Long Covid Roundtable

Robert F. Kennedy (00:00):

… of senators. Senator Young and Senator Marshall who's here, who have a deep interest and have been talking a lot about this issue. But also in response to my own personal experience and the calls that I get almost every day from people who are suffering from long COVID across the country and don't know where to go and feel that their voices aren't being listened to, including members of my own family. We wanted to do something different in response to this pandemic. In the past, the response to epidemics of this kind has been to pump a lot of money into ivory tower science to try to solve the problem. We've already bought $1.5 billion into NIH to solve long COVID, and we've got literally nothing from it. And one of the mistakes that we've made in the past is to not talk to the doctors who are actually treating the disease.

(01:07)
During the HIV epidemic, there was a policy in the federal government to simply stop talking to those doctors and to discredit them. There was extraordinary science going on and particularly with the gay doctors in New York, San Francisco and Los Angeles who were finding great success in treating their patients. And those doctors were shut down in the process, but also there was a initiative by the federal public health agencies to shut them down and to deny access to the repurposed drugs that they were using to treat patients very successfully.

(01:56)
There was a movie called Dallas Buyers Club that was made about this, and my uncle said, Senator Ted Kennedy actually became an advocate for those patients and ultimately made an agreement with Dr. Fauci who was shutting those doctors down to fast-track the treatment testing, clinical testing of the repurposed treatments, off-label treatments that they were having so much success with, and to allow patients to get access drugs that they and their physicians believed were going to be helpful and not having to import them from Mexico or Europe or Canada.

(02:41)
The same thing happened during the COVID pandemic where repurposed drugs that were being used by physicians across the world and being used very, very successfully were not only not investigated, but they were shut down and people's access to them was denied. And we want to make sure that that mistake never happens again during our disease crises, during contagion crises, and that we start listening to doctors who are on the front line and the doctors who are treating patients successfully all over the world. There's approximately 15 million front line physicians in the world and many of them are imaginative, they're great healers, and they find solutions that the ivory tower often doesn't see. And so we want to first of all open up a dialogue with those physicians and then give us some mechanisms for assessing the efficacy of their treatments and doing the other things that we need to do, for example, to identify biomarkers, to identify and characterize symptomology.

(04:02)
Right now, CDC lists about 300 symptoms to along COVID. And people, virtually everybody falls into one of those categories. And we want to do everything that we can to narrow that constellation of symptoms and then to be able to assess these unconventional treatments and protocols that people are using and find out from the patients themselves, from the physicians themselves, which ones are working. So this is partially a listening session, but it's a lot more than that. It's a session in which we are seeking to find alternatives. We're seeking to find solutions. Where we want to, for example, start a website and it helps Americans locate doctors who are successfully treating these diseases and gives us a way to assess the success and the efficacy of those treatments.

(05:04)
And we don't know exactly what that's going to look like. And one of the reasons we wanted to meet with these people, this esteemed panel today, is to get their ideas about how to construct a website that will really be useful to patients and physicians around the country. And that will give the public health establishment an ability to evaluate the success of various protocols. So I want to welcome all of you today, and let's begin by introducing ourselves. Maybe Dr. Redfield you would start, we'll go around clockwise.

Robert Redfield (05:46):

I'm the former CDC director. I'm an infectious disease physician by training, and I'm currently involved in clinical practice largely for long COVID and mRNA vaccine injury.

Holly Olson (06:02):

My name is Holly Olson. I am a long COVID survivor and my kids and I all have long COVID. I'm from Utah. I'm also a registered nurse with a bachelor's in science and have done a lot of research on this. I've had my journey of the long COVID affecting my connective tissue and all of my body where I could not even walk or move. Have utilized lots of different treatments and have found that stem cells and have helped quite a bit, ethical sources of stem cells. So I wrote a stem cell bill for Utah, which allows treatments to be done in Utah and have passed another one in Florida and I'm working in other states. I've also have found that monoclonals have been a huge helping factor in calming the immune system down along with peptides that have been very also very helpful and hyperbaric oxygen therapy has helped me and my kids and several of my long COVID friends. We are just grateful to be able to discuss this and to get some ideas to get people better and I appreciate this time.

Devin Russell (07:13):

Well, Mr. Secretary, thank you for having me. It's an honor to be here with you all. My name is Devin Russell. I'm-founder of the Long COVID Foundation. Thank you for affording me the liberty to wear my mask. I think once I explain my history here, you might understand why I would wear one. First, I want to hand out a one pager on… Thank you… on some of the long COVID community needs. I had long COVID starting in March of 2020. I've had it for five and a half years now. I did not take the COVID vaccine. I alone have had 170 plus symptoms, some very severe Guillain-Barre, blood clotting, heart issues, brain dysfunction, and even delirium at a time because my brain was so inflamed, which it still is inflamed but not to that level, but it's still a problem for me. I was near death at times and that's not a hyperbole, I thought I was going to die.

(08:25)
Prior to that. I had chronic Lyme for 11 years, which I recovered from, and I managed a chronic illness center clinic for four years. So based on that experience, I can tell you long COVID is a unique kind of hell. This is an urgent crisis that needs action now as I'm sure you know. People are suffering and even dying, and a lot are holding on by a thread. So some of the things we need of which there are many, but well-run common-sense trials, biomarkers and tests and development of antivirals and other drugs because we have no tests, no biomarkers and no treatments right now approved. So I look forward to discussing this in more detail today and thank you.

Robert F. Kennedy (09:11):

Thank you.

Darcie Johnston (09:12):

Good afternoon. I'm Darcie Johnston, the principal deputy director of the Intergovernmental and External Affairs Office in the Office of the Secretary.

Ken Callahan (09:21):

Hi, Ken Callahan, head of policy for the secretary. Just want to thank everyone for coming, and this is something the secretary has been very adamant and focused on making sure we brought together a roundtable of physicians and patients and other advocacy groups to make sure he could hear directly from them. This is something also he has stressed he wanted to make sure was live-streamed, so it was open to the public, part of his campaign to make sure there's radical transparency. And then also just wanted to address the invisible illness, which there are many in the US, and secretary and the team here is committed to making sure that we get a voice for everyone who is suffering from them. Thank you everyone for coming.

Jim O'Neil (10:04):

I'm Jim O'Neill. I'm the deputy secretary of HHS and acting director of CDC. So here in this room you have the heads of four of our science divisions and one of our data divisions. We're all eager to learn more about long COVID and do excellent research and come up with solutions for everyone. So I'd say long COVID is in the same clinical category as Lyme and Epstein-Barr and chronic fatigue syndrome, which is no consensus yet on biomarkers, no consensus yet on diagnosis, no consensus yet on causes or treatment, but definitely an important urgent challenge that we need to discover everything we can about it.

Robert F. Kennedy (10:53):

I also want to mention, and we're going to do a very similar roundtable, I think next month on Lyme disease, which has a lot of interactions and similarities.

Roger Marshall (11:06):

Right. Thank you Mr. Secretary, Roger Marshall from the great state of Kansas. I'm here today representing and speaking for, fighting for the 20 million Americans with long COVID. And it is personal just like your stories, Mr. Secretary and that I've had a loved one with long COVID for three years. And I want to take a moment to acknowledge some of the people in the room. It's different being the doctor on the other side rather than trying to help somebody out. It's been very humbling, but I'm so grateful for them. We've reached out to hundreds of doctors and tried to figure out who could help my son and acknowledge Dr. Jordan Vaughn here who's kind of the pioneer of vasculitis, something as an OB-GYN, we talked about pelvic congestion syndrome and cardiac output return. So great to see Dr. Vaughn here. And out in the audience in the next panel is Dr. Bruce Patterson who has a diagnostic tool.

(11:58)
He absolutely has one. I believe it's the right one. And thanks to Dr. Bhattacharya who's going to let him continue to prove that that's the right one. The secretary talks about confirming other people's studies and that's exactly what we're going to do. And the great thing, it helps delineate the difference between reactivation of Lyme's disease versus long COVID. So you're right, outside of the ivory towers, there are people that are out there at warp speed time trying to solve the problem. And of course, my mentor here, Dr. Redfield, has also helped my loved one in kind of quarterbacking all the different approaches out there and just kind of keep the keeper of all knowledge and just always brings a word of hope to all of us. So I'm honored to be here and we're we're going to whip this thing Mr. Secretary, we're going to get to the bottom of it. Thank you.

Marty Makary (12:52):

Great. Thank you Senator. Great to be here. And my name is Marty Makary. I'm the FDA commissioner. Mr. Secretary thank you for making this a priority. We have been talking about so many competing important areas in healthcare where we desperately need to push the field towards a cure. And this was a massive priority for this secretary, so that's why we're here today. Thank you. Long COVID is real. It's been underestimated and overestimated. We are here today to try to help those who are suffering from long COVID. We've spent $1.5 billion with essentially nothing to show for those dollars that were allocated. A lot of hospitals got rich with more MRIs and CAT scan revenue, but in the end, the people suffering with the condition are still struggling. We do know that we have some data points. The presence of long COVID appears to be proportional to the duration of COVID illness and the severity of COVID illness.

(14:03)
Thank God both of those have decreased significantly over time. And so we don't see as many new cases today as we did in the past. But people who developed their long COVID symptoms in the past still deserve answers. They've become forgotten to many people. We do know COVID illness is an antibody mediated phenomena, and antibodies can do a lot of things in the body that are not always anticipated or recognized early on. And we know that COVID illness creates general body inflammation. Guess what? Most illnesses in the entire field of medical science are due to generalized body inflammation, insulin resistance, and metabolic dysfunction. And so we are seeing some of the same common principles that could apply to other illnesses if we can crack this code. So I'm here to learn and to listen, but we are committed at the FDA to supporting this agenda. So thank you.

