COVID Webinar Series: Transcript of session with Kevin Tracey, MD

Kevin Tracey, MD, President & CEO, Feinstein Institutes for Medical Research
Recorded Wednesday, June 18th
His session is available for viewing online.  This is a transcript of the Q & A:

KRIS REBILLOT: You are in New York City, Long Island, and Upstate New York. That’s where Northwell is, 23 hospitals, 2 million patients served every year. What’s the status in your part of the world?

KEVIN TRACEY: We just… the status is good. We just saw some of the best kind of work that humans can do to help each other. Northwell, as you said, is 23 hospitals, 70,000 employees, hundreds of outpatient facilities and skilled nursing facilities. And in the early days of the response to this epidemic, these 70,000 people came together as one around an emergency. And the response was… frankly, it was awe-inspiring to be part of, and we’ve gotten through it quite well. We’ve treated about 50,000 patients, inpatients and outpatients, 11… discharged more than 11,000 patients from the hospital having survived COVID. And we didn’t run out of PPE or ventilators. We built 2,000 new hospital beds in a few weeks. It was an incredible thing to witness. It was an incredible thing to be part of.

KRIS:  Dexamethasone was shown to improve the odds of survival in those sickest patients compared to those who received standard care. What’s your take on it?

TRACEY: I think it’s good to be optimistic. I think the world is quite desperate for good news wherever it can find it in this horrible pandemic. I have some questions that haven’t been answered yet about this.

We haven’t seen… as you said, we haven’t seen the peer reviewed data. I did read the press release fairly carefully and I still have a lot of questions. It’s very hard to know if the control population was comparable to the sick population that was the... you know, the control population was comparable to the treated population. It’s very hard to know when you’re talking about… you know, Dexamethasone or Decadron, it’s a lot more potent than prednisone, it’s one of the more powerful steroids we have in the armamentarium. So it’s very hard to know what a low dose means relative to body weight and age. And it’s very hard to understand in the disease progression where the drug would have benefit versus risk. And I think that’s the part that hasn’t been well thought through yet, or it’s not possible to completely understand yet. Dexamethasone is a powerful immunosuppressing drug. And it’s not just about benefit, which has been talked about the most. The question that still remains is the risk-to-benefit ratio. And until we understand a lot more about the risk benefit ratio, it’s going to be hard to make a broad recommendation for this.

There’ve been lots of studies of steroids for pulmonary inflammation in the last 30 years, many of which I knew quite well. And, you know, what ends up happening is it seems like one year steroids are the answer for this problem and two years later they’re not, because of secondary infections, immunosuppression, fungal infections, or sepsis, as a complication. And without seeing all the primary data and understanding more about this, it’s very hard to know the risk-benefit ratio.

So, yes, I’m a fan of good news and I’m an optimistic person, but I think the school is still out on this.

KRIS:  Back to Northwell… you said that you got through it pretty well. Were you prepared? How did you manage?

TRACEY: So were we prepared? We were prepared, probably better than most. Going back 20 years or so we had experiences with Hurricane Sandy, which disrupted healthcare significantly in the Greater New York area. We also stood up an infectious disease and an emergency operation center response during the Ebola epidemic, because there was a real possibility that, you know, as the cases… a couple of cases flew into the United States, I believe through Miami, if I remember correctly, that cases could have come into New York. And so we put a lot of thought into that.

And I also participated in an evaluation of the response to the SARS-1, to the first epidemic that primarily affected North America, primarily Toronto. And we had been involved in making recommendations to the federal government to stockpile PPE, stockpile ventilators, stockpile, antibiotics. And so, we had some experience in thinking about preparation that went back for a long time.

The… Northwell is very uniquely arranged because… organized, because it’s a single management structure for all 23 hospitals and all 70,000 employees. And so when you stand up an emergency operation center with the leaders of medicine, nursing, operations, the GPO, the General Purchasing Organization that purchases billions of dollars of equipment every year, HR and planning, which can bring in nurses and doctors from all over the United States, which we did do… we started these conversations very, very early. We started them in January.

