Speaker 1: Pushkin from Pushkin Industries. This is Deep Background, the show
Speaker 1: where we explore the stories behind the stories in the news.
Speaker 1: I'm Noah Feldman. Today we're going to talk about the
Speaker 1: novel coronavirus and evolution. All viruses mutate and evolve, and
Speaker 1: that includes SARS cove two, the virus that produces COVID nineteen.
Speaker 1: The version of the virus that we saw when the
Speaker 1: pandemic first started this winter is slightly different from the
Speaker 1: version of the virus that has emerged today in ninety
Speaker 1: five percent of the cases that we're seeing. But what
Speaker 1: does that tiny, little single point difference mean one amino acid?
Speaker 1: Is it something we should be concerned about? That is
Speaker 1: something that scientists are in the process of figuring out
Speaker 1: to day. We're joined by one of those scientists, Nevill.
Speaker 1: Sanjana is a geneticist at the New York Genome Center
Speaker 1: and New York University. He has been researching and publishing
Speaker 1: about how the coronavirus is mutating. Nevill, thank you so
Speaker 1: much for joining me. Let's start with the call it
Speaker 1: the medium picture. Let's talk about the changes that we
Speaker 1: know have happened through mutation in the stars. CoV two
Speaker 1: virus since the original version surfaced in Wuhan over the
Speaker 1: course of the spring. Sure, so I think there's several
Speaker 1: different changes that have been found in different patient populations.
Speaker 1: Like many RNA viruses, I think one thing that is
Speaker 1: important to know about stars CoV two is it doesn't
Speaker 1: say the same it does mutate. There's elements of how
Speaker 1: the virus replicates where errors can be made during RNA transcription,
Speaker 1: and those errors can get packaged into new viruses and
Speaker 1: then propagated. Most of the time, most of those errors
Speaker 1: changes or variants or mutations probably have very little effect.
Speaker 1: But occasionally you have changes that really do have some
Speaker 1: functional impact on the virus. So one of the mutations,
Speaker 1: a single point mutation that you've been working on and
Speaker 1: that's gotten a fair amount of coverage, not as much,
Speaker 1: perhaps as it ought, is a mutation at the six
Speaker 1: hundred and fourteenth place in the genome of the starscoby
Speaker 1: two virus. Tell us about that one and tell us
Speaker 1: how it's moved through the population, right, Yeah, So the
Speaker 1: mutation that's in the spike protein. So Spike is really
Speaker 1: amongst the coronavirus proteins, probably the most famous proteins. So
Speaker 1: Corona just means crown. And the reason that coronavirus has
Speaker 1: this name with crown in it is because the individual
Speaker 1: viral particles, the varions are decorated with the spike protein
Speaker 1: that kind of sticks out and gives it this crown
Speaker 1: like appearance. So, just out of curiosity, because I've been
Speaker 1: wondering about this, It's called the spike protein because it
Speaker 1: literally spikes up and a number of spikes make the crown.
Speaker 1: It looks yeah, it looks like a spike. Yeah, it's
Speaker 1: by far the most distinguishable feature of any pictures we've
Speaker 1: seen at the virus. So the spike protein, the RNA
Speaker 1: port encodes a protein and that protein has thousands of
Speaker 1: amino acids in the six fourteenth position. Is this mutation
Speaker 1: that we've started to focus on, and the reason that
Speaker 1: we've started to think about this is totally accidental. My
Speaker 1: lab works on crisper and gene editing. We are very
Speaker 1: interested in using those tools to understand what are the
Speaker 1: host genes, what are the human genes that are essential
Speaker 1: for viral entry? And by figuring out which are the
Speaker 1: essential genes for viral entry, we were hoping that we
Speaker 1: could find ways to maybe block some of those genes
Speaker 1: or suppress the activity of some of those genes, and
Speaker 1: by doing that protect people from the virus entering. And
Speaker 1: this was just one of these accidents and science. You
Speaker 1: often hear about science that when you tell the story
Speaker 1: of science that it's like super linear, but when you're
Speaker 1: actually doing science, it actually is not so linear. There's
Speaker 1: twists and turns and different paths, sometimes dead ends. And
Speaker 1: so with the what we were trying to do in
Speaker 1: the lab to understand what are the host proteins that
Speaker 1: are required from viral entry, we started using a very
Speaker 1: safe virus that we use in the lab, and all
Speaker 1: we did was we attached to it the spike protein
Speaker 1: on the outside of that virus from stars Kobe two,
Speaker 1: because we know that the spike protein, because it spikes out,
Speaker 1: is the first point of contact between human cells and
Speaker 1: the coronavirus. And what we found actually was something pretty sad,
Speaker 1: which was that we were really barely able to get
Speaker 1: any cells infected with this virus that we had put
Speaker 1: the spike protein on. And so at that time in April,
Speaker 1: we had started to hear about this mutation that was
Speaker 1: circulating the population and looked like it was increasing it
Speaker 1: had come about sometime maybe in early February, likely in Europe,
Speaker 1: based on the best viral population genomics work with sequences viruses,
Speaker 1: and it looked very rapidly after it's kind of emerged
Speaker 1: in early February that it started to take over kind
Speaker 1: of the world populations. And that's true up to today
Speaker 1: where it's greater than ninety five percent of the circulating
Speaker 1: coronavirus today seems to be carrying the spike mutation, so
Speaker 1: new in February, but now here in July, it really
Speaker 1: seems to be quite dominant. So we thought, okay, let's
Speaker 1: modify the spike protein that we have in the lab.
