Speaker 1: Pushkin from Pushkin Industries. This is Deep Background, the podcast
Speaker 1: where we explore the stories behind the stories in the news.
Speaker 1: I'm Noah Feldman. If you've been listening to our show
Speaker 1: this past month, you'll know that coronavirus is basically the
Speaker 1: only thing we've been thinking about. We've tried to explore
Speaker 1: how this global pandemic is influencing every aspect of our lives.
Speaker 1: Our body is, of course, our economy, our civil liberties,
Speaker 1: our emotions, even how we cook. One topic, though, that
Speaker 1: we haven't yet covered is the question of treatment that
Speaker 1: takes on the virus directly. That may be one way
Speaker 1: for us to solve the corona problem, although it also
Speaker 1: may not be depending on the science. We may simply
Speaker 1: have to depend ultimately on social isolation to make the
Speaker 1: virus go down. So how far are we along the
Speaker 1: way to determining what drugs work? Here? Are the treatments
Speaker 1: that have gotten a lot of publicity actually working? Are
Speaker 1: they plausible? Have the studies that have been released actually
Speaker 1: demonstrated efficacy? Or are we much too early in the
Speaker 1: process to know how things are going to work out?
Speaker 1: If we find a treatment, will it be scalable? Here
Speaker 1: to discuss all of this with me is doctor Angela
Speaker 1: russ Mussel. She's a research scientist and a virologist at
Speaker 1: the Columbia University Mailman School of Public Health, and she's
Speaker 1: worked extensively on viruses and evola. Angela, first of all,
Speaker 1: thank you for taking the time to be here with us.
Speaker 1: What treatments are out there now that are being studied
Speaker 1: that you think potentially holds some promise And we're not
Speaker 1: talking about vaccines at all today, but we're going to
Speaker 1: start by talking just about treatments, right So, there are
Speaker 1: several treatments in clinical trial right now. It's important to
Speaker 1: note that there are no treatments at this time that
Speaker 1: have been demonstrated to be effective and safe for treating
Speaker 1: COVID nineteen. The main drugs that I've been hearing about
Speaker 1: are three different drug regiments. So there is a drug
Speaker 1: called rumdz a viere that was tested for ebola, and
Speaker 1: it wasn't effective for ebola, but it's a fairly broad
Speaker 1: spectrum anti viral drug and it has shown promise against
Speaker 1: MERS coronavirus in animals and against this coronavirus SARS coronavirus
Speaker 1: two in cell culture experiments. So that drug is being tested.
Speaker 1: It's not currently approved for use in humans, but there
Speaker 1: is quite a bit of safety data that was gathered
Speaker 1: during the trials for ebola, So if that drug does
Speaker 1: prove to be effective in a controlled trial, it should
Speaker 1: be relatively quick process to get it out to the public.
Speaker 1: Another drug that's being looked at is hydroxy chloroquin, which
Speaker 1: is an anti malarial drug that's also used to treat
Speaker 1: rheumatoid arthritis and lupus. Sometimes that has been tested with
Speaker 1: the antibiotic zithromycin. There was a lot of press about
Speaker 1: this also because President Trump has asserted that this is
Speaker 1: a game changing, miracle drug. It's really important to note
Speaker 1: that the controlled studies in a sufficient number of patients
Speaker 1: to determine whether or not it's effective are still ongoing.
Speaker 1: So the only papers that have been out about chloroquin
Speaker 1: or hydroxy chloroquin have used very very small numbers of
Speaker 1: patients and there were some issues with the trial design
Speaker 1: in terms of the controls that were used to evaluate
Speaker 1: its efficacy. So despite what we've heard some politicians talking about,
Speaker 1: those drugs are not proven at this time to be
Speaker 1: effective at treating COVID and then Finally, they're also looking
Speaker 1: at a combination of HIV protease inhibitors, and these drugs
Speaker 1: were chosen because they showed some efficacy anecdotally against SARS
Speaker 1: classic and so people thought that they might be useful here. Additionally,
Speaker 1: they were used with an anti influenza drug to treat
Speaker 1: a patient in Thailand. That patient recovered, so they concluded
Speaker 1: that it might have had an effect. But as with
Speaker 1: the other drugs that I just mentioned, it's critical to
Speaker 1: test those in a large group of patients with proper
Speaker 1: controls to determine if they actually are effective or not.