But I wouldn’t say… because your question was very specific. We were as ready as we could be, but no one, I don’t think, knew when we went from a few dozen cases in our hospitals to thousands, nobody knew when it was going to stop. And so it was an around the clock operation led by brilliant colleagues, who had, you know, sort of all trained and prepared for this for many years. And so like going to war, you train together and you get to know each other, and you know who you can rely on, but then you’re in it, and it’s very hard to… it’s a very hard… it was very… it’s very hard to describe what it felt like to be in the response. I did not treat patients myself. I focused on standing up a clinical trials unit. But, you know, my colleagues who were in the ICU every day, and, you know, been celebrated as heroes, I have to agree, I have to agree… you know, they’re my heroes, too. And the patients… because of all this, the patients… our patients did pretty well.

KRIS:  Northwell has, because of its size, it has an integrated medical health record. What was Northwell able to discover based on having all that data that’s connected and available?

TRACEY: Yeah, it’s an incredibly valuable data cohort at this point for several reasons. First, as you say, it’s all connected. Everything about Northwell is very connected. Second, we think it’s probably the largest, well-collated electronic data for any COVID cohort in the world because of the numbers. We treated 20% of all the cases in New York.

And so we’re still going through it. We’ve reported… as you know, and as many listeners probably know, we have reported out on several of our findings. We showed, clearly, the risk of hypertension, morbid obesity, and diabetes, the risk of age, and we showed the dangers of this disease in a separate study to the kidneys and how important acute kidney injury is to the pathogenesis of this disease. And we published several… my colleagues have published several manuscripts looking at the role of thrombosis and the importance of anticoagulation. And so we’re still going through the data. We are in a very unique position now to be able to follow these people because there’s some big questions still out there about what it means to have survived COVID and what are the long-term sequelae, if any. So it’s an important asset and a very active work in progress, as we speak.

KRIS:  Some folks don’t come out of this in great shape, or it takes a long time. What sort of things will you be asking? What will you be looking for going forward?

TRACEY: So I know what I would ask. I’m not personally doing those studies. You know, I’ve spent much of the last 30 years thinking about, directly or indirectly, the problem of sepsis. And what we know from sepsis survivors, severe sepsis survivors, those that sort of have a bad case of sepsis, spend some time in the ICU, but survive, we know that the mortality of sepsis survival is 50% at five years. It’s a huge mortality risk to having survived sepsis, which, of course worsens with age.

And so what we’re looking at now are patients who have had COVID-induced severe sepsis syndrome. Because sepsis is a syndrome, it doesn’t mean bacterial infection. And we have a lot of these people now introduced to the population for either chronic care, chronic respiratory care, or in some cases, back at work, back at home. But, you know, ‘I can’t run my five miles at the same speed I used to run,’ or ‘I noticed that my heart races when I do two flights of stairs and it never did that before.’ So those are the kinds of questions.

It also is going to be interesting and important to understand the long-term sequelae on the immune system. There’s a tremendous amount of questions on what does immunity to this disease mean? And does it develop in all patients who have had the disease, or some? Is it a B-cell antibody-based immunity, or a T-cell… primarily a T-cell protection that may be important? We don’t understand that yet. And we don’t understand all the sequelae in the nervous system. So the virus can attack nerves. It’s probably… although we don’t know for sure, it’s probably one of the reasons so many patients lose their sense of taste and smell. Some patients complain of feeling foggy afterwards for some days, weeks, or months. And the question is what is the long-term sequela of that? So these are all big unknowns.

I think people are used to having answers quickly and on their phone, and they’re not used to hearing experts say ‘I don’t know.’ But most of the experts still don’t know, including me, about what are the answers to these and some other important questions. It’s frustrating to many to realize that we’re confronting this together as an unknown. We will figure this out. There will be treatments that will be effective. There will be vaccines someday. There will be answers to these questions to mitigate risk and to improve long-term outcomes. But as of right now, we’re only a few months into it and we’re still figuring it out.

KRIS:  So back to the medical record and all the risk factors that your organization was able to develop, were you surprised by how impactful this virus is on the body?

TRACEY: I was surprised at the speed with which it causes severe ventilatory dependence, severe illness requiring intensive care in what seems to be a significant part of the population that had never seen the virus before. So it’s as if it comes in and very quickly identifies... it’s as if the virus was going around identifying a cohort of susceptible patients and they all got sick at the same time. That was really surprising to me.