Jay Bhattacharya (15:06):

I'm Jay Bhattacharya. I'm the director of the National Institute of Health. When I was in the Senate hearing for my confirmation as I was leaving the Senate floor after the hearing, a long COVID patient came up to me and said, "I'm desperate, please help." And I assured her that we're going to find an answer. The National Institute of Health, it has a long history of finding answers for patients. As a representative of the ivory tower class here, Mr. Secretary, let me just say, I want to make sure that we're not just in the ivory tower, there's folks in the room have learned from about long COVID in the ivory tower who've devoted their careers to trying to get answers. But also we have to acknowledge that we have not made as much progress as the patients that we are representing deserve.

(16:01)
And for the NIH, I don't want to wait to know everything about the physiology, the pathophysiology of the disease, I don't want to wait to be able to get the perfect diagnostic test before we start to have real answers for patients. I entirely agree with you Mr. Secretary, about listening to the physicians who treat patients, listening to the patients themselves. And then I want to see that those ideas are incorporated in our research agenda. Actually, one of the things I've learned since becoming an NIH director is that we've shifted how we're doing our investments in long COVID research toward more practical trials. And we are running, I think several of them now, but we need to expand them to more.

(16:52)
I've heard so many great ideas from some of the physicians in the room and from patients themselves, it's going to be a collaboration, it's not going to be us telling you from the ivory tower, here's what's real, what's not real. It's going to be us listening to you and our expertise helping to sift the answer so you can have, the next time we have a commission a year from now, it won't be 20 million people suffering, it'll be 20 million people with answers getting better.

Jordan Vaughn (17:26):

I'm Jordan Vaughn from Birmingham, Alabama. I am the founder of the Microvascular Research Foundation for Long COVID. I'm actually just an independent physician that had the resources to try to help people. And a lot of what's driven me is a lot of the data from the academic world, but being able to utilize that data and apply my understanding of mechanisms of medicines and actually discuss with the patient and figure out ways to help them based on their symptoms, the knowledge we get from the NIH, but also reusing medicines that we know help in those areas.

(17:59)
And I think that's one of the things that drives me the most is a lot of solutions even, There are things that will come, I think, but there's a lot of things already out there on the shelf that we need to evaluate and utilize and actually are very available for people and is very effective in many ways, especially in about the, again, I've treated about 4,000 people and just the data that I have within my clinical cohort is amazing, but it also informs me on when things don't work and when they do work.

(18:26)
And so in many ways, I think actually having a clinician- patient direction upward and actually suggesting models and pathology markers and… That is actually the direction it needs to go instead of from the top down. I think actually it's such a patient symptom-based disease with multi-systems that it's going to be very hard unless you listen to patients. And actually a lot of the things that I've learned is actually just by keeping my ears open and spending time with patients and believing what they tell me. And I think that is something that you're not going to get from a textbook.

(19:05)
And in fact, a lot of the time what the patient informs you, you utilize your medical education to come up with ways that that could happen and then try treatments that might work for it and they become effective. I mean, it's a very different pathway than the classical pathway, but especially when you're talking about probably something that's going to require multiple medications and has multiple systems involved, a monotherapy is probably going to be very hard to come up with, and I think we need to look at it in a very different light. So thank you.

Michael Paytas (19:37):

Good afternoon. I'm Michael Paytas, Mr. Secretary thank you for the invitation. I'm an obstetrician, I'm actually a maternal fetal medicine specialist and a physician scientist. I've been on the front lines for COVID for acute and long COVID since the beginning, and I desperately wanted to do something to help our patients from the very beginning. My laboratory focuses particularly on brain injury work and we've developed a therapeutic for acute and long COVID and we're in the pre-clinical setting and we're hoping to go into a clinical trial, and I hope I can be of help to this group.

Robert F. Kennedy (20:21):

Can you tell what the treatment is?

Michael Paytas (20:24):

Sure. It's a 15-amino-acid peptide that is called SPIKENET, that blankets the spike protein. And we developed because in the early days I wanted to develop an animal model that would help us to actually work with this in a safe way. So we developed a BSL-2 model, which means that it's not as if you will, as working with the SARS-CoV-2 virus. And that allowed us to help understand some of the pathologies. And we then went ahead and studied other aspects to it. So now we know it's different effects not only in binding the virus, but actually what it's doing to help heal and reverse some of the changes that are occurring in different organs.

Robert F. Kennedy (21:13):

Are you finding the same level of COVID in vaccinated versus unvaccinated people infected or? What are you seeing in that area?

Michael Paytas (21:25):

Yeah, that's a great question. So all of this in the preclinical model is not with using on the vaccine. What we're seeing now clinically is that we have a mix of patients that have been vaccine naive and patients that have had it. And I am seeing this in the hospital team, not in the high numbers that we saw initially, but certainly we're seeing it.

David Putrino (21:59):

Hi everyone. David Putrino. I'm the Nash family director of the Cohen Center for Recovery from Complex Chronic Illness in New York. We're a hybrid clinical and research center in New York City that treats long COVID, chronic Lyme disease, vaccine injury and other infection associated chronic illnesses such as ME/CFS. Long COVID first came on our radar in April of 2020, shortly after we'd been hit pretty hard in New York by COVID. And we started to notice some of our patients weren't recovering, so we stood up a clinical program. And since then we've seen over 5,000 people with long COVID at our clinic. And we recently released 167 page guide to assessment, intervention, all in an insurance covered clinic. So even in the manual, we cover what CPT codes to bill, how to write [inaudible 00:22:55].

(22:52)
(silence)

Robert F. Kennedy (23:18):

What are you finding that works?

David Putrino (23:21):

So what we've done in the handbook is similar to what you said, Secretary Kennedy, there's 300 symptoms, but there are much far fewer drivers. And so when we think about what could be causing the symptoms, there's autonomic dysfunction, there's vascular dysfunction, which Jordan does a lot of work with. There's immune dysfunction, there's viral persistence, there's reactivation of other viruses. So what we advocate for is an approach where also as Jordan said, your patient is your biomarker. You listen to what they're saying, you take a few blood tests, you say, oh look, I'm seeing EBV reactivation strongly in this person. Their spike antibody is really, really high. Maybe this person might benefit from a combination of antivirals such as, we've been working with a physician named Skip Pridgen, also in Alabama who pairs valacyclovir and Celebrex and Paxlovid. And his results have been really, really quite strong.

(24:25)
And so we're trying to bring some of his work into a randomized controlled trial so that we can go to the FDA and say, "Hey, here's some good quality data suggesting that this really moves the needle on patients who have these specific biomarkers." Because I think the one thing, if you take anything away from this meeting, there's no silver bullet. There's not going to be one drug that undoes everything for long COVID. We really have to look at each patient individually the same way that we do with HIV care, the same way that we do with cancer care. We need to really understand the uniqueness of each patient.

Robert F. Kennedy (25:02):

Dr. Redfield, what are you seeing that works in your clinic? And do you have interactions with other doctors like these?

Robert Redfield (25:09):

Well, I do interact with him. Jordan Vaughn and I work very closely together. He's taught me a lot, I think I've taught him a little, I tell people it's hard for me to say that he may be better at this than me because I'm pretty cocky. But again, the symptom complex is important. So I focused more on cognitive dysfunction and immune dysregulation. And in that regard, I looked at ways to try to trick the immune system to reset at set point. So I used some of the earlier drugs that I had used for treating HIV infection, for example, a drug called maraviroc, which I use quite frequently and have had some fairly dramatic impact on cognitive function in people who literally are so cognitively impaired that they can't speak in more than two or three words at a time and been able to get them back to speaking normally.

(26:07)
The other thing we've done a lot working with Jordan is become much more aware of pelvic vein congestion in patients, which who would've believed that I have patients that present that really feel like they're suffocating. And it's not a comfortable place to be in a room with these patients because they're 24/7 feel like they can't breathe, and yet their hearts are normal and their lungs are normal, so why can't they breathe? And Jordan helped elucidate and helped teach me, and I've followed up on it, is their problem is they're not returning blood, the heart and the lungs. And the reason they're not returning blood to the heart and lungs is because the integrity of their veins, they can't stay open under the pressure of an artery that's overtop it. So we see a lot of pelvic vein compression and what we end up doing, we both have a mutual patient today that's having the procedure done in Denver.

(27:08)
Believe it or not, what we end up doing is putting a pelvic stent in the iliac vein to keep the vein open and it resolves their symptomatology. So there's all different times, you got to really decide what you're going after. For me, largely it's been cognitive dysfunction, where I have a lot of high performing individuals that no longer can function their executive function, and how do I get their executive function back to the point that they can maintain their job. And again, as I mentioned, the drug I probably use a lot is maraviroc, rapamycin, probenecid in a combination. And again, all repurposed drugs, none of them approved for what I'm using, but I've had pretty good results in about 70% of the patients. And then if they have the pelvic vein congestion syndrome, getting intervention radiology or peripheral vascular surgery to evaluate them and potentially put stents in. We have other patients that as already mentioned, they have a tendency to reactivate other viruses, the herpes viruses in particular, and they cause a lot of the symptomatology of fatigue.

(28:16)
And then are there ways that we can help them regain control of their replication of herpes viruses. So it's a very complex disease. It is going to be important to limit the symptoms into categories and to try to compare apples to apples because if you just take people quote with "Long COVID." The last thing I'll say on this is there really is probably a difference between patients with post mRNA injury versus people that have post COVID symptoms. I will say my post mRNA injury, which is a real thing, it's real contrary to what a lot of people think, it's real.

Robert Redfield (29:01):

Those patients have a tendency of not improving. They just don't seem to be improving. I have a number of patients now that are out five years. It's painful. The COVID infection patients do have a tendency to improve over time despite me doing something or not doing something, although we try to accelerate that, particularly for those people that have so severe cognitive dysfunction.