Speaker 1: A smaller clinical trial done in China that was controlled
Speaker 1: and randomized looked at those two HIV drugs and saw
Speaker 1: no effect in overall outcome, meaning that whether a patient
Speaker 1: received those drugs or just supportive care, there was no
Speaker 1: difference in the number of patients that eventually died from
Speaker 1: severe COVID disease. So the WHO is evaluating that drug
Speaker 1: combination as well in a larger group of patients to
Speaker 1: see if at a population level that would have a
Speaker 1: more a greater impact in terms of treating COVID. So
Speaker 1: those are the three drug regimens that have advanced the
Speaker 1: furthest in clinical trials, and we should start seeing some
Speaker 1: trial data from those, I would think in the next
Speaker 1: couple months, so that we can have a better idea
Speaker 1: of whether or not some of these existing drugs can
Speaker 1: be repurposed for treating COVID. Why is the timescale months
Speaker 1: for clinical trials here? I mean, the course of the
Speaker 1: disease is not that long. And of course, ordinarily one
Speaker 1: would want to have very careful experimental design and when
Speaker 1: we would want to have peer review of the studies
Speaker 1: and so forth and so on. But under crisis conditions,
Speaker 1: the ordinary person, and I'm treating myself as that here, think,
Speaker 1: you know, why can't the duration of the study just
Speaker 1: be as long as the course of the disease runs.
Speaker 1: And even if you run it a couple of times,
Speaker 1: that doesn't mean that it has to take months. So
Speaker 1: why are we talking about months? There are several factors.
Speaker 1: In order to demonstrate efficacy, you really need to have
Speaker 1: larger patient groups. So people in different places are doing
Speaker 1: different things, they are in different environments, and they have
Speaker 1: different levels of hospital care. And also genetically we're very
Speaker 1: different from one another. There's a lot of individuals, individual
Speaker 1: variation in the population. So when you are trying to
Speaker 1: enroll patients in a clinical trial, you're going to be
Speaker 1: seeing people coming from all different sorts of circumstances with
Speaker 1: all different kinds of potentially confounding variables, so pre existing
Speaker 1: medical conditions. People are going to be different ages, They're
Speaker 1: going to be both male and female. Each case will
Speaker 1: be different. So in order to understand how these drugs
Speaker 1: work in general for a person off the street, you
Speaker 1: really need to look at a lot of people, and
Speaker 1: that just takes a lot of time. Another issue is
Speaker 1: the ethics of it. So when clinical trials are done,
Speaker 1: you need to have informed consent from all of those patients,
Speaker 1: and patients are allowed to drop out of the trial
Speaker 1: at any time. In addition, many clinical trials will have
Speaker 1: criteria for patients to be removed from the trial if
Speaker 1: it appears that they are being harmed by the trial itself.
Speaker 1: Let's say somebody has an allergic reaction to an experimental drug.
Speaker 1: You would not want to continue treating that patient with
Speaker 1: that drug because that could potentially harm them. So in
Speaker 1: order to get these types of numbers that we really
Speaker 1: need to apply the knowledge of whether a drug is
Speaker 1: effective or not and safe to a large population of people.
Speaker 1: You just really need to enroll a lot of patients,
Speaker 1: and they have to be able to remain in the trial,
Speaker 1: and you have to do quite a lot of statistical
Speaker 1: analysis to make sure that you're accounting for all of
Speaker 1: these potential variables that a large diverse population of people bring.
Speaker 1: Everything you just said seems completely logical and appropriate for
Speaker 1: a well designed clinical trial of a drug. It makes
Speaker 1: me very happy and relieved to think that under ordinary circumstances,
Speaker 1: when scientists start checking on the efficacy of a new
Speaker 1: potential treatment, they do everything you've said, large sample size,
Speaker 1: sophisticated statistical analysis, ethical constraints, and allowing people to withdraw.