It’s not surprising to me that it affects so many organs. As I said, technically, COVID-19 is a form of severe sepsis, and that’s exactly what severe sepsis does. It affects the brain, the heart, the lungs, the kidneys, the liver. So I wasn’t particularly surprised by the progression of the multiple organ damage. I wasn’t particularly surprised by the severity of the organ damage because of the severity of the cytokine responses, which were… you know, which were known before in China. No, I was just surprised at the speed at which it comes in.

And then I was surprised… I remain surprised at the speed at which it falls, at which the infection rate seems to have fallen. I don’t think we understand yet what reopening means. Will there be just a chronic steady state of infection that percolates through the population or will there be a second wave? No one knows. It’s interesting, now, as things start to reopen, we’re not seeing massive surges yet in the states that have reopened. You’re seeing increased infection rates, but you’re not seeing that overwhelming onslaught into the hospitals and medical centers that we saw in New York in those early days. So that was the biggest surprise, how quickly it came on and then how quickly it tailed off.

KRIS:  Got it.

TRACEY: That said… I’m sorry, Kris. That said, we still now have hundreds of patients on ventilators in our hospitals, and they… some of them look to be there for a long time.

KRIS:  Northwell and with your help pivoted to doing clinical trials. The first one, you did something with Gilead sciences on the drug Remdesivir`. What was that about?

TRACEY: With Gilead, we looked at their antiviral drug, Remdesivir. And the question there was does administering this nucleotide-based drug intravenously to patients who are in the hospital, does it shorten the hospital stay or improve mortality? Now, just to put a really important data point around this, which some people don’t think about very often, I said ‘admitted to the hospital.’ We were admitting people to the hospital who were very sick, whose PO2s, or oxygen levels in the blood were less than 90%. Now, three months ago, if you showed up in the hospital and had a PO2 of 92, 93, 94, you would have been admitted to the hospital. So the bar for being admitted had been raised significantly. You had to be really sick just to get admitted. So many, many thousands of patients were treated… not just in New York, but around the world, were treated with low oxygen levels at home because they weren’t, quote/unquote, sick enough to be admitted.

In those patients receiving Remdesivir, Gilead recently reported that there was benefit in shortening hospital stay, but they had not… the last data I’ve seen, anyways, they had not achieved statistical significance on 30-day, all-cause mortality. But that drug is now recommended by most in the treatment paradigm for COVID. The big question is if we, or anyone, could give the drug earlier to people who were less sick, would it be even more beneficial?

KRIS:  It seems like we need to get drugs to people earlier in the course of the disease, right?

TRACEY: I agree. There’s been a lot written about that, and, you know, it’s one thing to recognize it’s the right thing to do, it’s another thing to say we should do it, and it’s a third thing to live in the real world and try to actually do it. It’s really, really, really difficult. You know, we put together an army of almost 200 people to enroll 1,500 patients into six or seven clinical trials in eight weeks. I mean, those kinds of numbers are mind-boggling. You know, a typical clinical trial you’ll enroll 10, maybe 20 patients in a year, and we enrolled… we enrolled 10% of our COVID patients into clinical trials in eight weeks. And… but it re… […skip in recording…] runners, laboratory staff, data-cleaning people and back office folks, regulatory folks, reporting folks.

And so when you think of the logistics of doing this and COVID, you have to start thinking about what does it look like to get a consent when you’re wearing PPE? How many times do you have to go in and out of the house? Who do you have to report your presence in the house to, what authorities, and who’s tracking you and who’s tracking the patient? What… you know, back to your point, how sick is this person and how sick… where are they in the time course of the disease? Day one or day 14? These… the logistics of this are absolutely… are absolutely unprecedented. You know, it’s Ebola with a much lower mortality, but it evokes the same sort of fear response in some people and logistical difficulties for others trying to do this.

KRIS:  Northwell was also involved, and you were involved with a clinical trial with Regeneron and Sanofi. What happened there?