(29:27)
I mean, I can tell you the one lady, Joy, is a beautiful woman that I take care of, executive function, mid-fifties. She got to the point that she could only speak in about two words, three words at a time. And, she came to see me and I told her at the end of our first visit that she was the sickest person from cognitive dysfunction that I'd ever seen and she immediately burst into tears. It was very awkward. And, she left and I told my wife the story and my wife lectured me on being more caring-

Robert F. Kennedy (29:59):

You need to improve your bedside manner, Doctor.

Robert Redfield (30:01):

Improve my bedside manner. And so, Joy came back the following week and the first thing I did was I apologized to her and I said, "I told you the truth, but maybe I could have done it in a better way," and Joy looked at me, speaking in two-word blurbs. She said, "Dr. Redfield, I didn't cry because you said I was the sickest patient that you've ever seen. I cried because you're the first doctor that acknowledged I was sick." And, that's the problem with most of these patients.

(30:25)
I'd say five years ago, 95% of my patients came to me from psychiatry. They were all told it's a problem. Now some of them actually get to me before they see the psychiatrist but these patients have really been told there's nothing wrong with them, it's anxiety, they're making it up. No, it's organic. And, Joy, I got to put on this combination [inaudible 00:30:50] rapamycin, [inaudible 00:30:51]. And, within three weeks she was speaking normally. Her insurance company decided not to renew the prescription. Within three to four weeks she couldn't speak again. We got her back on the medicine and within three to four weeks she was speaking normally.

(31:07)
So, there are things that work. I don't know why they work. I do think one of the problems with COVID, that I'm more of an expert on, is this post-inflammatory immunoregulatory problem and the immune system that's stuck over here, how do I get it back in the middle so that individuals can function more readily?

Roger Marshall (31:30):

Mr. Secretary-

Robert F. Kennedy (31:31):

Yeah.

Roger Marshall (31:32):

If I could just… Quickly, I tried to talk to the folks at home now on this pelvic congestion syndrome and it's a pretty easy way to self-diagnose yourself if you've got this or not. And, it's maybe just as simple as, if you feel better in a swimming pool, if that gives you some relief, would that be… What else can they do at home just to sort that out?

Jordan Vaughn (31:57):

[inaudible 00:31:58] non recovery in the legs. A lot of them additionally have lots of fullness below the belly button. They also have a lot of POTS-like symptoms because of the preload failure of the right ventricle, meaning you're not getting blood back to your heart, which also additionally means pulmonary perfusion is compromised, which makes you short of breath.

Roger Marshall (32:15):

What can they do at home to diagnose-

Jordan Vaughn (32:15):

So, the main thing would be, yes, "Do you feel better in water?" But also a lot of these people, a lot of us don't realize the reason we sleep horizontal is because of the venous system, because it's a low-pressure system. So, most of these people were people that woke up, ready to run, ready to go and a lot of them now will say, "Look, it takes me an hour in moving in the morning to get going." And, that's a good signal that there is basically venous stasis or venous issues.

(32:41)
And, again, I go back to this that I didn't even realize, 72% plus of your blood is in your venous system and it's not good blood. It's low oxygen, it's inflammatory, it's coagulable. And, if it's not moving, in a sense it's like your sewage not moving.

Robert Redfield (32:54):

One of the things on for your website, Mr. Secretary, would be so useful, Jordan and I have talked about it, is just to have these patients tell their story. I mean, when you hear this story… I mean, when I first heard it, I didn't understand it but now that I've heard the story, I can pick it up like that. You guys have pelvic pain congestion and we finally get them to a professional vascular surgeon or a special radiology and lo and behold, we find out they are 85%, 95% compressed. So, I think patients hearing other patients stories can begin to position themselves correctly because the average physician, I think, is not educated about this at all. I won't tell you how many people think that this can't be true.

Jordan Vaughn (33:38):

But, me and Dr. Redfield, we argue about what's causing it, which I think is where the NIH comes in. It's so, okay, we see this phenomenon. It's usually happened in women historically. Now about 40% of my patients are male. Usually they're athletic males that are hypermobile, a little more flexible than average, probably some laxity in the veins. But, why? And, I'm a vascular guy so I think the vasa vasorum, the small vessels to the veins, are being compromised, which compromises the smooth muscle integrity of the veins. Dr. Redfield agrees with me so it's probably right. I'm just kidding. But, we need-

Robert Redfield (34:09):

Those kind of, I tell them that the veins' major receptor is the H2 receptor and basically it's a problem with the spike protein dysregulating the H2 receptor and causing inflammation in the valve wall. But, we don't know what the-

Jordan Vaughn (34:20):

Yeah. And, that's where I'm saying the clinical things, the phenotypes we're seeing, being able to have some type of mechanism that's really in the background, picking up and seeing these kind of phenomenon that drives translational research to say, "What the heck is actually going on here?" That's kind of my… Very different than the top down because you're looking at it from the patient reporting it as opposed to some phenomenon above.

Jay Bhattacharya (34:43):

So, one of the things that the recovered TLC, this is sort of the next step in what the NIH is trying to do with long COVID is we had essentially a formal listening session where we had submissions from patients, from doctors. And, we got 403 submissions about drugs, 64 on diet and nutrition, 29 on manual and physical therapies, 27 on complementary integrative health and then 28 device submissions and 21 other which, I mean, I thought I had gone through all the categories.

(35:19)
The point is that there's a lot to study and the question is, for us, it's prioritization, right? How do we decide which of these are the most promising? This is partly why I said earlier, I don't want to wait. I don't want what we did in HIV where we're telling patients, "Just wait. Wait until the next randomized trial, wait until the randomized trial."

(35:39)
We have to be pragmatic. There's so many different conditions and we have four that we're currently doing, four trials. We're doing recover TLC, low dose naltrexone, this is something we heard from the patient community that worked for some folks, GLP-1 drugs actually again works for some folks, stellate ganglion block and then baricitinib. So, those are the four we're doing and it's not enough I have to say. It's a good step forward because we're not waiting to find a full characterization of all the… You can hear among these [inaudible 00:36:18] doctors that we're still struggling to figure out exactly what the right mechanisms are. And, I mean, you guys have seen hundreds and hundreds of cases, so-

David Putrino (36:26):

Well, if I may, I mean, we're currently running dozens of clinical trials ourselves, interventional clinical trials, randomized controlled trials, without any NIH funding. And, the reason for that is, and with respect, I grew up in NIH system, so NIH is very good at doing incremental innovation which, as Jordan mentioned, that's what we need to understand mechanisms, that's what we need to understand things. And, I'm an implementation scientist so I know these numbers but, when it comes to things that the NIH have funded, we go from bench to bedside on average in the United States in 17 years. That is too long.

(37:08)
And so, I think we need to advocate for more public-private partnerships. We need to get drug companies involved. There's a company called Invivid that we're working with right now that produces a monoclonal that could be helpful for both long COVID and for vaccine injury because it can neutralize spike protein that is circulating in the body. We have not yet had a good size mechanistic trial of a monoclonal to neutralize spike protein. This is an urgent need and this is something that I think we can achieve rapidly through public-private partnerships. We can go to the FDA and we can say, "These are the sorts of things that we need to get emergency use authorization and urgent labeling for these patients who are currently paying out of pocket." I met with a patient just yesterday, went out to New Jersey, spent $30 grand on a monoclonal infusion. That's not achievable to most people, not even 1% of people.

Michael Paytas (38:11):

[inaudible 00:38:13]

Robert Redfield (38:13):

If I can just echo one comment, I think, Mr. Secretary, for you to reflect on, and I've mentioned it to Jay. I think it's so important to get the private sector involved. All right? When I think about how we motivated, for better or worse, the vaccine companies and Operation W [inaudible 00:38:30], we got the private sector involved. I remember Tony Fauci and Collins said that we didn't need to do that, just give the $15 billion to NIH and they would take care of it in three to seven years. And, I made a lot of friends that day, I said, "Yeah. We'll probably take seven years if that's how we do it."

(38:42)
I think we've got to get the private sector involved. There's a lot of private sector. I know a number of companies that have very exciting, innovative stuff and we've got to get them involved. Even in this little room right here, you're looking with clinicians in long COVID between 4 of us, we're probably taking care of over 15,000 people. I mean, it's not that complicated to put a consortium together and then partner that with the private sector to bring some of these new innovative therapists.

Roger Marshall (39:12):

How [inaudible 00:39:13]-

Robert Redfield (39:19):

Well, I think that's part of the things you have to engage them. I mean, not everybody in the private sector is adverse to using repurposed drugs.

Jay Bhattacharya (39:29):

That's something the NIH ought to solve. There's something we haven't done enough of and it's something… I mean, I hear you. You're right, absolutely right. We need to do this much faster, be more agile, and with private sector collaboration, there are mechanisms inside the government to do that and we just need to use them more.

Michael Paytas (39:49):

Yeah. I would just follow up with that. I've had three now of STTR/SBIRs and that's where you really get at that private and academic partnership supported by the NIH, which I think is a great program for drug discovery and acceleration, getting to clinical.

(40:08)
The second comment I just wanted to make is, you have a number of OBs and GYNs across the country. We do ultrasound all the time. I'm looking at the uterine artery Doppler and all of this day in and day out. So, just thinking logistically, we can just engage our colleagues to incorporate this because we're doing this all the time on the uterine artery and the pelvic veins.

Holly Olson (40:37):

I just want to add, that's why I wrote the stem cell bill was because we were waiting for FDA to approve ethical sources of stem cells for treatments. And so, writing the bill, getting it passed unanimously both in the house and the Senate, I'd love to do something at a federal level, that allows… And, it's not just going to help with the long COVID, it helps with autism and dementia and Parkinson's and all these other different diseases. I believe the peptides too will also help with that along with hyperbarics. So, the congestion stuff that was going on, my hands and feet were pretty much black and purple, but when I did hyperbarics, it brought back all of the circulation. I also phlebotomized.