Speaker 1: Let's just insert this little mutation that seems to be dominating.
Speaker 1: This is back in April. We did this and let's
Speaker 1: give it a try in the lab. And what we
Speaker 1: found was indeed it solved our problem. Our problem is
Speaker 1: we couldn't get the virus are kind of safe virus,
Speaker 1: the pseudovirus that we have decorated with the spike protein,
Speaker 1: we couldn't get it to enter our human cells. But
Speaker 1: when we changed it to have this mutation, we were
Speaker 1: able to see it enter much much better, five to
Speaker 1: ten times better, and we thought, great, we've solved our
Speaker 1: technical problem we had here in the lab. And then
Speaker 1: a day or two later we started to think about
Speaker 1: this and we said, wait a minute, this is pretty important.
Speaker 1: Maybe instead of just running on from this technical problem,
Speaker 1: we should maybe we should report this. Maybe we should
Speaker 1: tell people like, look, this is a functional change in
Speaker 1: how the virus infects humanselves. There are many fascinating things
Speaker 1: in the story you just told, and I want to
Speaker 1: just break them down a bit at a time. So
Speaker 1: let's start with the kind of astonishing fact that in January,
Speaker 1: when the first sequencing of the stars COVID two genome began,
Speaker 1: almost none and maybe none of the viruses that were
Speaker 1: sequenced had this mutation at place six fourteen. By March
Speaker 1: the number was noticeable. By April, it was sufficiently noticeable
Speaker 1: that your lab was thinking, let's try it out. By
Speaker 1: May it was in seventy percent of reported cases, and
Speaker 1: now it's at ninety five percent. So the first question
Speaker 1: I want to ask is does this count as strong
Speaker 1: evidence to you, as among other things such geneticist, that
Speaker 1: there must be some adaptive feature of this change, or
Speaker 1: is there some way that this could have happened without
Speaker 1: this particular mutation helping the virus to replicate more successfully. Yeah,
Speaker 1: so I think scientists are naturally very careful. So when
Speaker 1: we got this first functional data in late April early May,
Speaker 1: we weren't sure whether to believe it. And one of
Speaker 1: the great things about science during the COVID era is
Speaker 1: that there's been a lot of sharing and very rapid
Speaker 1: sharing new results. And in May what we saw were
Speaker 1: lots of different groups steadying the viral genomics and the
Speaker 1: evolution of viral sampling through the world, and there was
Speaker 1: really quite a dichotomy of views. There were folks who
Speaker 1: thought this is clear evidence of selection going on for
Speaker 1: the spike mutation, and then there was completely opposing views,
Speaker 1: which is less so today, but was more then where
Speaker 1: people thought, maybe it's something about a founder effect. You know,
Speaker 1: if hasn't seen coronavirus before, but just the first introduction
Speaker 1: of coronavirus into that country happens to be the one
Speaker 1: that carries this variant, and then maybe the next introduction
Speaker 1: into that country happens a week later. Well, you know,
Speaker 1: exponential growth, So if you have a week of lead time,
Speaker 1: that can really result in a lot more infections, especially
Speaker 1: because we know asymptomatic people can infect others, you know,
Speaker 1: I think sitting where we are right now, especially with
Speaker 1: all the functional data that's come out, there's about five
Speaker 1: or six different groups that have shown functional data is
Speaker 1: similar to what we did here in the lab, I
Speaker 1: think it's pretty clear that this version of the virus
Speaker 1: is more transmissible. And it's not just laboratory experiments, but
Speaker 1: something that we do in our preprint is we look
Speaker 1: at data from Sheffield University in the UK and also
Speaker 1: the University of Washington in Seattle. So these are two
Speaker 1: totally different groups sampling different populations UK population and US population,
Speaker 1: and they're basically looking at data from the qPCR test,
Speaker 1: which is the test that involves the nasal swab and
Speaker 1: qPCR just stands for quantitative polymerate chain reaction. It's actually
Speaker 1: quite a standard lab technique and because it's got that
Speaker 1: q and it quantitative, it can actually detect how many
Speaker 1: viral copies they are in a particular nasal swab. And
Speaker 1: what's super consistent over the two sites is the difference
Speaker 1: between the people who have the D variant or the
Speaker 1: G variant. These are the two different spike variants. The
Speaker 1: D is the original one, the G is the new one.