TRACEY: So the Regeneron trial was a… it is a drug that inhibits the signaling of IL-6, which is one of the cytokines that was thought to be important in the COVID damage to the lung, or the cytokine storm. And I remember on Friday, March 13th, a date I’ll never forget myself, I began speaking to David Weinreich, the Chief Medical Officer at Regeneron, and said, ‘David, we have dozens of patients and we’re soon going to have hundreds and hundreds. And I wonder if it would be possible for you to tell me before we start this trial that you’ll give me as much drug as I need?’ And he said, ‘I will.’ And so it was sort of a verbal handshake on the phone, if you will, and within five days we had launched that trial.

We enrolled with Regeneron 225 or 226 subjects in the matter of weeks. That was by far the largest enrollment from any center in that trial. And we had some of our physicians quite convinced it was working, that it was a beneficial effect in many patients. But when the code was broken, it turned out that there was not a significant benefit in the patients who had not been on a ventilator yet. And the question was still unknown, and I believe still is unknown, of whether there might be benefit of using this agent in people who are already on a ventilator.

So, you know, the teaching point here for many of us was people, even very objective, critical scientists, work really hard in these life and death situations where the patients are dying, the family is distraught, the physicians and nurses are often distraught, and you see things that you form a pattern in your mind that you want to be true. And many folks have become convinced that steroids, like dexamethasone, is working, or IL-6 is working, or Remdesivir is working, and, arguably, in many cases, we still don’t really know.

KRIS:  Northwell got some press for doing a clinical trial involving the main ingredient in Pepcid, the antacid drug. Where’s that sit?

TRACEY: So that study that we’re looking at… we’re analyzing the data for that study now. And the drug is called famotidine, which is the generic version of Pepcid. And it turns out that a colleague of mine, actually one of the physicians who was on this committee of three that wrote this report in 2003 for the White House on preparedness for epidemics… that physician was Michael Callahan, an infectious disease physician at Mass General. And he called me the week of March 17th and said, ‘Kevin, I was in China. I was in Wuhan, deployed by the Department of Health and Human Services to work with the Chinese physicians on the response to COVID. And we observed in a large cohort of Chinese patients that the patients taking famotidine had significantly improved outcomes.’ We don’t know why, but there were… by this time now, March, there had been done back in the United States some in silico modeling of viral proteases and computer in silico structure… function analysis of these proteases with famotidine suggested possibilities that famotidine could be a viral protease inhibitor. Famotidine, it turns out, is one of the safest drugs in the pharmacopeia. It has few, few drug interactions. The LD50 is on the order of 300 milligrams per kilogram, or something. It’s widely used and safe. The side effects are minimal.

And so Michael asked if I would be interested in doing a clinical trial considering the use of famotidine in these hospitalized patients. And we said we would be very interested because, remember, there was no drugs, there still are, arguably, there were no drugs for this disease, and this is one that many people were taking anyway. So that started a pretty big trial for us that we’ve since enrolled about 230 patients. And as of today, we’re still looking at the data, fingers crossed.

KRIS:  We talked earlier about your hopes to use the convalescent plasma from folks who have survived COVID-19 as a possible treatment. That ran into a snag. I think it’s probably a good example of how difficult this can be. Can you talk about that experience?

TRACEY: Sure. Yes, there’s lots of snags and lots of learning points for the future, hopefully, for the world, actually.

So in the case of convalescent plasma, we had been exploring sort of quietly the feasibility of doing this and the scientific validity of doing it. And we concluded early on that there wasn’t good data for the risk-benefit analysis to commit major precious resources to that as a prioritized clinical trial in our early response. We had set up this COVID Clinical Trials Unit, that’s what we called it, with this army of 200 people, and we were prioritizing clinical trials by their scientific rigor and feasibility. And what happened was, we started getting phone calls from patient’s family members, and it seemed as if sort of the more connected the patient was to whoever, the more phone calls we got. And so it became very political. And the typical phone call was, ‘I just saw on TV that this is going to save my grandfather, you know, who has Stage 4 lung cancer, and is 86-year-old, and has been on a ventilator for two weeks. You have to give them convalescent plasma.’