(41:16)
I think there's a lot of things out there that we can look into that are going to help us. And, I mean, I was waiting for doctors to help me and was not getting the help or even the hospitals. I had to take it into my own hands and into my own kids. I have four kids that all have it and we have vaccine injury. We also have long COVID just, I mean, from COVID itself. And so, working with some doctors that think outside of the box, Dr. Jones was amazing. He's the one that found the monoclonals. He ran all my interleukins and then figuring out the hyperbarics and then the stem cells and the peptides. So, there's hope. And, that's the thing is, when I felt a little bit better, it gave me hope of knowing this isn't permanent, that we can find things that are going to help us to get even better, so…

Jordan Vaughn (42:00):

I would say in this disease process, most patients probably know more about it than your typical physician or internist when you walk in. There's very few diseases like that. And, a lot of actually the ideas or things that they come to, sometimes just listening to what worked actually creates ideas in my head on why it worked, if that makes sense. And, I think getting back to listening to patients but, it's amazing right now the resources that patients have to be able to find out about their issue.

(42:31)
The problem is, is when they try to find something to execute help for the issue that they've discovered is very difficult because physicians are unaware that this is causing issues, especially even within their specialty and domains. And so, imagine going with a disease that you know have and a physician that, first of all, may not even believe in it, second of all, may have never even heard of it. What kind of help are you going to get unless you have a physician that's willing to learn and then try things?

David Putrino (42:58):

I do think education is important there, Jordan. I mean, great point, but when we released our handbook, I did a series of educational talks across the West Coast to a thousand PCPs because I really think PCPs are going to solve all my problems here. No pressure on the PCPs but they're the people who, when you walk in the door and say, "Look, I got sick two weeks ago or a tick bit me and I haven't felt the same since," they're the ones who should be identifying, "Oh, you have chronic Lyme, you have long COVID, you have any ME/CFS or chronic EBV." And, we got to a thousand PCPs in that tour so we really went for it. And, 30% in the door at our pre-seminar interview did not believe that long COVID was real. So, they were happy to mark themselves on a survey saying, "I do not believe in the authenticity of this." An hour and a half later, 0% said that. And, it was just presenting good quality data to them and saying, "This is what you…" And also, "This is a plan. Here are the things you can try when someone comes in your door."

Roger Marshall (44:07):

Right. And, I think this gets back to we do need a good diagnostic tool. And, I just can't emphasize enough the mental help of being told that, "Yes. You're not crazy." Let's just be frank here. These patients have been told they're crazy. "There's nothing wrong with you physically." To have a test that confirms, "It's Lyme's disease. Okay. Great." And, I think that maybe we have some of those secrets now unfolding as we… You say there's 70 symptoms, 150, you probably are starting to put them in buckets now? And, based upon those buckets, is there a correlation with some of the testing that we're doing? I'm looking at Dr. Patterson to come and tell us the next roundtable. And then, your primary care doctors, get them to first base at least. We want to get the PCPs to first base with a little bit more data.

Jim O'Neil (44:58):

So, I think this roundtable already is a significant watershed in validating this disease, putting a lot of information on the table. I'm learning a lot. Mr. Secretary, I'm very grateful that you convened this. And, you also asked us to build a website to scale this meeting up into a national level and provide a single place, a platform, where patients and providers and pharma companies can all share information about symptoms and diagnosis and repurpose drugs and treatments and probably a lot of other things that we haven't thought of yet. And, we have our chief technology officer of HHS, Zach Terrell, here listening. Secretary's asking to build a website at CDC for all this information. We have Kristen Honey, our chief data officer. We have Dr. Willy Chertman, our science policy advisor. We are all listening. I'm learning a lot and we are going to scale this up.

Devin Russell (45:52):

I'd like to add something if I may.

Robert F. Kennedy (45:54):

Can I ask [inaudible 00:45:55].

David Putrino (46:02):

Yes. A hundred percent.

Robert F. Kennedy (46:04):

Sorry. My question was, are any of you seeing an interaction with mold?

David Putrino (46:09):

Yes. I think along with, as Dr. Redfield mentioned, there's this immune dysregulation and I think immune dysregulation makes your body more susceptible to everything. So, for instance, as you mentioned, your chronic Lyme meeting, roundtable, something you can take into that is we have data to suggest that a significant portion of our long COVID patients are now testing positive for reactivated Babesia, which is a tick-borne pathogen.

(46:38)
And, what we think is that they were carrying that pathogen, that parasite, for a very long time. And SARS-CoV-2 reactivated it because where does Babesia hide? Our vascular people? In the vasculature. It hides in the endothelium. So, spike protein agitates the endothelium and so these other pathogens get reactivated and agitated. And, similarly, this immune dysregulation, the immune exhaustion that people with long COVID experience also make them susceptible to mold exposure, make them susceptible to mold injury and other toxins as well.

Robert Redfield (47:14):

There's cells in our body we call mast cells that are very unstable in people with long COVID.

David Putrino (47:20):

Yes.

Robert Redfield (47:21):

And, what they end up doing is causing all of this allergic symptomatology. So, mold, whether it's mold hyper reaction, I will tell you that when they get intercurrent illnesses, patients who get an intercurrent respiratory illness, they get it much worse with long COVID than say before they had it. So, there's clearly a hyper reactivity of the body to allergens, to infectious diseases. Jordan and I do a number of things to try to stabilize the mast cells in the human body. A lot of repurposed drugs that we know can actually help stabilize these cells and patients do get a lot of benefit from it when we stabilize their mast cells.

Robert F. Kennedy (48:06):

Devin, did you have a comment?

Devin Russell (48:09):

Yes. I just didn't want to lose track of the virus because the virus persists and people get reinfected as well. And, that's a big problem for people with long COVID. And I know we want to characterize everything, but when I had chronic Lyme, my chronic Lyme symptoms didn't present like somebody else's but we still had the same underlying problem, which was Borrelia was chronic. So, I just want to be cautious about putting everybody into groups when the main underlying problem may be the same thing, even though there are reactivated pathogens and damaged and other things going on, the virus itself and included with the spike, I think we need to keep a great focus on that because Lyme is the great imitator and I think long COVID is the greater imitator.

Robert Redfield (49:00):

I think it's a real important point. I mean, I'm sort of a clinical virologist and I will tell you four years, five years ago, I would've argued pretty aggressively that there's not viral persistence with COVID. Now, in the last two and a half, three years, I'm totally convinced that there's viral persistence in long COVID. A number of the patients that they failed to clear the virus. This is a chronic viral infection. And so then, that raises a whole different ways to approach it. How do we stimulate the body to facilitate viral clearance?

(49:35)
And, I think the group at Yale has done some really good work. I think there's a lot of evidence now. We have a paper that we're going to review now that's highlighting all the evidence today that there is viral persistence. And, that's important because, as we get into what's the pathogenesis of long COVID, I think more than we appreciated, it's the lack of viral clearance.

David Putrino (50:00):

And, to that point, just earlier this year, a consortium of us came together and published in Lancet Infectious Diseases, a roadmap. So, for anyone who wants to use it, FDA, CDC, NIH, a roadmap for how to address viral persistence in long COVID cases, which really talked about combination antivirals, long duration combination antivirals, mixing antivirals with monoclonals. Because, as we know, once a pathogen is persisting, i.e. once it's in the tissue, it's much, much harder to eradicate than just two weeks of Paxlovid or boost your immune system for a little while and hope for the best.

Robert Redfield (50:42):

And, one of the important mechanisms that we have as humans to clear pathogens is an aspect of the immune system we call the cellular immune system. And I think, if you watch closely, there'll be more and more data coming out that there's significant defects in cellular immunity in people with long COVID.

(51:00)
And, that opens the possibility not only could you use antibody, but could you look at ways to trigger your cellular immunity because it's really cellular immunity that our body uses to clear these pathogens at the end of the day. So, I'm very optimistic that, with significant investment in the science of this, and Jay and I have talked about this, is that we can really go after therapeutic strategies that are based on a pathogenic understanding that… I think I argued with Jay probably five years ago and I told him, "There's no viral persistence. There's no viral persistence. This is self-limited virus." Well, I was wrong. There probably is viral persistence.

Robert F. Kennedy (51:43):

I think Dr. Redfield's optimism is a good place to end this session. We're going to have a half an hour. We're going to start our next session on innovation and I welcome all of you at home to rejoin us and thank you all very much for being part of this.

MUSIC (51:59):

(instrumental music)

Robert F. Kennedy (01:24:46):

Welcome back to the late afternoon session of our Long COVID [inaudible 01:24:50]. Sorry [inaudible 01:24:50] do that again. Welcome back to the late afternoon session of our Long COVID Consortium. This morning we had physicians and patients in to talk, and now we have a group of innovators and researchers, and we're going to talk about the path to a cure to treatments. One of the things, for those of you who weren't here this morning, we talked about the need to do something different at this agency, which is not just to develop science out of NIH, but actually to go out and talk to physicians, talk to patients, and find out what's working on the front line.

(01:25:29)
And we had a very successful meeting just now, and now we have a new group of people. And why don't we start over here? Why doesn't each person introduce themselves and then talk about some of the things that they're working on? And I do want to say we have Senator Todd Young with us today. During my confirmation hearings, he asked me to include ARPA-H and discussions about Long COVID and bring them in. And we have Dr. Jason Roos, who is from ARPA-H. So that is… Now we're even. Thank you.

Speaker 1 (01:26:17):

Thank you.

Robert F. Kennedy (01:26:17):

Thank you.