Speaker 1: All that makes perfect sense. None of that makes sense
Speaker 1: to me under crisis conditions. And help me out here,
Speaker 1: because my instincts are clearly at odds with that of
Speaker 1: at least some of the scientific community here. But it
Speaker 1: just seems very difficult for me to get my head
Speaker 1: around the idea that we should proceed as normal when
Speaker 1: we're in the middle of a global pandemic. Certainly this
Speaker 1: has been accelerated. The process of approving the trial, of
Speaker 1: coordinating a trial has been accelerated. Another thing that is
Speaker 1: being done sort of to balance potential benefit of these
Speaker 1: drugs for patients who need it most, who don't have
Speaker 1: time to wait for a clinical trial, because as you
Speaker 1: pointed out, it is a public health crisis. The FDA
Speaker 1: has approved the use of hydroxychloroquin prescriptions off label for
Speaker 1: compassionate use in patients that really have nothing left to lose,
Speaker 1: that patients who will die without some kind of intervention.
Speaker 1: So there is a balance between doing these types of randomized,
Speaker 1: properly controlled, properly statistically powered clinical trials as well as
Speaker 1: access to the drugs for patients who really have nothing
Speaker 1: left to lose, and well, even if they don't benefit,
Speaker 1: it's worth a try. The danger in that is that
Speaker 1: when people are deciding to self medicate or demanding these
Speaker 1: prescriptions off label for disease that's potentially not very severe,
Speaker 1: that's the type of thing that should be avoided. But
Speaker 1: you are correct that it is a crisis and that
Speaker 1: patients who are in the most dire condition, with the
Speaker 1: most severe need should have access to some of these
Speaker 1: experimental medications. Whether we have proof that they work or not.
Speaker 1: We'll be back in just a moment. I now want
Speaker 1: to ask you about the French study which I myself read,
Speaker 1: where on a very very small sample size there were
Speaker 1: fewer than forty five people in the entire trial, and
Speaker 1: of those only a very very small number I think,
Speaker 1: only six if I remember correctly, got the particular combination
Speaker 1: of hydroxy chloroquine and zethromycin together. But that study was exciting,
Speaker 1: and you could sort of understand why there was such
Speaker 1: a reaction to it, even from the President, by virtue
Speaker 1: of the fact that among that tiny number of people,
Speaker 1: those six people, the study reported that all had been
Speaker 1: completely cleared of signs of the virus when they study
Speaker 1: them quite a short time later, something like six days later.
Speaker 1: I mean, reading that study shows you what got everybody excited,
Speaker 1: also shows you the limitations of the study. What do
Speaker 1: you think of as the real problem with that study?
Speaker 1: If there is one? Oh boy, there are several problems
Speaker 1: with that study. One of the issues were the controls
Speaker 1: that were selected for that study. They were patients from
Speaker 1: a different institution, and usually when you're doing a study
Speaker 1: like that, you want to use patients from the same
Speaker 1: cohort of patients, so the same patient pool that you're
Speaker 1: treating people in. They effectively from what I can tell,
Speaker 1: selected patients, just other patients to compare it to, and
Speaker 1: that's not really a great comparison. Also, you pointed out
Speaker 1: it was very small, So when you're talking about six
Speaker 1: patients out of a group of I think there were
Speaker 1: twenty in the total treatment group, that is not sufficiently
Speaker 1: powered to make any conclusions at all. Those patients could
Speaker 1: have cleared the virus on their own, they could have
Speaker 1: gotten better, we just can't say because not enough patients
Speaker 1: were investigated. There are some other issues as well. One
Speaker 1: issue is that the journal that that paper was originally
Speaker 1: published in after a very short time of being a preprint,
Speaker 1: is controlled. The editor in chief of that journal is
Speaker 1: the senior author of the paper. Did he a Raoul?