Speaker 1: And what both the sites find is that there's about
Speaker 1: a threefold increase in viral RNA detected in the nasal
Speaker 1: swabs of people with this new G variant, and that's
Speaker 1: consistent between Sheffield and the group in Seattle. And so
Speaker 1: to me that that suggests, I mean, we can't say
Speaker 1: something about person to person transmission, but something that we
Speaker 1: can definitely say with that data is that perhaps within
Speaker 1: the body, and remember the body is kind of a
Speaker 1: collection of cells, independent cells, where you know, you can
Speaker 1: have cells that are infected in cells that are not
Speaker 1: that are just fine. So perhaps within the body there's
Speaker 1: greater infection, greater distribution of the virus amongst cells when
Speaker 1: they are carrying the SPIKE variant. That sounds like it's
Speaker 1: a very powerful reason to think that the spike variant
Speaker 1: is superior with respect from the virus perspective, inferior from
Speaker 1: our perspective, and that it is adaptive. Let's talk about
Speaker 1: the question of why it seems to be better at
Speaker 1: effectuating transmission. What is it about the crown that works
Speaker 1: better from the virus's perspective at latching on to your
Speaker 1: cells in the G variant compared to the D variant
Speaker 1: with which the virus began. That's a great question. Yet,
Speaker 1: so if it is more infectious, like we show in
Speaker 1: a few different cell types, why is it what's you know,
Speaker 1: how does this one amino acid change create such a
Speaker 1: big difference in infectivity. That's a great question. We have
Speaker 1: the exact same question. And so when you look at
Speaker 1: the structure of the protein, there's different functional domains across
Speaker 1: the length of the protein. Something that we noticed is
Speaker 1: that kind of the closest functional domain to where this
Speaker 1: mutation is the receptor binding domain. That's the thing that
Speaker 1: actually makes contact with the human receptor for coronavirus, which
Speaker 1: we think is in a receptor called ACE two. So
Speaker 1: we said, okay, it's it's not in the receptor binding domain,
Speaker 1: but it's very close to. It's the closest kind of
Speaker 1: domain of the protein that has this well defined function.
Speaker 1: So it must be that, right, It must be. You know,
Speaker 1: something that this mutation is doing. It's increasing its affinity
Speaker 1: for ACE two. It's just like you know, if you're
Speaker 1: able to have kind of a tighter handshake, then that's
Speaker 1: a going to increase infection versus somebody that just kind
Speaker 1: of waves from a distance. Right, So we set about
Speaker 1: actually with some collaborators here at NYU to really to
Speaker 1: test this. And you know, as is often the case
Speaker 1: in science, you know, you have some very strong hypothesis
Speaker 1: about here's what the data should look like, and you know,
Speaker 1: reality and tells you, hey, you're wrong, And that's exactly
Speaker 1: what happened here. You know, our hypausis going into this
Speaker 1: was it was likely stronger binding to the receptor ACE two.
Speaker 1: We found that there was basically no difference between the
Speaker 1: purified spike or the spike variant with ACE two binding.