Hossein Estir (01:26:17):

Thank you, Mr. Secretary, for inviting us. I'm Hossein Estir. I'm an associate professor of medicine at Mass General Hospital. I would like to start by stating that I'm here as an individual, not representing my institution. I'm here as a scientist, deeply rooted in rigorous scientific evidence. I'm an empirical scientist. I believe in gold standard science, and I'm also have personal experiences with Long COVID. I'm not a clinician, I'm a data scientist, social scientist, but I work very closely with a lot of clinicians. All of my perspectives are

Hossein Estir (01:27:00):

Basically from my research over the past five years on long COVID and deep appreciations of the complexities of human health. Should we go a little bit about what we do?

(01:27:15)
All right, so most of my work is on defining the problem, which I think is part of the bigger problem of why all of the investment hasn't resulted or anything. I believe that what we do is that we use computational basically techniques and AI and big data sets to define complex temporal human phenotypes. And I believe one of the main challenges is that we've been trying to target something that is elusive, has never been decided, they're defined and it's all over. So I think that part of lack of success is it probably is one of the hardest thing to actually ask for treatment when you don't still know what is exactly out there, because it manifests in several different ways and it can be very individual, treatments can be very individual also. So we probably are talking about a lot of different sub-phenotype definitions here, and we've never had enough power in our data, in the legacy approaches to define this disease so far.

Robert F. Kennedy (01:28:33):

Thank you very much, Doctor. And that was one of the themes that we hit on this morning is that this is a constellation of symptoms that each patient needs to be treated individually and that we don't have biomarkers and we don't have many of the characterizations that we have for other diseases. So thank you for adding to that. Now Bruce Patterson, who's also a clinician who has had great success in treating COVID patients from all across the country.

Bruce Patterson (01:29:09):

Thank you, Secretary Kennedy. It's my pleasure to be here. I am a physician-scientist. I was trained at Northwestern in viral pathology. I went in to start my research career in HIV in 1990, so I've lived through these pandemics, and the words you said in the previous session couldn't be more true. The fact that we're sitting here together discussing the issues and the struggles is such an enormous step and so different than how HIV was treated back in the day.

(01:29:43)
I went on to do a head of virology at Stanford where I continued my HIV research on reservoirs, viral replication, and what I call replication competence, which is the ability for viruses to make more of themselves, to replicate. And at the time we started studying monocytes, which are a white blood cell, and harbored many viruses including what we published in 2009 with hepatitis C of all viruses.

(01:30:21)
And it brought an issue to me was that these monocytes, which are human scavengers, basically can take up or get infected with viruses. And so when I got back from China in January 2020, we used 158 biomarkers, the immunophenotype acute COVID, and we found that patients at 60 days and 90 days may have been better, but by no stretch of the imagination was your immune system normal. It was highly dysregulated, as Dr. Redfield had mentioned, and it was abnormal in a very different way in acute COVID.

(01:31:02)
So we took these 500 patients at a time where there was only one variant and we modeled using machine learning and AI that the two algorithms that set apart acute COVID and this population of individuals who had symptoms at 90 days, now recognized as long COVID. So even then we had the two algorithms that were a composite of cytokines and chemokines that were biomarkers that allowed us to separate long COVID.

(01:31:35)
We then went on to model chronic Lyme, chronic fatigue syndrome, and now we're working on mold mycotoxins as was mentioned in the previous meeting, where we can actually use the diagnostic to obtain a pure population of patients with long COVID, chronic Lyme, and other chronic inflammatory conditions. That is paramount to doing obviously very informed clinical trials where patients get enrolled properly.

(01:32:06)
We also use that data in now 20,000 patients. We've treated 12,000 patients. We have a database of 20,000 patients where we used that information in a data analytics portal to develop a therapeutic that could address long COVID and we're very excited to be on the precipice of launching our FDA trials in that combination drug that was approved to proceed 18 months ago. And it's fortunate that we're sitting here because this trial could have been done, but I have spent the last 18 months trying to raise money to fund this trial.

(01:32:48)
But in long and short is we discovered a new mechanism through our data analytics that there can be viral persistence in the absence of replication. So there's fragments of virus, viral RNA in monocytes, there's fragments of viral protein in monocytes. We showed that in long COVID. We showed that in post-vaccination syndrome. So that's almost proof that you don't need a replicating virus to basically have the same symptoms as long COVID. And the clincher was, we just found the same mechanism in Lyme disease. In other words, retention of Borrelia protein in long-lived non-classical monocytes, that their sole reason to live is to traverse to the blood vessels and cause vascular inflammation. And that's how we're treating long COVID and chronic Lyme. But it was very prophetic that you, Mr. Secretary, brought together ideas about long COVID and Lyme because personally I think they're very much related from a pathogenesis standpoint.

Robert F. Kennedy (01:34:03):

And what is the name of your drug?

Bruce Patterson (01:34:05):

It's a combination of Maraviroc and Atorvastatin. So it was similar to what Dr. Redfield was talking about, but the base is Maraviroc, a CCR5 antagonist, that has a very unique role. It was used as an HIV entry inhibitor, but it's a profound immune modulator and it prevents inflammatory cells from migrating all over the body. Most importantly, it reprograms monocytes away from a pro-inflammatory phenotype reducing this immune dysregulation in long COVID patients. And last, the lymphopenia or the low levels of CD8 T-cells that you see in long COVID, Dr. Iwasaki has published that as well, is a function of the CCR5 pathway, and that lymphopenia low lymphocytes gets restored by using a CCR5 antagonist like Maraviroc.

Robert F. Kennedy (01:35:06):

Thank you, Doctor.

Michael Peluso (01:35:11):

Hi, everybody. I'm really grateful for the opportunity to be here. My name's Michael Peluso and I'm a long COVID physician researcher and clinical trialist at the University of California, San Francisco. I've overseen our long COVID program since way back in March of 2020 and our program is really focused on two things. First, understanding the biological root causes of long COVID. We also have evidence for things like viral persistence and ongoing immune dysfunction, immune dysregulation, and secondly, conducting clinical trials with the goal of getting people better.

(01:35:51)
We are involved with about seven different clinical trials, really trying to push the envelope on long COVID therapeutics, and I'm really here today to advocate for what's been mentioned already, which is the importance of really scaling up our portfolio of clinical trials for people with long COVID. So I think that there are basically three, briefly three things that we need to do that.

(01:36:17)
The first is really to implement a flagship biomarker program to figure out who is most likely to benefit from each of the types of clinical trials that we might do, and to also get diagnostics into the clinical setting so people can get a diagnosis and we don't continue gaslighting our patients and telling them that this is all in their head.

(01:36:42)
The second is that we have so many leads on what actually needs to go forward into clinical trials. Dr. Bhattacharya mentioned this before, and we need to be chasing them all down right now. The pace of clinical trials has been too slow. We need to get more trials into the field, like this year. To do that, I really think we need to invest in a bottom-up approach to clinical trial implementation, with a variety of different groups that are each running their own trials but with shared enrollment criteria and outcome measures so that they can be directly compared when we have results.

(01:37:18)
And then the third thing that we really need to do, which also came up this morning, is to promote industry investment and engagement in this problem. We saw for HIV how important it was in the '90s to have pharmaceutical partners on board with developing drugs and investing tremendously in getting people onto ART, figuring out what treatments would work. We need that level of commitment for long COVID. Thank you.

Jason Roos (01:37:48):

Well, good afternoon-

Robert F. Kennedy (01:37:48):

Dr. Roos-

Jason Roos (01:37:49):

Sorry.

Robert F. Kennedy (01:37:49):

Go ahead.

Jason Roos (01:37:49):

Go ahead.

Robert F. Kennedy (01:37:51):

No, I'm just introducing you.

Jason Roos (01:37:55):

Well, good afternoon. I'm Jason Roos. I'm the acting director at the Advanced Research Projects Agency for Health. First, I want to thank everybody for taking the time to come here, the patients, the providers in the previous session, all of our research colleagues here, and Senator Young, appreciate your support as well.

(01:38:14)
ARPA-H was born in the model of DARPA with the goal of going after the hardest problems in the healthcare space. And our mandate is to really focus our investments on those high-risk, high-impact research areas that can really push the boundaries beyond those incremental improvements and really be transformative. And I can't think of any other problem right now we're dealing with in long COVID in terms of what fits into that, into that bucket. But we are not in any way, shape or form going to solve this problem on our own. My whole of government colleagues here, Jay and Marty and CDC and others, this is a problem we all have to tackle together. But importantly, as was brought out earlier, in the earlier session, it's going to be very important to involve you all and public-private partnership engaging with the community outside of the government as we try to tackle these problems.

(01:39:12)
So I'm here today to listen to what you all think we should be placing our investment. How do we maximize the use of our resources? Who do we need to be partnering with to really try to make some significant progress here? And I can say that we are committed to really trying to move the needle and being true to our model. And the output from today is going to help inform the investments that we are intending to make in the very near term on the long COVID problem. We were talking earlier there, we're already starting to look at this idea of repurposing which came up before, we have some investments there on the rare disease space, how might that be applied in this world? And then certainly on the biomarker front, that's an area of great opportunity. So again, I just want to thank you all and thank you, Mr. Secretary, for your strong interest and push in this area.

Jay Bhattacharya (01:40:09):

I'm Jay Bhattacharya, the director of the National Institutes of Health. I already gave comments earlier so I don't know how much I should repeat myself, but I'll say that the need of patients that I have heard from on this is just tremendous. It's the heart of and soul of everything that we at the NIH are working on this. And, Bobby, your passion for this is truly inspiring.