Speaker 1: And furthermore, Elizabeth Bake from microbiome Digest has pointed out
Speaker 1: that there are some issues with his publication record. There
Speaker 1: are some papers that he has published with questionable data,
Speaker 1: and not necessarily that that indicates that he's falsifying data
Speaker 1: or or engaging in any intentionally nefarious work. But some
Speaker 1: questions have been raised about the research integrity in general
Speaker 1: of papers that he has authored, and just the conflict
Speaker 1: of interest with you know, him being the editor in
Speaker 1: chief of the journal that this was rushed to publication
Speaker 1: in does not do a lot to support the notion
Speaker 1: that the trial was rigorously evaluated by a panel of
Speaker 1: non conflicted peers. So there are a lot of questions
Speaker 1: about that particular investigator and the studies coming out of
Speaker 1: his group, as well as some of the claims that
Speaker 1: he has made on social media and in the media,
Speaker 1: which is you know, has sort of fueled this their
Speaker 1: miracle drugs and they're going to solve everything. There are
Speaker 1: both scientific as well as really ethical reason That's why
Speaker 1: that work may be somewhat problematic. So we've now evaluated
Speaker 1: that study and you've called it significantly into question and
Speaker 1: very helpful ways. There's a lot there that I had
Speaker 1: not known before and that I think is not generally
Speaker 1: available outside of the expert sphere. However, and here to
Speaker 1: the big However, if I were someone who were very
Speaker 1: sick with coronavirus right now, we're pretty sick, significant shortness
Speaker 1: of breath enough to have to be admitted to a hospital,
Speaker 1: and I had to choose among available options, I'm pretty
Speaker 1: sure that I would ask for this treatment combination. Not
Speaker 1: because I would be convinced of the rigor of the
Speaker 1: study just because there isn't any really other option out there.
Speaker 1: And indeed, you know, just anecdotally, someone who might know
Speaker 1: who was in the hospital, was really sick, was on
Speaker 1: eventilator in New York, was actually given this treatment. And
Speaker 1: I thought to myself, good, So, I guess what I'm
Speaker 1: wondering is about a kind of paradox, right. I mean,
Speaker 1: here you are saying the science is bad and inadequate,
Speaker 1: and yet it still might be better evidence than anything
Speaker 1: else we have, and therefore a reason to give it
Speaker 1: a try in an individual case. Now, I don't think
Speaker 1: I'm crazy. I mean, is that what you would do
Speaker 1: if you were suddenly hospitalized or someone close to you
Speaker 1: were suddenly hospitalized with a serious case. I mean, I
Speaker 1: think that for that reason this has been used in
Speaker 1: those circumstances that would be an appropriate circumstance in which
Speaker 1: to use this. But with the caveat that that is
Speaker 1: definitely a decision for the physician treating a particular patient
Speaker 1: to make. There may be counter indications for taking either
Speaker 1: of those medications. I have read that there are potentially
Speaker 1: drug interactions that can occur between zithromycin and hydroxy chloroquin specifically.
Speaker 1: I'm not sure personally why for the rationale of including
Speaker 1: a zithromycin other than it's an antibiotic that could potentially
Speaker 1: treat secondary bacterial infections, which are probably playing a big
Speaker 1: role in the most severe patients. So it's possible bole
Speaker 1: that a different drug besides zithromycin for somebody, for example,
Speaker 1: who might be allergic to a zithromycin, or have a
Speaker 1: bad reaction to a zithromycin, or have a drug interaction problem,
Speaker 1: they could be given potentially a different antibiotic, and those
Speaker 1: would all be decisions that would be made by the
Speaker 1: physician treating the patient in each individual circumstance. I agree
Speaker 1: with you that for patients who are on a ventilator
Speaker 1: where there is no other option, a physician should be
Speaker 1: able to make a decision about whether to treat that
Speaker 1: patient with an unproven medication that is available and FDA
Speaker 1: approved for other uses. That is a really individual decision
Speaker 1: that needs to be made in terms of patient physician care.