Speaker 1: So this was definitely not the right answer. It's fascinating
Speaker 1: to hear about a hypothesis that doesn't pan out, and
Speaker 1: it helps the rest of the world to trust science,
Speaker 1: to realize that it's not that the scientists start with
Speaker 1: the hypothesis then claim to prove it. Some things work,
Speaker 1: some things don't. That's part of the process. So what
Speaker 1: did you do next when you realize that the ACE
Speaker 1: two wasn't the answer? You know, there are other aspects
Speaker 1: of what spike you know, which, after all, is just
Speaker 1: this little micromachine that helps the virus. It is not
Speaker 1: there just to have the handshake with the ACE two receptor,
Speaker 1: it performs a lot of other functions that are very
Speaker 1: important for the virus to actually enter an inject it's
Speaker 1: genetic material into the human cell. The handshake is really
Speaker 1: just the first part. After that, the spike protein actually
Speaker 1: sheds kind of a piece of it and unveils this
Speaker 1: very hydrophobic piece, which is a way to say it's fatty.
Speaker 1: It's made of lipids, and why is that important. Lipids
Speaker 1: like to stick to other lipids, and the membranes of
Speaker 1: our cells are all fats, and so basically by unveiling
Speaker 1: this hydrophobic piece, it can stick into the plasma membrane,
Speaker 1: the fatty lipid by layer of our cells, and that
Speaker 1: way fuse basically make kind of this fusion between the
Speaker 1: viral membrane, which is also a lipid and the cell membranye.
Speaker 1: But this little dance, you know, is well orchestrated, and
Speaker 1: so what we eventually did find is that one difference
Speaker 1: we could see between the variant, the mutant form of
Speaker 1: spike and the original form of spike is that this
Speaker 1: kind of processing that enables the protein to go through
Speaker 1: this dance that in the end unveils. This piece that
Speaker 1: sticks into the host cell seems to be different between
Speaker 1: the wild type spike and the variant spike that it
Speaker 1: seems to be more resistant to certain kinds of premature unveiling,
Speaker 1: let's say, of this fatty region, and that actually might
Speaker 1: help it, because if you think about it, these viral proteins,
Speaker 1: they don't just come out and start to infect cells.
Speaker 1: They're produced inside a cell that's already infected. And if
Speaker 1: the spike protein has to go through this kind of
Speaker 1: complicated dance where it changes its confirmation a little bit,
Speaker 1: if that happens too early, it might be an irreversible change.
Speaker 1: It might not be able to become functional again. And
Speaker 1: so if that happens, say in the cell that produces
Speaker 1: the spike, then maybe that's too early. It really has
Speaker 1: to happen after it sees ACE two, it does the
Speaker 1: handshake with ACE two, and then it can kind of
Speaker 1: undergo this conformational change to stick itself into the membrane.
Speaker 1: And if that's happening too early, which is something that
Speaker 1: our data suggests, that might actually lead to varians that
Speaker 1: have spike on them. But the spike is not really functional,
Speaker 1: and perhaps what the mutant spike does is it just
Speaker 1: leads to more functional spike on the surface of the viruses. Now, well,
Speaker 1: let's turn now to the bigger picture consequences of these
Speaker 1: really remarkable findings that you and your co authors have
Speaker 1: contributed to making. When the ordinary person hears that possibly
Speaker 1: the new version of stars covy two is five to
Speaker 1: ten times better at transmitting itself than the old version,
Speaker 1: the natural thought is, oh boy, that's scary. So first question,
Speaker 1: is there any reason to think that an initial mutation
Speaker 1: of that sort would be an indicator that there could
Speaker 1: be future mutations that might similarly improve the transmission rate,
Speaker 1: that is, make it worse for us better for the virus.
Speaker 1: Or is it the case that just because this was
Speaker 1: a random point mutation, there's just no reason to think
Speaker 1: that there would be some other random mutation that would
Speaker 1: make this an even better virus at transmitting itself. Yeah,
Speaker 1: that's a fantastic question. I mean the real answer is,
Speaker 1: of course, like many things COVID related, we really don't know.