(01:40:39)
I think the key thing in my mind is that there's a lot to learn from patients, a lot to learn from clinicians who manage patients, and the RECOVER-TLC program, the NIH's program on clinical trials and long COVID, we did essentially a listening session where we got literally hundreds of possible agents, drug agents, a whole host of other therapies. There's a lot of expertise out there. And, Dr. Peluso, you mentioned the imperative that we start evaluating rapidly. That is absolutely true, and we've been way too slow just by spending $1.7 billion. We've been way too slow at evaluating them. And I think let me just make a defense of evaluating them, just because I think it's important. I think it's very important to listen to patients, and I think it's very important to get the therapeutics out there as rapidly as we can, but if we don't evaluate them, things that don't work will be given to patients as false hope. So the idea is for us to work together with the patient community, to work together with clinicians on the front line, but we have to work much more rapidly in academics than we're used to to do this right.

(01:42:04)
And I've been listening, I have tremendous hope. There's so many ideas that seem to me like they're very, very promising, expertise that's been developed over the course of now years, and I think we will have an answer, but it'll take way too long if we move at the normal pace of science. The kinds of consortia that have been developed, the sort of a clinical trial network, the capacity to use these networks to accumulate our learning and then communicate with others, that's what I'm absolutely focused on. And I'm delighted that Secretary Kennedy has convened these panels just so we can continue to have that engagement. The website you were talking about is going to be fantastic I think for patients to get to see what's available, and we're just going to keep moving forward. For all the long COVID patients out there, we're going to have an answer for you.

Todd Young (01:43:07):

Well, Mr. Secretary, thank you for your leadership on this and for not just keeping your promise, but going above and beyond the call of duty and highlighting the importance of this issue. We know that millions and millions of Americans have been adversely impacted by the after effects of COVID, and I do think it's going to take all of government's multi-stakeholder engagement to address this unique challenge, NIH, ARPA-H, our university research community, private sector, to have them all here and figuring out ways in a very transparent setting to cross-cut this issue, to tackle these challenges is going to be essential.

(01:43:55)
So I wanted to deliver my word of gratitude, Mr. Secretary, but also assure you that members of Congress are engaged in a bipartisan way on this issue. Very interested in the development of therapeutics and other ways we can tackle this, prepared to resource evidence-based interventions where we can, and really eager to engage with our constituents, whether they be members of our family or the business community or rank and file Americans who just are at wits end trying to make life work at the time that they've been debilitated by this condition. So thank you, sign me and other members of Congress up to continue this positive progress.

Robert F. Kennedy (01:44:42):

Thank you, sir.

Jim O'Neil (01:44:47):

I'm Jim O'Neill. I'm the Deputy Secretary of HHS and acting director of CDC. We've learned a lot about symptoms of long COVID, a long list, an informal list so far, and I would like to add one symptom of long COVID that I don't think we've mentioned yet, and that's alienation. So many people are suffering and people around them don't believe them, don't take them seriously. It adds alienation to all of their other symptoms. And I want to thank you, Mr. Secretary, for convening this conversation, putting it on the web. I'm hoping you'll provide validation and support for people that are suffering from alienation and also hope and optimism that we are putting more facts on the table, bringing more expertise, taking unstructured data and starting to add structure to it so that can lead to more solutions that everyone will have access to.

(01:45:46)
And you've asked us to build a website at CDC to put all this information together, information from patients, from providers, from manufacturers about repurposed drugs, about symptoms, about possible causes. I think this will be a great aid to all of our research. We have our chief technology officers, Zach Terrell, in the room who's listening very carefully. We have Kristen Honey, our chief data officer. We are taking all this information and suggestions on how this new website can best be a central repository for the world to gather this information. So thank you all for participating in this.

Ken Callahan (01:46:24):

Just want to echo, thank you everyone for coming. My name is Ken Kelly and I work on policy for Secretary Kennedy. As he had mentioned the first session was very much focused on giving providers and patients a voice and a platform to share what's worked, and this session is very focused on finding a cure, improving diagnostic testing, and just seeing what we can be doing on the government side to improve innovation in this space. So just want to echo the secretary and deputy secretary and thank you everyone for being here.

Darcie Johnston (01:46:57):

Good afternoon. I'm Darcie Johnston. I'm the principal deputy director of the Intergovernmental External Affairs Office. Thank you for being here today.

Speaker 2 (01:47:08):

Thank you, Mr. Secretary, for the opportunity to be here and for convening these two panels on long COVID. So I think we all agree that long COVID is a serious national crisis. There are at least 20 million Americans who are suffering from long COVID. Some actually disabled because of long COVID. Long COVID affects people across political lines and in every corner of the United States, wherever I go, there's always people with long COVID. While the NIH's RECOVER initiative was a well-intentioned start, it was very clear that its results so far have not matched the scale of the investment and the urgency of the crisis. We think we can all agree on that.

(01:47:49)
The number of people suffering from long COVID actually continues to rise. It's a misnomer where people don't really understand this, that even in 2025 people are still getting long COVID from COVID-19, even in 2025. It didn't go away. The number of people who are suffering from long COVID actually continues to rise and these people need answers yesterday. Need answers and treatment yesterday. To that end, I have three suggestions or initiatives for your consideration.

(01:48:16)
First, facilitate data liberation. And what do I mean by that? Create a national data comments for long COVID. A major roadblock to progress on long COVID is that the RECOVER's vast data set is literally locked for only RECOVER investigators, and actually that data was paid for by US taxpayers. I paid for that data. All US scientists should be able to access that data to help us solve the puzzle of long COVID.

(01:48:44)
Two, fund a diverse portfolio of drug repurposing programs. This is really, really important. We've made a lot of progress on AI over the past several years. I don't see that leveraged to really help us solve the problem of long COVID. We can and should do it. It's not beyond us. It's not beyond the might of the United States to solve the problem of long COVID. It's not beyond us to solve it, and we can and must solve it. And how you can do that? You can really study using AI and existing data, thousands of drugs for repurposing, identify the most promising candidates and then give them to NIH instead of testing a hundred, which it will not have the resource to test 100. Four is not enough, but maybe these are the top 15 that can really, you can put your money in and then try to investigate those.

(01:49:35)
Three, really galvanize research on studying the epidemiology and mechanisms. While we focus a lot on treatment, and that's really, really important 'cause people are hurting and they want treatment yesterday, they really want treatment yesterday, but there is really, we need also to understand epidemiology and mechanisms. For example, somebody said, "Oh, a lot of people in my family have long COVID." Why some people get afflicted with long COVID and most of us are just fine? I got COVID, I'm fine. Most of us when we get COVID, we're fine. Why do some people get long COVID and some people don't? We need to understand that.

(01:50:05)
We also need to understand what happens to people five years down the road after long COVID, seven years down the road, 10 years down the road. These are really, really important questions that need to be solved. We are in a race against time. We must make progress on long COVID. With both leadership, I'm grateful, grateful to you and to you, Senator, and to the NIH and to the rest of you for actually convening this, great enormous gratitude for doing this. With your leadership, I believe we can move the ball forward on long COVID. It's not beyond the power of the people in the room and the United States people to really solve this problem. We can and must solve it. Thank you.

Robert F. Kennedy (01:50:41):

Will you just talk about the database that you're talking about that we don't have access to?

Speaker 2 (01:50:49):

Correct. So RECOVER has in the observational arm and also in recruiting patients that amass troves of data, but those are primarily available to only RECOVER investigators, and they make really only the secondary or tertiary data sets available to people outside of RECOVER. If we are really, truly, truly serious about solving the puzzle of long COVID, you would want the best and brightest minds in the United States to really get access to that data and help you solve the puzzle of long COVID. Of course, no shorting privacy and security and must be done correctly and must be done by upholding the high standard of security and privacy. We're not cutting corners, but you ask people who are actually invested in helping you solve long COVID should be able to access that data and help you unlock or help you solve the puzzle of long COVID. That currently is not the case.

Jay Bhattacharya (01:51:37):

[inaudible 01:51:39]

Robert F. Kennedy (01:51:39):

What is the impediment? It seems like a no-brainer.

Jay Bhattacharya (01:51:43):

Yeah, no, this is what the real-world data platform that we're working on is supposed to be exactly for. And not just long COVID, the RECOVER data, but just the data sets that the United States government has for on a host of … a whole panoply of data sets that we have, making them available to researchers. It's not just for long COVID, for chronic disease after chronic disease. We need to unleash those data resources so that researchers of the world can use them.

(01:52:12)
I mean, I can tell you before I was an NIH director on the outside, I was quite frustrated and same-

Speaker 2 (01:52:16):

Yes!

Jay Bhattacharya (01:52:16):

… I can hear the same frustration in your voice.

Speaker 2 (01:52:18):

Yes!

Jay Bhattacharya (01:52:18):

I mean, I'm absolutely committed to making that happen, which you said also before about the patient privacy is very, very, very important. Right? We made a essentially comm pact with patients that we're not going to violate their privacy, but there are ways to do that now and make those data available, protect the privacy, and then allow researchers to … That's what the real-world data platform they're working on is exactly about.

Hossein Estir (01:52:39):

May I add a comment to that data, because I've worked with different networks as a repositor, I think that one of the main challenges is validation. The data, until it's not connected to the patient and you cannot go back and trace it back and validate and potentially follow up the recovery for the patient, it's not useful. It's not a centralized solution in my opinion is not useful. It has to be a federated way. So it can go back, look at the entry, C4C, all those practices. I don't think the answer is in secondary use of data because a lot of unvalidated work was out during the pandemic and a lot of misinformation, honestly, went out through even scientific publications without any validation.

(01:53:25)
And I really want to emphasize that is important because this secondary data, even the surveys data, these are not … I mean, the surveys, they have their own biases, but secondary data, EHR data, claims data, they were not yet collected for research. There's a lot of inconsistency, there is a lot of quality issues. I just wanted to say that there are solutions. I completely agree that we should utilize the data, but I don't think it's federated way is going to be traceable back to the patient to validate.

Jay Bhattacharya (01:53:56):

We can discuss that offline, but I think that those secondary data actually could be useful if they're analyzed properly and within ways that are, again, we can talk about that. These are the kind of problems that we're tackling in this real-world data platform.