Speaker 1: That's separate from doing a large scale clinical trial to
Speaker 1: determine definitively whether those drugs actually work. You mentioned that
Speaker 1: Zythromycin is a broad spectrum antibiotic. It's not an anti
Speaker 1: viral agent, and so you were speculating that, you know,
Speaker 1: if it's having an effect, maybe the effect that it's
Speaker 1: just having is helping to deal with whatever other bacterial
Speaker 1: infections maybe going on simultaneous to the viral infection. What's
Speaker 1: the mechanism for hydroxy chloroquin that is an antiviral agent? Right,
Speaker 1: So what is the mechanism if you can explain it
Speaker 1: in lay person's terms for us, by which that's supposed
Speaker 1: to have an effect If it is indeed having an effect,
Speaker 1: So that's not known. Hydroxy Chloroquine is actually an anti
Speaker 1: malarial and malaria parasites are not viruses. Actually they're single
Speaker 1: celled parasitic organisms. A group in China looked at the
Speaker 1: effect of chloroquine, which is a related drug in vitro
Speaker 1: on SARS coronavirus and SARS coronavirus to replication and they
Speaker 1: speculate that the block occurs during the entry process. So
Speaker 1: when a virus infects a cell, the virus attaches to
Speaker 1: a host receptor and is taken up inside the cell
Speaker 1: in a compartment called an endosome in order for the
Speaker 1: virus to begin replicating its genome, which is a critical
Speaker 1: step in viral replication, the virus has to escape, essentially
Speaker 1: from that endosomal compartment. That escape process is triggered by
Speaker 1: the acidification of the endosome, so the endosome pH drops
Speaker 1: and that provides a chemical environment in which the virus
Speaker 1: confuse with the endosomal membrane and get inside the cell.
Speaker 1: What hydroxychloroquine and chloroquin do is they prevent endosomal acidification,
Speaker 1: and that has been proposed as a mechanism for how
Speaker 1: it would act as an antiviral drug, So it prevents
Speaker 1: the virus from actually getting into the part of the
Speaker 1: cell that it's going to replicate in by blocking that
Speaker 1: acidification process and keeping it trapped in those endosomes. Another
Speaker 1: one of the potential treatments that's being tested that you
Speaker 1: mentioned is remdesvere, an antiviral drug that I think said
Speaker 1: did not work against ebola, but did have some effects
Speaker 1: against mers. Tell us a little bit about this drug
Speaker 1: and why it's thought that it might actually be effective
Speaker 1: against this coronavirus. So, remdesiviere is a broad spectrum anti
Speaker 1: viral drug that's in a class of drugs called nucleoside analogs,
Speaker 1: and they are a chemical mimic of the ATCG molecules
Speaker 1: that make up DNA or RNA. Technically an RNA it's
Speaker 1: you instead of T, but they're called nucleoside bases. And
Speaker 1: most people are familiar with, you know, the genetic code
Speaker 1: which is made up of at season gs and the enzymine, cytosine,
Speaker 1: and guanidine, and these When the virus genome is replicating,
Speaker 1: these are put by an enzyme called, in the case
Speaker 1: of viruses, an RNA polymerase. They are put into a
Speaker 1: chain and that makes the new genetic material. What these
Speaker 1: nucleoside analogs do is they get inserted into this chain
Speaker 1: instead of the atcorg that is actually supposed to be there,
Speaker 1: and that can cause the genome to be catastrophically mutated
Speaker 1: effectively with these non functional base analogs. It's also been
Speaker 1: proposed that these nucleoside analog drugs can also activate certain
Speaker 1: innate antiviral signaling pathways, and they can also interfere with
Speaker 1: the activity of the polymerase enzyme that is making the
Speaker 1: new copies of RNA. In the case of a coronavirus.