These kinds of requests became something that could not be ignored. You’ve got people who are sick and dying, you have family and medical staff who are desperate to try something. And so we contacted the National Coalition through Johns Hopkins and Mayo Clinic, and registered with that group to begin collecting plasma for what we hoped would be, and intended to be, randomized clinical trials comparing the effect of convalescent plasma as a therapy versus plasma that had been collected pre-COVID, meaning control plasma. By the time we got the paperwork approved and were ready to start processing plasma for treating our patients, which was only a few days, a week, maybe, the FDA had pulled the ability from Hopkins to offer a randomization. So, essentially, we were now… we had now just jumped into a massive anecdotal trial with no controls, other than historical, which are very imperfect in a disease for which the therapy is changing daily or weekly.

We have since enrolled 500 patients in the convalescent plasma study, which is a huge number, potentially the largest cohort in the world, and we are analyzing that data against historical controls. All I can say is I hope it worked. You know, I’m concerned that it may not have worked in a statistically significant way for the whole population. And I’m concerned that it may have worked in some sub-group of patients that without controls we’ll never be able to figure out.

So, yeah, it was… many, many, many, many aspects of this response were very, very politicized.

KRIS:  What was your experience with hydroxychloroquine at Northwell?

TRACEY: It wasn’t good. We had designed the trial using famotidine to be a randomized double blind placebo-controlled study. And, literally, a few days before we were ready to start infusing the first… and we had to essentially buy all of the intravenous famotidine that was available, had not been already put in hospitals, to have enough drug to complete the study, and… because we knew once that it was announced that there would be a run on famotidine just like there had been a run Remdesivir and just like there had been a run on hydroxychloroquine when the president started talking about it. Once the president started talking about hydroxychloroquine, this was… people forget how fast this all happened and how scared people were. But, again, like with convalescent plasma, patients and their families were demanding hydroxychloroquine because the president said so. Now, in some cases you could have the doctor-patient relationship and you could sit down and say, ‘The risk-benefit ratio is not proved, and, yes, the president said that but we still don’t know.’ And in some cases, you know, the doctors would say, ‘No, I’m not giving hydroxychloroquine for the following reasons.’ But in the absence of any drug with proven approval or effectiveness or benefit, zero drugs and people dying, you know, eventually, hydroxychloroquine in many, many centers was adopted as one of the standards of care right before we started the famotidine trial.

So we literally had to include hydroxychloroquine as one of the standards of care, like oxygen and intravenous fluids, in the famotidine trial. And so now we’re actually not sitting on a double blind randomized trial, a placebo versus famotidine. We’re sitting on the data of a hydroxychloroquine plus or minus famotidine study.

While all this was going on, Columbia Presbyterian, our colleagues there, led by Tim Wang, and others, looked at their data, 1,600 patients or so, if I have the number right, and found that the patients on famotidine had a significantly improved outcome from ventilator requirements and death, like few less than .02. So that was very encouraging.  And we, then, did an outpatient study, uncontrolled, and published that recently, and got… looking at 10 patients who seemed to have a biological response to famotidine.

So hydroxychloroquine, clearly… the politicization of hydroxychloroquine clearly complicated our ability to get a scientifically rigorous answer in a timely way. We now have to go back and start a new famotidine trial on the outpatient side.

KRIS:  When you talk about all this complexity and the snags, do you have any sense of a timeline probability for vaccines and other treatments? In the atmosphere you describe, what’s your sense of how this is all going to play out?

TRACEY: I think we have to bet on both at this point and do the work in both. Both meaning… well threefold. I think we need to do work on direct antiviral agents like Remdesivir. I think we have to do work on drugs like famotidine that are broadly available, cheap, and safe that may work targeting the virus, probably not, may work by doing something to the immune system, which seems more likely at this point, although we certainly don’t know, I don’t know. But I think we can’t… we can’t not work on improving… and we need to do more work on dexamethasone. We can’t bet the farm on the vaccines at that point because... I said, you know, we’re not seeing yet massive surging waves that could come in the fall, and we better have a better handle on what drugs help these people who really need them or we’re going to be in trouble.