Todd Young (01:54:11):

Mr. Secretary?

Robert F. Kennedy (01:54:12):

Yes.

Todd Young (01:54:13):

Do you mind if I ask sort of a question of the group?

Robert F. Kennedy (01:54:16):

No, You and I are co-chairing this.

Todd Young (01:54:18):

Oh, great. All right. Kind of you. So thank you for hosting again. This is thematically I think a good point to ask a question, not only how we can repurpose existing pharmaceuticals, but whether there are ways to get more companies at the table to help solve these problems. It seems to me that the FDA does amazing work. There's been some, I think, thoughtful reflection about how to reform the FDA or how to impose leadership to cut through bureaucratic delays and bring more solutions to those who need it. Mr. Secretary or others, are there things that we can be doing, perhaps a pharma roundtable at some point to bring stakeholders to the table and figure out collectively how we can accelerate US long COVID research through FDA reforms?

Robert F. Kennedy (01:55:13):

Yeah, this is exactly the question that I asked at the last session is how do you bring in a public-private partnership? How do we incentivize private companies to get involved in, particularly when there's repurposed medicines involved, where the patents may have expired or somebody doesn't own the patent? It's a little trickier than it was during COVID when we were just focused on vaccines and there was a huge profit potential, but maybe other people have ideas about how to do that.

Todd Young (01:55:48):

So yeah, existing drugs, but also drugs in development. Are there things we can do through the FDA process? Maybe others have thoughts about that?

Michael Peluso (01:55:56):

I think-

Speaker 3 (01:55:57):

Do you mind if I introduce myself?

Robert F. Kennedy (01:55:59):

Yes.

Speaker 3 (00:00):

Michael Peluso (01:56:00):

God.

Dr. Akiko Iwasaki (01:56:01):

I think we still have two more people. So I'm Akiko Iwasaki, Professor of Immunobiology at Yale University School of Medicine, and I'm also director of the Yale Center for Infection and Immunity. We started the center two years ago to tackle chronic diseases that happened after an acute infection like SARS-CoV-2. We also realized that many other pathogens can cause similar outcomes, which we're calling post-acute infection syndromes from Lyme disease, Epstein-Barr virus, and multiple other causes.

(01:56:32)
What we're understanding from long COVID research is very precious because it informs immune dysregulation for other types of post-acute infection syndromes. What is happening, seems to be, is that there is a fundamental inability in some people to clear the virus at the acute phase, which then leads to persistence of the virus, or the viral antigen, or the RNA. That then leads to things like herpes virus reactivation, Epstein-Barr virus, as well as induction of autoimmunity, autoantibodies that we can detect in about 20 to 25% of people and also chronic inflammation that's not resolved.

(01:57:14)
So we are seeing these features from multiple studies, and we believe that tackling these root causes of disease is going to make the biggest impact in patients' lives because it's not just the symptomatic treatment, but getting at the root cause and getting rid of the cause of disease.

(01:57:32)
So for instance, for viral persistence, we can deploy things like antivirals, monoclonal antibodies. We also heard about Invivyd, which makes Pemgarda, and they have a next-generation monoclonal that's even more potent that we can trial in patients with COVID. For people who unfortunately already developed autoimmune diseases, there are many, many amazing drugs in the space of autoimmunity that we can retool and repurpose and to do a randomized clinical trial.

(01:58:04)
For herpes virus reactivation, we really need to develop better drugs and vaccines against these herpes viruses. For instance, investment into antivirals is key for preventing future pandemics and future occurrence of these post-acute infection syndrome, as well as developing better innate immune agonists, which allows your host cells to remove these pathogens on their own.

(01:58:32)
Again, also, using immunotherapeutics to remove the persistent virus, whether it be SARS-CoV-2 or Epstein-Barr virus. Also, I believe that more support in basic research is needed. So from the NIH, we need to really look at root causes in a more rigorous fashion with much larger cohort of studies in addition to doing randomized clinical trials and trying to do deep immune phenotyping so that we can identify people who benefit from a particular medication and who don't. So we won't be wasting people's resources and time and energy into giving wrong treatment for patients.

(01:59:16)
Just as an example, if somebody has an autoimmunity, you don't want to be giving that person antivirals. It may not be relevant and vice versa. So understanding what they have and what the root causes are important, and biomarkers, many of us already talked about this, but having a validated biomarker to identify people who have persistent virus antigen versus people who have autoantibody versus people who have chronic inflammation will go a really long way to doing a targeted randomized clinical trial, and for engaging industry, academia, and regulatory agencies all together to expedite this process, because as many of us already said, we really needed this randomized clinical trial yesterday.

(02:00:02)
So I agree with it, and I'm here to serve and be a resource for this group.

Robert F. Kennedy (02:00:10):

Ed, do you want to respond to that?

Jay Bhattacharya (02:00:12):

I mean, I agree with all of that. I've learned a lot from your work over the years, and I'm grateful for it. So thank you. I think we have to invest in all of the above. It really is a tragedy that we've spent so much money and time and not gotten those validated biomarkers. But I don't want to wait. I don't want to wait. I want those randomized trials happening now as fast as we can.

(02:00:36)
We can't do hundreds, but we can do a lot, and I've heard the possibility of other private collaborations. I think that's one way to accelerate things. We have to do all of the above.

Robert F. Kennedy (02:00:49):

Dr. Peloza, you had a comment about how to bring in a private [inaudible 02:00:55]?

Michael Peluso (02:00:55):

Yeah, I just wanted to make a quick comment. So I spend a lot of time as a clinical trialist, doing kind of proof of concept or early phase two trials, knocking on doors of different companies that have drugs that I think can and should be tested for this condition, and there's, I perceive, this hesitancy because this is considered a really risky investment on the part of a lot of these potential industry partners.

(02:01:23)
The other question that comes up, by far, the most often is how do you know that the people that you enroll in this trial actually stand to benefit? That sort of gets at this biomarker issue. I think that they are concerned that a bad outcome in a long COVID trial, which is not going to be straightforward, could harm their product development pipeline.

(02:01:47)
So I really like the idea of actually having a roundtable event like this with industry partners to really get a sense of what their concerns are and what would facilitate this. The last thing I'll say is it's not at all clear what the FDA would accept as an outcome in a clinical trial for an indication. So guidance from the FDA perhaps as part of a round table, that would be extremely helpful, I think, in engaging that key group of stakeholders.

Robert F. Kennedy (02:02:14):

Dr. Patterson.

Bruce Patterson (02:02:16):

I think that was such a great idea. I think in terms of biomarkers and in terms of how we use our diagnostics, it's two-fold. Number one, you need a diagnostic to stratify, ensure that you're enrolling long COVID patients into a trial and you're not enrolling Lyme patients into your long COVID trial. That's been the focus of our trial design.

(02:02:42)
Number two, you need a biomarker or a collection of biomarkers as in our Long Hauler Index that shows response to therapy. So you have a companion diagnostic in addition to a diagnostic that can stratify. So it goes much beyond a discussion maybe because we're kind of beyond what biomarkers should we use, where we're actually using, deciding how to deploy that diagnostic, deploy those biomarkers, and like I said, one to stratify, to get a pure long COVID population, and one to monitor response to therapy. That brings up the point.

(02:03:23)
I think long COVID in the term PASC are two different definitions. I think SARS-CoV-2 in of itself is capable of a post-infectious condition, Dr. Iwasaki mentioned, I think PASC encompasses the fact that SARS-CoV-I2 causes profound immunosuppression CD8 T-cell counts in the single digits when we started in February 2020, and, of course, you get the herpes family virus reactivation, you get Lyme recrudescence or reactivation, and now, mold mycotoxins, we're studying. So that is truly post-acute sequelae of COVID. That's past. I think with long COVID and pure COVID, it's not Epstein-Barr reactivation. It's not CMV reactivation. It's not Lyme, and I think that's how we've kind of framed our development of diagnostic to decide on that. So we get pure long COVID in our trial.

Robert F. Kennedy (02:04:28):

I would ask all of you, including Dr. Iwasaki, what is your confidence that you can distinguish between Lyme, and long COVID, and short COVID, for example?

Bruce Patterson (02:04:39):

Well, we've published that already in two papers, so we're very confident. We've studied over four oh patients in each of those papers, and we have real world data on over 12,000 patients. So we have supreme confidence. If we had more bandwidth and more people, we would be submitting our drug trial and our diagnostic to the agency at the same time.

(02:05:07)
Right now, we're just trying to get our drug trial started, but we're going to use the clinical data derived from our clinical trial for the drug as our clinical portion of our biomarker studies because our biomarker is incorporated into our clinical trial design.

Robert F. Kennedy (02:05:24):

Can you comment on that, Dr. Iwasaki? Could you treat both Lyme and long COVID?

Dr. Akiko Iwasaki (02:05:30):

Yes. So I'm a basic scientist, so I collaborate with clinicians who treat both long COVID and post-Lyme. In terms of diagnosis for post-COVID, it's still challenging. I wish there was a blood biomarker that says, "Okay, you have long COVID versus you have long Lyme. You have long EVB." But these things, they're fairly overlapping. So some people may have all of these things going at the same time, while others may only have one of these things.

(02:06:01)
So I think we're not there yet, and maybe your diagnostics works well to dissociate these things, but often, patients come with multiple of these pathogens. The other thing is that people who have Lyme tend to be more susceptible to getting long COVID and other post acute infection syndromes. So it's a little bit difficult to disentangle all this, but the root cause driver may be shared, for instance, persistent pathogen, whether it be Lyme bacteria, or SARS-CoV-2 virus, or EBV, if we can treat that root cause, it may still benefit these patients. We may have to use multiple antimicrobial to get rid of all this.