Speaker 1: So these drugs did show promise in preclinical studies against ebola,
Speaker 1: but then it turned out not to work in actually
Speaker 1: Bola patients. There might be some reasons for that that
Speaker 1: don't actually have to do necessarily with the mechanism of
Speaker 1: the drug. One thing about ebola patients is that they
Speaker 1: aren't necessarily coming into an ebola treatment unit or ETU
Speaker 1: when they are early on an infection. Oftentimes, when an
Speaker 1: ebola patient is symptomatic, they will show up at the
Speaker 1: ETU after they're already very sick. And I study ebola,
Speaker 1: I study the host response to ebola in my animal
Speaker 1: models that I study. Once those animals have sort of
Speaker 1: reached a point of no return in terms of their
Speaker 1: host response just being completely screwed up by systemic ebola infection,
Speaker 1: then targeting the virus's ability to replicate may not be
Speaker 1: very helpful. And I wonder if that is why in
Speaker 1: patient trials, why remdzevir was not as effective as it
Speaker 1: appeared to be in preclinical trials, Because often in preclinical trials,
Speaker 1: when you're working with an animal model, you know exactly
Speaker 1: how much that animal was infected with and at what
Speaker 1: time that animal was infected. People don't necessarily know when
Speaker 1: they got infected, so remdesivir's ability to treat ebola patients
Speaker 1: will have a lot to do with at what point
Speaker 1: in the infection you can treat them. For COVID, we
Speaker 1: know that remdesivir has some efficacy against SARS coronavirus two
Speaker 1: in vitro in cultured cells, and we know that it
Speaker 1: seems effective in non human primates that were infected with
Speaker 1: Mer's coronavirus, which is another related coronavirus that causes a
Speaker 1: similar type of disease. Whither it will work in patients,
Speaker 1: I think will be dependent on when those patients are diagnosed.
Speaker 1: So remdesivir treatment as a last resort for patients who
Speaker 1: are already severely ill may or may not have an effect.
Speaker 1: If remdesivir does work by triggering some of these anti
Speaker 1: viral immune responses, it's possible that some of those responses
Speaker 1: may be protective. We just don't know until we are
Speaker 1: able to test this. But that is why it's so
Speaker 1: important to test these treatments on people at different stages
Speaker 1: of the disease and with different clinical manifestations of the disease,
Speaker 1: because we really need to know if, for example, remdesivir
Speaker 1: does appear to work, if treatment begins very early, then
Speaker 1: we need to know that so that patients can begin
Speaker 1: treatment initially when they are diagnosed, rather than waiting for
Speaker 1: them to progress to severe disease, for example. So those
Speaker 1: have a lot of implications for the types of decisions
Speaker 1: that physicians and clinicians will make if that drug does
Speaker 1: prove to be effective. Just a quick mention of the
Speaker 1: HIV protease inhibitors which in one patient seem to maybe
Speaker 1: anecdotally have an effect, what would the theory of the
Speaker 1: mechanism be there, and what's your virological instinct about the
Speaker 1: probabilities of that approach panning out. So I've seen a
Speaker 1: couple preprints that have suggested using in silico, meaning in
Speaker 1: computers analysis alone, showing that there may be some interaction
Speaker 1: with the M one protease of coronaviruses. I'm not clear
Speaker 1: if that is the mechanism. I haven't personally seen data
Speaker 1: to suggest that those protease inhibitors that normally target the
Speaker 1: HIV proteases also would have an impact on the coronavirus protease.
Speaker 1: It's certainly possible many proteases have conserved structural features in
Speaker 1: terms of how they work. I haven't seen any data though,
Speaker 1: that conclusively demonstrates the mechanism by which those HIV protease
Speaker 1: inhibitors would be functional. And I'm really grateful to you
Speaker 1: for your time. Before I let you go, I just
Speaker 1: want to ask, is there something I'm not asking you
Speaker 1: that I should be asking you with respect to the
Speaker 1: treatments that are out there. Is there some important point
Speaker 1: that you think we need to hear that I haven't
Speaker 1: directed you towards. I think the only important point that
Speaker 1: I like to get across is that the trials that
Speaker 1: are proceeding now are going as fast as they can.