I hope the vaccine comes as fast as some people have advocated for or promised, but, you know, I’m concerned. We don’t have vaccines for the common cold, which is a similar viral family member. We don’t have a vaccine for HIV. And with HIV, you know, we spent decades and billions of dollars by some of the best companies in the world and some of the best scientists in the world and we don’t have a vaccine for HIV. I’m not equating COVID with HIV. There are clearly some as yet unexplained features of the immune response to this virus that seem to be somewhat immunosuppressive. You’re not seeing robust antibody responses. What does that mean? It’s not clear how long immunity lasts to this virus. And you can say, ‘Well, it’s a virus like any other virus and we’ll have a vaccine.’ But, to me, that’s sort of like saying HIV is a virus like any other virus and we don’t have a vaccine.

I think we need to stay very cognizant of the fact that we need a vaccine, absolutely. That has to happen as a population response. But we also have to keep studying drugs and molecules, particularly ones that are available and safe, to see if we can come up with combinations of drugs to help people who are really, really sick before there’s a vaccine.

KRIS:  What’s your sense on where we are with antibody testing?

TRACEY: I think we’re doing it. My take is it’s happening, and it’s happening with lots of different tests against lots of different antigens, based on lots of different definitions of a positive test or a negative test. And we’re learning. My take on it is that we’re learning. We don’t know what the best test is, we don’t know what an IgM versus an IgE versus an IgG response really means. We don’t know why some people don’t seem to have a good antibody response. We don’t understand the role of T-cell immunity. You know, there’s been some recent work published in Cell that people who didn’t even know they had been infected seemed to have a very specific T-cell repertoire, or memory against very specifically the current COVID virus. So there’s more questions than answers about this.

We’re almost done testing virtually all of our employees, and approximately 15% of them seem to have some sort of positive antibody assays. We had 20 deaths of our 70,000 employees from COVID, and so we’re taking very, very seriously the testing to understand what it means. We’re now tracking all of our employees in and out of every building to maintain the safety of our buildings for our patients, but also for our workforce, itself.

And, you know, you ask about the testing. I don’t think you can really think about what the testing means, unless you put it into the context of the army of people that you need in every town or every city to follow up on the results of the tests. And so, you know, you look at a place like China, and they have the army, ‘Just go take care of it. Follow everybody, find out who they talk to, talk to all of those people, write it all down and make a map.’  You know, the United States, sadly, with absence of leadership from Washington in this response, we weren’t ready for this. Some states were more ready than others. I saw a report earlier today that a handful of states have sufficient staff to do the effective contact tracing, a handful of states. Three-quarters of the states don’t have anywhere near enough people in place to follow up on the results of these tests. So I think there’s a rush to criticize, ‘We didn’t have this test and we didn’t have that test.’ We were missing a lot more than a few tests. We didn’t have the whole infrastructure in place on the public health side to deal with the results of the tests that we didn’t have.

KRIS:  I know that you were part of a group in 2003 that made recommendations. Talk about that. And what happened with that?

TRACEY: So after the SARS epidemic, the first one that came into United States from China, actually. from Wuhan, again, I believe, and really hit hardest in Toronto… it killed about 800 people worldwide. And Mike Callahan, actually, the physician I mentioned before, who called me about the famotidine idea, Mike invited me down to Washington with Dr. Mitch Fink, God rest his soul, and another physician from the White House, and we studied models of a virus that would be about 10 times more lethal than the current virus. And looking at transmission similar to the virus that we have now, the estimates were that it would kill between 20 and 50 million Americans in six months, not 200,000, 20 to 50 million. At which point, hospitals would be overrun, doctors and nurses would be dead, and the best kind of preparation response at that point is to have stockpiled millions of ventilators, millions of PPEs, millions of intravenous setups, and millions of doses of antibiotics. I mean, that’s exactly what we recommended in our report to the White House. And that report has been around for 20 years or 17 years.

Some of the stockpile was created, based… I don’t know… I’m sure we weren’t the only one to think that up in a two-day meeting. I know groups in Minnesota and elsewhere have made… and the Gates have made recommendations like that to the government over the years. But the point is it was concrete recommendations which were not followed through on. And, you know, we went so far as to recommend the kind of ventilators that should be stockpiled, the kind of that the Green Berets or Navy seals carry, which are like jetpack ventilators. And we recommended deploying them into schools and/or fire stations in towns, because if the hospitals shut down or became tense in parking lots, there might be a few medically-savvy people in the towns who could access the stockpiles and use it to treat, you know, their neighbors and their...