Todd Young (02:06:47):

Mr. Secretary, I just wanted to pull on a thread here. Dr. Peloza and Dr. Patterson both indicated they thought it would be helpful to convene a pharma roundtable. You and I can perhaps discuss that offline or work with your team on whether that makes sense. I can tell you I have an interest regardless of perhaps convening such a roundtable on Capitol Hill. So for all watching this, know that that strikes me as something that is worthy of doing.

Robert F. Kennedy (02:07:23):

Dr. Willy Chertman, do you want to introduce yourself and give us any comments?

Willy Chertman (02:07:28):

Sure. I'm Willy Chertman. I work for the secretary and the deputy secretary as a science advisor. I actually used to work in Senator Todd Young's office where he was a champion of oversight on long COVID efforts, and I think the fact that this roundtable brings together the leadership from all parts of HHS shows that this HHS is really committed to solving hard problems, because everybody here, I think, probably agrees that long COVID, chronic Lyme, these are among the trickiest medical problems out there, and we're committed to doing it transparently.

(02:07:59)
So I'm learning a lot from everybody, and feel free to follow up with me after on the concrete ideas that you've all come up with so far.

Robert F. Kennedy (02:08:08):

Dr. Patterson, I know Senator Young has been open about his own struggles with, and I'd love to hear what your experience is and what your experience with your patients is.

Bruce Patterson (02:08:23):

I'm running a pharmaceutical company myself, and people ask me, "Why do you still see patients?" I can't tell you how valuable it's been over the last five years to see over 12,000 patients sit in front of them, hear their stories of disability, how it affects their families. There is no doubt that this is something that is so pervasive in this country, and it goes well beyond the 20 to 30 million people who have it. There's no doubt that it's more than a trillion costs to the healthcare group.

(02:09:01)
But the fact is hearing their story, symptoms, and then seeing their biomarker data, and relating the two. And testing our basic science hypotheses and approaches in a real-world case where we're seeing patients, we're using repurposed drugs, and we think it's been very successful to date, and we look forward to our trial. But that interconnection between the patient and the science is invaluable, and it's all captured in our data analytics portal where we're doing a lot of the things that have been suggested here by ourselves.

(02:09:49)
We have our data scientists who are digging into our 12,000 patients laboratory symptom data and looking at the connections and response to therapy. I mean, subjective responses to therapy are so difficult. This population has been so sick that it's really hard to say, "Well, I feel better. Maybe I'm better. I don't know if I'm better, but I'm better." But to see their immune system resetting and getting back to normal on our panel is so reassuring, not only to us, but to them that, "Hey, you know, what we're trying right now is at least working and getting your immune system back to normal." Dor the most part, we see symptoms following. I wouldn't trade that feeling for anything in the world.

Robert F. Kennedy (02:10:43):

How would you describe your success rate?

Bruce Patterson (02:10:47):

People always ask that, and I think, early on, we didn't even have a diagnostic that could separate long COVID from line. Early on, I would say 70 to 80%. It could be even higher now that we're able to say, "Well, no, you have a Long Hauler Index over six," or, "You have high interleukin eight plus high interferon gamma," or, "High interleukin 13 plus high interferon gamma, you have Lyme."

(02:11:13)
Being able to make that distinction in our real-world data, I think, has been invaluable. Maybe our success rate is over 80, 85%. But I think in terms of the clinical trial, that is absolutely critical. So please.

Michael Peluso (02:11:32):

Yeah, no, I think my perspective on this is that it's so important to learn from the experiences of patients who are trying different therapeutics and then to, like you said, get those therapeutics into clinical trials that can be done safely and with rigor to prove that a therapeutic does or does not truly work. I think we've seen some things advanced to clinical trials based on that.

(02:12:06)
For example, there have been several trials of short-term antivirals based on patient experiences. But the other thing that I just want to kind of state for the group is that often clinical trials are negative, but a negative clinical trial is not useless. We actually learn a tremendous amount from trying and not seeing an effect because we can understand whether the drug did or did not have a biological effect in the first place.

(02:12:35)
Then we can really try to hone in on whether there's a subset of people… I'd love to hear thoughts on this, whether there's a subset of people that do truly benefit, how do we understand who those people are, and then how do we identify those people for the next clinical trial, which would really give us the best opportunity to find something that truly works for a subset of people, because as we've mentioned repeatedly in this, this is a heterogeneous condition. That is a challenge, but that should not be an unsolvable problem, and I think that we can learn even from clinical trials that don't hit a home run for how to inform move forward.

Dr. Akiko Iwasaki (02:13:14):

Yeah, thank you very much, Dr. Peloza. So one of those, an example of this is the PAX LC trial. We did a Paxlovid fifteen-day course of treatment in patients with long COVID in collaboration with Pfizer, and we did not see an effect in terms of the primary outcome of improving the health of these people sufficiently.

(02:13:36)
However, we did a deep dive immunophenotyping in these people, and we are seeing some signatures that may be predictive of who recovers versus who don't. Again, it's not in everyone who took the drug, but these signatures are then going to inform us what might be the next target that we should go after.

(02:13:56)
So Dr. Peloza is absolutely right. A failed clinical trial is a learning experience, and we have to learn from each of these, because they're very expensive, laborious, and the patient's time and effort, we cannot waste that.

Hossein Estir (02:14:10):

Let me just a brief comment about, because everybody agrees that we need to accelerate clinical trials. We also agree that it's a heterogeneous problem. Paxlovid trial, how long did it take for you to start and do it? Several months, right?

Dr. Akiko Iwasaki (02:14:25):

Oh, yeah. So our Paxlovid trial was relatively quick and cheap because we did it in a decentralized trial, which is really amazing effort by Dr. Harlan Krumholz at Yale who specializes in these next-generation trial platforms. This is what I would recommend to everyone, because patient with long COVID and other post-acute infection syndromes are quite ill. Even if they wanted to participate in a trial, they're unable to come to these sites.

(02:14:56)
So we sent the phlebotomists to their homes. We send all the surveys electronically, and the drugs are sent to their homes, again, remotely. So none of the patients had to come to any given sites to do the trial, and I think it's cheaper and faster, and this is something that we should consider going forward, especially when we're having this discussion with the pharma partners.

Hossein Estir (02:15:19):

Now, my comment is that we can actually do this kind of trials on multiple hypothesis using data. In fact, we have done that, and we found that Paxlovid doesn't have any effect, and we have curated this cohort of the largest curated precision cohort in the country. 150,000 patients, 21,000 of them have unexplained chronic conditions post-COVID that associated with COVID. That's about more than 14%.

(02:15:45)
So we have this data of about 80% accuracy, which is still great given the validation. We are testing hypothesis that takes several months to just test in the standard ways. I think with the power of data, with the data that is available in all academic medical centers, we can do things like PheWAS-type analysis and look at a lot of different things and accelerate the beginning part of the trials and have the hypothesis be driven by data.

Todd Young (02:16:19):

This is a high-risk, high-reward public health condition. ARPA-H has a high-risk, high-reward model. This is why you were established as I understand it. So, Dr. Roos, I wonder whether you have a timeline for initial planning to assist with this public health condition and whether you might be able to give us a sense of when you might potentially launch or long COVID work.

Jason Roos (02:16:50):

So we've already begun this discussion in coordination with the secretary's office, and his counselors, and the community of interest here. We felt that this forum, and as we were engaging with the secretary, this forum was vital to help informing that. We don't want to just jump out and presume that we have the best path forward.

(02:17:10)
So I'm very confident in saying that, in short order after this forum that we can come up with a plan, work that through the secretary's office and get that out to the community to react to. We're talking weeks, not months, years. Speed is our middle name. As you know, our job is to accelerate better health outcomes, and we are, as I said in the beginning, very committed to doing this quickly.

(02:17:37)
To that point, one key question for me is, clearly, money is required here, so I don't want to dismiss that. But what are the barriers right now? Like, why can't we be sitting in this room next year and have that validated panel of biomarkers or have the mechanisms of action well articulated so we can move to the next step in the game? That's the thing that we're interested in, because, again, we know it's going to take money, but what are those things that are going to really give us that exponential game?

Michael Peluso (02:18:14):

Yeah, so, obviously, I do think that this can be solved with resources. I think that one of the challenges that we've had is just the timelines for reviews of proposals to kind of get them from a proposal stage to actually in action. It often takes a year or longer to get through peer review. These processes are meant to be deliberate and thoughtful, but that timeline doesn't really work for what we're talking about.

(02:18:45)
So what I'd like to see are things like dedicated review panels with expertise in these conditions so that we're not kind of starting from scratch, explaining to someone in a different field why they should care about long COVID or these related conditions.

(02:19:03)
Then I'd like to see an accelerated sort of timeline for grants in these agencies. Programs like that have existed, historically, for other conditions that are a priority like HIV. but 18 months from proposal stage to funding, at best, is not really the speed that we need to be going at. Those are structural problems that I think could be addressed.

Bruce Patterson (02:19:27):

Just to add to that, because it's such a great point, is it dissuaded us from applying for grants two years ago. We figured that we could raise the money privately quicker than we would write a grant, have it reviewed. The 18 months, I think, is very accurate. I realized that when we were submitting RO1s back in the day, and that's an impediment. To us, that was like, "We're going to go at it alone and try and raise this money." That became a slog. So you know what? I think that is a critical point to really expedite the review process and get the money moving.

Jim O'Neil (02:20:11):

So CDER at FDA has a biomarker validation process program, and obviously, this is a priority for this administration. So when you have biomarkers that are well-characterized, let-

Bruce Patterson (02:20:33):

Say, two years ago, and it was sent back to us. So I hope that's true, and I would love to resubmit it.

Jim O'Neil (02:20:41):

I'll follow up on that. Thank you for bringing it to our attention.

Robert F. Kennedy (02:20:45):

Well, we've come to the end of our session. I want to thank this extraordinary pantheon of great researchers for being here.