Speaker 1: I think based on this rapid evolution that we've seen
Speaker 1: just you know, with months of this virus circulating, I
Speaker 1: think it certainly is not beyond a shadow of a
Speaker 1: doubt kind of possibility that there might be another mutation,
Speaker 1: maybe in the spike protein, maybe in some of the
Speaker 1: other twenty five odd proteins that are in this virus
Speaker 1: that either leads to increased transmissibility or you could lead
Speaker 1: to hopefully not but some sort of increased lethality of
Speaker 1: the virus. And that sounds very scary. I don't think
Speaker 1: it has to be scary. I mean, one thing that
Speaker 1: is very great to see right now, which we certainly
Speaker 1: didn't have during the nineteen eighteen you know, flu pandemic,
Speaker 1: is the use of rapidly deployable genomics thing. It's like
Speaker 1: the work that I'm talking to you about today, where
Speaker 1: we've been able to very quickly functionally characterize the impact
Speaker 1: of some of these mutations. There's a large scientific community
Speaker 1: of people working on this right now, and I do
Speaker 1: think we can either react in real time to a
Speaker 1: lot of these mutations at least understand what their functional
Speaker 1: impact is, or but the kinds of cool DNA synthesis
Speaker 1: technologies and RNA synthesis technologies that exist, we can actually
Speaker 1: make mutations and test them in a massively parallel way
Speaker 1: to kind of figure out, hey, what does this mutation do,
Speaker 1: what does that mutation do, and really fully characterize what's
Speaker 1: kind of a broad spectrum of what these proteins are
Speaker 1: capable of. And that way maybe we can start to
Speaker 1: predict and already think about, well, how do we improve
Speaker 1: our vaccines, how do we improve our therapeutics. And this
Speaker 1: has been done before with highly mutating viruses, so this
Speaker 1: is not a crazy idea to suggest. Perhaps the most
Speaker 1: mutagenic RNA virus that everyone knows well is HIV, the
Speaker 1: virus that causes aids. That virus is tremendously mutagenic, and
Speaker 1: what was found in the in the early and mid
Speaker 1: nineties was that drugs that were seemingly effective against HIV
Speaker 1: didn't really work in the long term, meaning that the
Speaker 1: virus was able to evolve ways around the drugs. You know.
Speaker 1: The real break through was in the late nineties the
Speaker 1: development of what we now referred to as the cocktail,
Speaker 1: which was a few different attacks on the virus, three
Speaker 1: different drugs brought together, and it turns out that even
Speaker 1: though the virus is very good at mutating that RNA virus,
Speaker 1: the three drugs together proved to be kind of a
Speaker 1: knockout punch and still to this date, twenty years twus
Speaker 1: after the development of the HIV cocktail, it is still effective.
Speaker 1: And so I think that provides a really nice roadmap,
Speaker 1: you know, I think it should inspire us that we've
Speaker 1: been able to lead with science. Let's talk then about
Speaker 1: vaccines and reinfection and what the practical consequences will be
Speaker 1: for those of this observed mutation. Let's start with reinfection.
Speaker 1: If you're in China, this may matter much more if
Speaker 1: you're in China than if you're in Europe or the
Speaker 1: United States. But you got the early version and now
Speaker 1: here comes the mutated version back around it comes back
Speaker 1: via Europe or the United States. I know there was
Speaker 1: concern initially in China that it might be that whatever
Speaker 1: immunity people have, and I realize we don't fully know
Speaker 1: how much community people have when they have been infected,
Speaker 1: but whatever immunity people did have might no longer be
Speaker 1: sufficient to hold off this new mutation of the virus.
Speaker 1: Is there data on that yet or do you have
Speaker 1: an intuitive sense absent the data, what is likely to
Speaker 1: be the case with respect your reinfection of people who
Speaker 1: got it the first time. Yeah, there's not data from US,
Speaker 1: But there's data from several other groups that have now
Speaker 1: started to look either at therapeutic antibodies that are being
Speaker 1: tested or antibodies isolated from patients who have had a
Speaker 1: COVID nineteen disease. Course, what they found is that many
Speaker 1: of these antibodies targets, say, for instance, that ACE two
Speaker 1: binding domain, which is the part of spike that's kind
Speaker 1: of on the farthest away from the virus. It's on
Speaker 1: the surface really of the virus. And so the good
Speaker 1: news is again because the mutation doesn't really seem to
Speaker 1: alter that receptor binding domain so much that most of
Speaker 1: those antibodies still are very effective against the mutant spike.
Speaker 1: So that'll suggests that this one mutation probably doesn't wipe
Speaker 1: out that kind of immunity. And just so I understand,
Speaker 1: is that because you did a great job of describing
Speaker 1: the two part process of how the virus gets you.