So there was a stockpile. It did have a lot of stuff in it. Apparently the stockpile was depleted. There was just a failure of leadership from Washington in this response, and it was really unfortunate.

KRIS: Given the lack of leadership, and given where we are now, is it really up to the states? Do we need to start thinking about and preparing for surges?

TRACEY: Well, I think, fortunately, we didn’t have leadership from Washington, but we did have it from the Governor of New York, we did have it from Tony Fauci, we did have it from a few other governors, Ohio comes to mind. And these… you know, because of the… you know, I’m proud to say, we hosted Governor Cuomo, several of his press releases from my labs at the Feinstein Institutes, and from our core laboratories where we did a lot of the COVID testing. And governor Cuomo’s leadership was critical to the New York response. It took responsibility for the hard decisions. His leadership took responsibility for the hard decisions, and his leadership clearly explain what was going on to a lot of people around the world, as it turned out. And he clearly explained how decisions were being made, including now, as we begin reopening, he’s explaining how and why we’re reopening. And you reopen when these hospitalization numbers do this, and when the new infection numbers do that, and when the number of contact tracing folks are in place, we do that. And so leadership did come, you know, in our case, fortunately, from the governor, and that was incredibly helpful.

But it also came… it also comes from places like my boss, Michael Dowling, who runs Northwell Health. You know, over the years, it’s been very easy for many people to cast stones at these large healthcare systems that are so inefficient and are robbing us blind, and, you know, we need a centralized… we need a centralized government healthcare system. Well, thank goodness, we didn’t have Washington’s healthcare system to rely on for the last two months. And thank goodness, my boss, Michael Dowling, had set up a healthcare system that because we’re so large and because we’re so efficient, we could marshal a response to save lives that would fill in for where the government, frankly, wasn’t prepared. Andrew Cuomo’s leadership was terrific, but New York State was barely prepared for this. Northwell was prepared, and we shared, and we opened the Javits Center, and we made recommendations and guidance to the SS Hope when it pulled into town.

So, you know, the good news is there are leaders out there and they’re ready to lead us. You’re asking me to direct you to them to what to do next, that’s above my pay grade.

KRIS:  When we talked about developing treatments and vaccines, what needs to happen with drug manufacturing?

TRACEY: Well, one of our recommendations 17 years ago, was to set up manufacturing plants for… oxygen, would be a good start, and antibiotics would be a good start in the United States, so that we’re not relying... I mean, the US Army doesn’t have its bullets manufactured in Russia or China, and there’s a reason for that. And the famotidine, again, was a good example. We’re pretty sure… it was really a bad timing, of course, in many ways, but Zantac had just been pulled from the market over manufacturing safety concerns, like in the weeks right before we announced the potential of famotidine to be effective, which created a massive run on famotidine. So you couldn’t find famotidine in many drug stores for weeks. Pepcid, generic famotidine, famotidine on Amazon was sold out. And so, I also think some of that is because most of the generic famotidine is made overseas in China and India, and it’s shipped in huge bulk supply. Big, you know, oil drum-size shipments come from overseas of these trucks, and then they’re reprocessed for USP or UPS, whatever it is, USP standards for manufacture and FDA clients in the US. The FDA approval is actually on the final processing step in the US. We need to move more of that manufacturing back to the US, because had the epidemic shutdown Asia worse than it did, or killed more people in Asia than it did, we’re at risk of running out a lot of drugs, if not all of them. So those questions have been called to the front.

I mean, my fear is that we’ve asked all these questions, and everybody wants to do something right now. And my fear is that people forget, you know, and the vaccine comes out, or the disease goes away, like SARS one did, no one knows where that went, and then all of a sudden, it’s back to everyone worrying about their 401(k) and their 403(b), and we got to get the stock market back, and then, ‘Let’s not invest in research now, we’ll do it next year.’

So my fear is we know what to do now, what has to be done, and it requires significant long-term investment in research infrastructure, and, also, in your case, with this question, pharmaceutical manufacturing.

