprise in various respects,
Speaker 1: most particularly in how different it is than the variance
Speaker 1: that came before it, thereby suggesting that for various possible
Speaker 1: reasons that we're not yet sure of the evolutionary process
Speaker 1: is happening faster than we previously expect it. Third, and
Speaker 1: this is to my mind very important, we should not
Speaker 1: accept the viewpoint which we sometimes here expressed by non experts,
Speaker 1: that all viruses necessarily evolve in the direction of becoming
Speaker 1: less virulent. In fact, the virus will do whatever it
Speaker 1: takes to replicate itself, seen in evolutionary metaphorical terms, and
Speaker 1: that means that if it turns out that the virus
Speaker 1: can spread more effectively while being less virulent, it will
Speaker 1: do so. But if the virus needs to be more
Speaker 1: virulent in order to spread more effectively, it will do
Speaker 1: that too. Consequently, we cannot generalize and assume that we
Speaker 1: are on the way to things automatically gradually getting better
Speaker 1: via omicron Fourth, we are certainly approaching some quality that
Speaker 1: could be called endemicity, or a state of being endemic
Speaker 1: for COVID nineteen, defined to mean that almost everybody in
Speaker 1: the population will have been exposed to the disease, often
Speaker 1: relatively early in life. However, and this is the big however,
Speaker 1: whether that matters in the long run in terms of
Speaker 1: making it less likely that people get very sick depends
Speaker 1: entirely on how good future variants are at avoiding immunity.
Speaker 1: If people get sick when young and retain immunity, then
Speaker 1: that is a good result in terms of the effects
Speaker 1: of endemicity. But if future variants on the virus can
Speaker 1: still infect people who have nevertheless been exposed, the serious
Speaker 1: and indeed severe problems associated with the healthcare system and
Speaker 1: COVID nineteen could in principle continue even when the disease
Speaker 1: is endemic last and very much not least. Mark says
Speaker 1: that the possibility of a vaccine that would effectively block
Speaker 1: future variance by virtue of it being general enough to
Speaker 1: prevent all forms of the coronavirus from spreading or alternatively
Speaker 1: from getting the people who get them very sick, is
Speaker 1: worth pursuing. Whether it will succeed or not, of course,
Speaker 1: remains an unknown and not something on which it's possible
Speaker 1: to put a probabilistic numerical judgment. At the human level,
Speaker 1: Mark says he thinks it's very unlikely that in a
Speaker 1: couple of years or even sooner than that will all
Speaker 1: still be walking around wearing masks. That, for one leaves
Speaker 1: me some reason to continue to be hopeful. Ultimately, and
Speaker 1: this is me talking, not Mark. The power of this
Speaker 1: virus has been to shape the way we in the
Speaker 1: world respond to it in a broad set of complicated
Speaker 1: ways that themselves deploy our own conception of social power.
Speaker 1: Disease has power, Humans have power in responding to disease.
Speaker 1: All of it involves us in a set of complex
Speaker 1: trade offs and choices. The difference between us and evolution
Speaker 1: is that evolution is making those choices blindly, with no
Speaker 1: normative vision of how it wants to be or how
Speaker 1: the world should be arranged. We as humans are in
Speaker 1: a different position. Our judgments can be thoughtful, strategic, and
Speaker 1: ethically inclined, and with any luck, they will continue to be.
Speaker 1: As I mentioned at the beginning of the show, we
Speaker 1: hear a deep background are going to take a hiatus
Speaker 1: for a few months as we work on our next season.
Speaker 1: We'll miss you, but I very much hope to hear
Speaker 1: your voices through reaching me on Twitter at Noah are
Speaker 1: Feldman or perhaps even more efficiently, on my website at
Speaker 1: Noah Dashfeldman dot com. Until the next time I speak
Speaker 1: to you, breathe deep, think deep thoughts, and, if at
Speaker 1: all possible, under the circumstances of our world, try to
Speaker 1: have a little fun. Deep Background is brought to you
Speaker 1: by Pushkin Industries. Our producer is mo La Board, our
Speaker 1: engineer is Ben Taliday, and our showrunner is Sophie Crane mckibbon.
Speaker 1: Editorial support from noahm Osband. Theme music by Luis Guerra
Speaker 1: at Pushkin. Thanks to Mia Lobell, Julia Barton, Lydia, Jean Coott,
Speaker 1: Heather Faine, Carlie mcgliori, Maggie Taylor, Eric Sandler, and Jacob Weisberg.
Speaker 1: You can find me on Twitter at Noah R. Feldman.
Speaker 1: I also write a column for Bloomberg Opinion, which you
Speaker 1: can find at Bloomberg dot com slash Feldman. To discover
Speaker 1: Bloomberg's original slate of podcasts, go to Bloomberg dot com
Speaker 1: slash podcasts, and if you liked what you heard today,
Speaker 1: please write a review or tell a friend. This is
Speaker 1: Deep Background.