Speaker 1: First it shakes hands and then it's in the door,
Speaker 1: and then it takes off its hat or something like
Speaker 1: that or its mask and reveals the fatty lipid bind
Speaker 1: to you and then you're stuck. Are you saying that
Speaker 1: the reason that the antibodies are likely to work. Nevertheless,
Speaker 1: is that they primarily target the initial handshake, and as
Speaker 1: you showed in your initial lab efforts, there's not actually
Speaker 1: a major change in the nature of the handshake derived
Speaker 1: from this mutation. It's the later part. It's the taking
Speaker 1: off the mask. Yeah, I think that's that's exactly the case.
Speaker 1: Let's talk about vaccines in that case. Sure. So. Obviously,
Speaker 1: some of the vaccines seek to replicate precisely the antibodies
Speaker 1: that occur naturally, but there are also different kinds of
Speaker 1: vaccines that are being experimented with. Now. There are these
Speaker 1: so called trojan horse vaccines like the Oxford approach, there's
Speaker 1: the RNA vaccine like the Maderna approach. What does the
Speaker 1: evolution in the virus suggest with respect to those vaccines
Speaker 1: that would those also be just as effective on the
Speaker 1: earlier version as the late version or is it trickier
Speaker 1: than that? Yeah, I think the implication for vaccines is
Speaker 1: something that definitely merits some research. So there's about one
Speaker 1: hundred and thirty or so vaccines under in various stages
Speaker 1: of clinical development right now. In terms of how we
Speaker 1: think about virus manufacturing, one thing that I think was
Speaker 1: really impressive was how quickly some of these, especially the
Speaker 1: new clique acid based vaccines, the DNA and the RNA vaccines.
Speaker 1: How quickly we can go from sequencing the virus, you know,
Speaker 1: the first coronavirus sequence that was released in January, to
Speaker 1: having a vaccine ready to go, which was also in January,
Speaker 1: as you mentioned with maderna. And so what might be
Speaker 1: more important than being too worried about is this vaccine
Speaker 1: out of date? Has it kept up with all the
Speaker 1: newest spike mutations? Is to think, how can we develop
Speaker 1: a process or a pipeline where we can quickly capture
Speaker 1: population genomic data and I mean circulating virus data, sequence
Speaker 1: the genomes quickly, and then quickly update the vaccines to
Speaker 1: take into account new restraints and this kind of whatever
Speaker 1: you want to call it, like tightly closed loop sort
Speaker 1: of system or something like that. You know, that's really
Speaker 1: that could be a powerful process that doesn't just protect
Speaker 1: against this spike variant, but perhaps any future spike variants
Speaker 1: we might be worried about. Are there any general lessons
Speaker 1: from other viruses and the course of their mutations that
Speaker 1: are relevant to us here? Yeah? I think you know,
Speaker 1: HIV is a great example because enormous resources were dedicated
Speaker 1: starting the late eighties onwards to fighting HIV, and there
Speaker 1: it still took more than ten years to have a
Speaker 1: truly effective therapy. So that's I mean, that's one thing
Speaker 1: to say, but we did end up with an effective therapy.
Speaker 1: Another reason why HIV, I think is a particularly good
Speaker 1: example is because, as some folks might know, there has
Speaker 1: been a long, decades long quest for a vaccine for HIV.
Speaker 1: But today, even though there's any promising candidates kind of
Speaker 1: better time now than ever before, we still don't have
Speaker 1: an approved vaccine. This is a virus where we've known
Speaker 1: about it since the eighties, So that's you know, to
Speaker 1: me that that's kind of a scary thing, right that
Speaker 1: we can expend tremendous effort and many years and it
Speaker 1: still can be difficult to have vaccines. Now, that's one case.
Speaker 1: There are other cases where vaccines have been developed in
Speaker 1: much shorter periods of time, just a few years here.