Speaker 1: But it really is critical to show efficacy. And another
Speaker 1: great example of this is Ebola. So during the West
Speaker 1: African Ebola outbreak, a number of patients that were evacuated
Speaker 1: from West Africa were then treated with an experimental drug
Speaker 1: called ZMP that everybody heard about, and many of those
Speaker 1: patients recovered and people attributed to that to look at
Speaker 1: wonderful z MAP. It works so well. Z MAP failed
Speaker 1: the same clinical trial that m Dozevier did. It now
Speaker 1: appears quite clear that getting just supportive care, so fluids,
Speaker 1: potentially breathing support, other types of treatments for the symptoms
Speaker 1: of Ebola disease. That type of supportive hospital care has
Speaker 1: been itself effective at really improving the case fatality rates
Speaker 1: for ebola. So it's possible that all those patients that
Speaker 1: go z MAP, who were all you know, in the
Speaker 1: United States for the most part, or Europe in state
Speaker 1: of the art, I see us getting world class supportive
Speaker 1: care that may have had more of an impact than
Speaker 1: z MAP, But because it was a handful of patients
Speaker 1: with no control group, we couldn't evaluate z MAP, so people,
Speaker 1: I think sort of jumped to the conclusion that it
Speaker 1: was z MAP that was doing this and not the
Speaker 1: other different types of care that those patients were receiving.
Speaker 1: So we just need to be really careful about attributing
Speaker 1: positive outcomes to the wrong thing. Lest you know, people
Speaker 1: start prescribing these drugs widely. They don't do anything. It
Speaker 1: gives people a false sense of security, and it could
Speaker 1: ultimately be more harmful to public health and helpful. Angela,
Speaker 1: thank you so much for your time and your expertise
Speaker 1: and your extremely clear headed analysis and your excellent way
Speaker 1: of making it all understandable even to a layman like me.
Speaker 1: Thank you so much for your time. Well, it's my pleasure.
Speaker 1: Thank you for having me on and giving me the
Speaker 1: opportunity to talk to your listeners about this. I learned
Speaker 1: a lot from talking to doctor Angela russ Mussen. In particular,
Speaker 1: she was extremely clear about the necessity of patience and
Speaker 1: good scientific technique in trying to figure out what treatment
Speaker 1: actually will respond to the novel coronavirus in a way
Speaker 1: that works. Like a lot of people, I'm eager for
Speaker 1: there to be a treatment that works right away. And
Speaker 1: you might have heard in my voice some wish, some
Speaker 1: fantasy that we could sidestep some of the most slow
Speaker 1: moving and precise scientific features of experimentation in order to
Speaker 1: get to a treatment, but Angela made it extremely clear
Speaker 1: that the danger in doing so is that we might
Speaker 1: end up mistakenly treating people with drugs that aren't actually
Speaker 1: solving the problem, a phenomenon that she noted did happen
Speaker 1: in some instances in ebola. Response, that means that we
Speaker 1: need to do the slow, careful science in order to
Speaker 1: make sure that people are cured, and in the mean time,
Speaker 1: physicians will keep on using experimental treatments, even if they
Speaker 1: don't know that they work for certain, in the hopes
Speaker 1: that they will have some effect. That combination makes me
Speaker 1: a little more hardened. But at the same time, my
Speaker 1: ultimate takeaway from listening to Angela is that randomness is
Speaker 1: a real risk. It is simply possible that we don't
Speaker 1: have immediately to hand any treatment that will effectively address
Speaker 1: the health challenges that we're facing. And if that's so,
Speaker 1: it's social distancing for all of us and for a
Speaker 1: lot longer. If there's progress with respect to any of
Speaker 1: these treatments, you can be sure we'll discuss that issue
Speaker 1: and get behind the story of the science until I
Speaker 1: speak to you next time. Be careful, be safe, be well.
Speaker 1: Deep background is brought to you by Pushkin Industries. Our
Speaker 1: producer is Lydia Jane Cott, with research help from zooe Wynn.
Speaker 1: Mastering is by Jason Gambrell and Martin Gonzalez. Our showrunner
Speaker 1: is soph Given. Our theme music is composed by Luis
Speaker 1: Gera special thanks to the Pushkin Brass Malcolm Gladwell, Jacob Weisberg,
Speaker 1: and Mia Loebell. I'm Noah Feldman. I also write a
Speaker 1: regular column for Bloomberg Opinion, which you can find at
Speaker 1: bloomberg dot com slash Feldman. To discover Bloomberg's original slate
Speaker 1: of podcasts, go to Bloomberg dot com slash Podcasts. You
Speaker 1: can follow me on Twitter at Noah R. Feldman. This
Speaker 1: is deep background