KRIS:  That’s the scariest thing for you, right, that we’re just not going to make the investment where it needs to be, and we need  more people in science, right?

TRACEY: Yeah, in… yes. In my role as Institute Director for Research at the Feinstein Institute and the Executive Vice President for Northwell Health, I have a fiduciary responsibility to look at what you just said. And when I look, I find that investments by the US government into research have not kept pace with inflation for 17 years. And that, to me, is a national crisis. China, Israel, Germany, Sweden, the UK, pretty much everybody is eating our lunch and investing more money in research than we are. And if we don’t turn that around as a result of this epidemic, then shame on us. The idea that you can mobilize billions of dollars in a couple of weeks… which, arguably, the federal government has done, and good for them to do that… to solve a problem, that’s fine. That’s a fine first step. But if you haven’t built-out the infrastructure, and maintained it, and trained the young scientists, the young students, and post docs, and junior faculty to pursue a career in this, and work on the same problem for 20 years, so that they’re ready to solve the next epidemic when it comes. And it will come. And if we don’t make those investments now in a sustained way, then shame on all of us.

And it is all of us, we have to all take responsibility to this. You know, Sputnik, you know, flew over America a few months before I was born, and it terrified people. And that fear was translated into so many things that created people like me, and my generation. It created NASA, obviously, it created DARPA, it indirectly created NIH. And this idea of people coming together to do the right thing, investing heavily for the long-term, in a funny way, it had its birth in Sputnik. And I hope if this is our Sputnik moment, that we don’t blow it.

KRIS: When you talked about planning, you gave an example about New Orleans and the Netherlands.

TRACEY: So those are two cities… well, one city, one country, I guess, underwater relative to sea level. And, you know, New Orleans called in the Army Corps of Engineers, and they made plans for a 100-year flood, and what kind of dam or dike or levee would you have to build for a 100-year flood. But then, for whatever reason—political corruption, graft, errors in judgment—they essentially built a levee for a 50-year flood. And, of course, with global warming, we’re now having 100-year floods every 10 or 20 years. So, obviously, New Orleans, has… those dams have been breached several times. In Holland, faced with a similar situation, they made plans for a 100-year flood and built a dike for a 1,000-year flood.

And, you know, that’s kind of what we’re facing now in our response. We should be… this will happen again. And if you want to imagine the scenarios that we looked at 17 years ago, this virus wasn’t very lethal. This virus is killing a small cohort of people at risk. It’s very unusual for this virus to kill someone without one of the major risk factors that have been very carefully studied. Clearly, it does. Clearly, there are some cases of very healthy people, with… who are young, with no risk factor, who get this and die, and it’s horrible.  But that’s not the major problem here. If you imagine a virus 10 times more lethal that comes on as quickly as this one, we are not prepared to that, and that would be the 100-year flood, not the 1,000-year flood.

KRIS:  You’re talking about pandemics in terms of national security, right?

TRACEY: Absolutely. What else is it?

KRIS:  Given the current situation, what do you find most heartening? 

TRACEY: Yeah, I think in a situation like this you always want to have a message of hope and a call to action. We just did the call to action first. The call to action is everybody has to get out and make sure that their congressmen, their senators, their representatives, that their kids, and their parents, and their friends and family know that if we don’t invest now in research we’re making a huge mistake. That’s the call to action.  Spend money on research.

The message of hope is research eliminates diseases. We beat viruses all the time. HIV, no, we don’t have a vaccine, but we… but it’s, by and large, medically controlled with pretty safe, cheap, widely available drugs.  Polio is gone. Polio… my grandfather worked on polio when he was a young doctor as a Yale. He worked on the polio vaccine.  I mean, it’s gone. You know, small pox is gone. Diphtheria and many other serious illnesses that my grandfather couldn’t treat and have kids die in his arms when he was a pediatrician, those diseases are gone. Science will beat this disease. We’ll beat it first with… probably with drugs that treat the people who are really sick and get them home to their families, and, second, we’ll beat it with a vaccine.

I’m very optimistic we’re going to win this war. I’m, actually, very hopeful that this is a solvable problem, as long as we pursue the call to action.

KRIS:  Thank you.