Speaker 1: I mean, we really do have the whole world focused
Speaker 1: on this, so I'm you know, I'm all for these
Speaker 1: optimistic estimates that we hear from you respected infectious disease
Speaker 1: doctors like doctor Fauci and others of you know, six
Speaker 1: months to a year, and I certainly hope that that's
Speaker 1: the case. I mean, we all want our lives to
Speaker 1: go back to normal, but I think it's important with
Speaker 1: the historical perspective, we have to say that, you know,
Speaker 1: developing safe, effective therapies, safe effective vaccines, it's not easy,
Speaker 1: and I'm only hopeful that there's so much effort going
Speaker 1: into it right now that it will greatly accelerate those efforts. Well,
Speaker 1: thank you for the work that you're doing and for
Speaker 1: explaining why we should be a concern about the irritation
Speaker 1: and why we should also recognize that it's not necessarily
Speaker 1: the end of the world. Thanks for the opportunity to
Speaker 1: be here. To me, it's a rather remarkable fact that
Speaker 1: we can see in real time how the stars Cove
Speaker 1: two virus has been evolving the fact that the variation
Speaker 1: at place six fourteen was not visible almost at all
Speaker 1: in January, in February, was noticeable in March, was really
Speaker 1: noticeable in April, was at seventy percent in May, and
Speaker 1: it is now at ninety five percent provides significant reason
Speaker 1: to think that it's actually doing something to help the
Speaker 1: virus transmit itself. Nevland his group have suggested that by
Speaker 1: improving the spike protein, the new version maybe five to
Speaker 1: ten times better at transmitting the virus than the version
Speaker 1: that existed before, and they've made significant progress in trying
Speaker 1: to figure out where and why that is happening. The
Speaker 1: consequences of this development are significant, and they're also subtle.
Speaker 1: On the one hand, Nevil says we shouldn't assume that
Speaker 1: just because there's been one mutation that made the disease
Speaker 1: easier to spread, that there will be others. There might be,
Speaker 1: there might not be. On the other hand, he says,
Speaker 1: sometimes the reality is that we do get rapid evolution
Speaker 1: in a virus in a way that makes it difficult
Speaker 1: to contain the virus with a vaccine. The upshot is
Speaker 1: that we need to watch the development of this virus quickly.
Speaker 1: The good news is we can now do that. The
Speaker 1: speed and cheapness of sequencing genomes now makes it possible
Speaker 1: in almost real time, to track what's happening in a virus.
Speaker 1: Never before in the history of pandemics has it been
Speaker 1: possible to keep as close an eye on the genetic
Speaker 1: variation and evolutionary pressures that are taking place within a
Speaker 1: disease as it spreads. The worrisome bit is that no
Speaker 1: matter how much science we have, and no matter how
Speaker 1: sophisticated we are at understanding what's happening, we don't necessarily
Speaker 1: have all the tools to solve the problem. We're going
Speaker 1: to continue to watch this story. If the virus evolves more,
Speaker 1: you can be sure that we will talk about it
Speaker 1: right here on deep background. We'll be right back. Welcome
Speaker 1: to this week's playback. Hi, this is Anne with the
Speaker 1: Warranty Department. Our records show that your vehicle warranty has
Speaker 1: expired or it's about to expire. That is a sound
Speaker 1: that no one likes to hear, the sound of a
Speaker 1: robocall reaching you on your mobile phone. The Supreme Court
Speaker 1: weighed in on the robocall issued this past week in
Speaker 1: a case where Justice Brett Kavanaugh wrote, Americans passionately disagree
Speaker 1: about many things, but they are largely united in their
Speaker 1: disdain for robocalls. The Supreme Court struck down a twenty
Speaker 1: fifteen law that made an exception from the general ban
Speaker 1: on robocalls to your cell phone for collection of debts
Speaker 1: that are backed by the government, which would include, for example,
Speaker 1: your student loans. On the surface, nothing could sound more straightforward.
Speaker 1: How great that the Supreme Court, in the exercise of
Speaker 1: its infinite wisdom, has protected us further from robocalls. But
Speaker 1: that's not really what was going on. What was actually
Speaker 1: happening at the Supreme Court was an intense fight between
Speaker 1: the courts conservatives and the courts liberals about what standard
Speaker 1: they should use to analyze questions about the freedom of speech.
Speaker 1: The conservatives want to use the highest standard called strict scrutiny,
Speaker 1: where the Court almost always strikes down a law that
Speaker 1: is seen to implicate free speech, and the liberals are
Speaker 1: concerned that the conservatives are going to use free speech
Speaker 1: doctrine to overturn progressive regulation on things like food and
Speaker 1: drug regulation, workplace safety, or the regulation of the al
Speaker 1: of securities on the stock market. To understand what was
Speaker 1: really going on beneath the service in the robotcall case,
Speaker 1: you need thirty seconds on the constitutional law of free speech. Historically,
Speaker 1: the Supreme Court applied its toughest level of scrutiny to
Speaker 1: laws that seemed to treat different statements differently from each
Speaker 1: other based on the ideas expressed in them. Sometimes the
Speaker 1: Court called that viewpoint discrimination. That is a law that
Speaker 1: treats two people differently based on their viewpoint. Perhaps one
Speaker 1: is a Republican and one is a Democrat, and the
Speaker 1: law treats them differently under those circumstances. The Court always said,
Speaker 1: we're going to look at this law very carefully, and
Speaker 1: we're almost certainly going to strike it down. That all
Speaker 1: changed a few years ago in a case called Read
Speaker 1: against the Town of Gilbert, when Justice Clarence Thomas wrote
Speaker 1: an opinion saying that strict scrutinies should apply whenever a
Speaker 1: law differentiated between different kinds of expression based on their content,
Speaker 1: not based on the ideas they expressed, but just based
Speaker 1: on their content at all. In the robocall case, the
Speaker 1: Supreme Court relied on exactly that idea. The Court held
Speaker 1: that what was wrong with the government giving an exception
Speaker 1: to the robocall ban for government backed debt collection is
Speaker 1: that to do so, it had to ask what is
Speaker 1: the robocall about? The mine? You're asking what the robocall
Speaker 1: is about, said the Court. You're looking at the content
Speaker 1: of expression, and any law, the Court said, that looks
Speaker 1: at the content of expression automatically gets stick scrutiny and
Speaker 1: gets struck down. Writing in dissent, Justice Stephen Bryer forcefully
Speaker 1: expressed his serious worry that applying that kind of content
Speaker 1: based analysis to government regulations about speech could end up
Speaker 1: invalidating the laws that tell companies you must disclose what's
Speaker 1: in your product, you must tell the truth about your
Speaker 1: security's offerings. You must provide workplace warnings to workers so
Speaker 1: that they know what the dangers are that are facing
Speaker 1: them in all of those instances. Brier pointed out, the
Speaker 1: rule in question regulates content. It says that certain things
Speaker 1: must be said and other things must not be said.
Speaker 1: Bryer is worried that the Conservatives are going to use
Speaker 1: this very idea that all content based rules deserve strict scrutiny,
Speaker 1: to chip away and maybe go all in and strike
Speaker 1: down huge swaths of government regulation. All of this may
Speaker 1: sound to you pretty far from robo calls, but you
Speaker 1: know what, that's often how things happen at the Supreme Court.
Speaker 1: On the surface, a decision that seems to touch on
Speaker 1: something relatively minor, the irritation of robocalls, and it seems
Speaker 1: to give you a good result. Meanwhile, beneath the surface,
Speaker 1: a long run battle between conservatives and liberals for the
Speaker 1: future of our country and how government is allowed to
Speaker 1: operate under the constraints of our constitution. They're going to
Speaker 1: be several more Supreme Court decisions in the next week
Speaker 1: or two, which are likely to be high profile and significant.
Speaker 1: Will come back to those in a future playback. Until
Speaker 1: next time, Be careful, be safe, Be well. Deep background
Speaker 1: is brought to you by Pushkin Industries. Our producer is
Speaker 1: Lydia Jane Cott, with mastering by Jason Gambrell and Martin Gonzalez.
Speaker 1: Our showrunner is Sophie mckibbon. Our theme music is composed
Speaker 1: by Luis GERA special thanks to the Pushkin Brass, Malcolm Gladwell,
Speaker 1: Jacob Weisberg, and Mia Lobel. I'm Noah Feldman. I also
Speaker 1: write a regular column for Bloomberg Opinion, which you can
Speaker 1: find at Bloomberg dot com slash Feldman. To discover Bloomberg's
Speaker 1: original slate of podcasts, wrote Bloomberg dot Com slash Podcasts
Speaker 1: and one last thing. I just wrote a book called
Speaker 1: The Arab Winter, a Tragedy. I would be delighted if
Speaker 1: you checked it out. If you liked what you heard today,
Speaker 1: please write a review, or tell a friend. You can
Speaker 1: always let me know what you think. On Twitter, my
Speaker 1: handle is Noah R. Feldman. This is deep background