Why You Still Feel Sick After COVID with Dr. Nancy Klimas
If you've recovered from COVID-19 but still don't feel like yourself — the fatigue, the brain fog, the crashes after even mild exertion — you are not imagining it. And you are not alone.
In this episode of Fast Metabolism Matters, Haylie Pomroy sits down with Dr. Nancy Klimas, Director of the Institute for Neuro-Immune Medicine at Nova Southeastern University, to dig into one of the most pressing and under-addressed questions in medicine right now: why do so many people still feel sick long after COVID is "over"?
What Is Long COVID, Exactly?
Dr. Klimas brings clinical precision to a condition that is often dismissed or misunderstood. Long COVID is not simply "feeling tired after being sick." It is a complex, multi-system illness characterized by persistent symptoms that last weeks, months, or even years after the initial infection — and it involves real, measurable changes in the body.
At the center of it is something called neuroinflammation — inflammation in the brain and nervous system that disrupts everything from energy production to cognitive function to the body's ability to regulate itself.
The Spike Protein Problem
One of the most important things Dr. Klimas explains in this episode is the role of the spike protein in driving ongoing symptoms. For many long COVID patients, fragments of the SARS-CoV-2 spike protein persist in the body long after the active infection has cleared. This persistent spike protein continues to trigger an immune response — keeping the body in a state of low-grade inflammation and immune activation that never fully resolves.
This isn't a theory. It's one of the leading mechanisms being actively researched and treated at Dr. Klimas's institute.
Post-Exertional Malaise: Why "Pushing Through" Makes Things Worse
One of the most misunderstood aspects of long COVID is post-exertional malaise (PEM) — the significant worsening of symptoms that follows physical or mental exertion. For people with long COVID, what would seem like a normal day of activity can trigger a multi-day crash.
Dr. Klimas explains the physiological mechanism behind this, and why the common advice to "just push through it" can actually cause harm. Understanding PEM is essential — not just for patients, but for the doctors, family members, and employers trying to support them.
Long COVID and ME/CFS: A Critical Overlap
Dr. Klimas has spent decades studying ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome), and she draws a striking parallel in this episode: the symptom profiles of long COVID and ME/CFS overlap significantly.
This matters because ME/CFS research — though historically underfunded — has produced real insights into how these illnesses work at a biological level. The long COVID surge has brought new attention and funding to this area, and Dr. Klimas explains how that research is now accelerating treatment options for both conditions.
The Rise of POTS After COVID
Postural Orthostatic Tachycardia Syndrome (POTS) — a condition affecting the autonomic nervous system that causes heart rate spikes, dizziness, and fainting upon standing — has seen a significant increase since the pandemic began. Dr. Klimas discusses why COVID appears to trigger POTS in some patients, what it looks and feels like, and how it fits into the broader picture of post-COVID dysautonomia.
How to Talk to Your Doctor About Your Symptoms
One of the most practical parts of this conversation is Dr. Klimas's guidance on how to advocate for yourself in a medical setting. Many long COVID patients report being dismissed, misdiagnosed, or told their symptoms are anxiety or stress. Dr. Klimas offers specific language and framing that can help patients be taken seriously and get the care they need.
What's Coming: Monoclonal Antibody Trials
Dr. Klimas also shares exciting updates on monoclonal antibody trials currently underway at the Institute for Neuro-Immune Medicine. These therapies are being studied for their potential to target and clear persistent spike protein from the body — a direct intervention into one of the root mechanisms driving long COVID symptoms.
This is leading-edge research that could represent a real turning point for patients who have been struggling without answers.
About Dr. Nancy Klimas
Dr. Nancy Klimas is a clinical immunologist and one of the world's leading experts in complex, chronic immune-mediated illnesses. As Director of the Institute for Neuro-Immune Medicine and Professor and Chair of the Department of Clinical Immunology at Nova Southeastern University, she has dedicated her career to patients whose conditions have historically been dismissed by mainstream medicine.
She also serves as Director of Environmental Medicine Research at the Miami VA Medical Center GRECC, where her work extends to veterans dealing with Gulf War illness and related conditions.
Connect with Dr. Klimas:
About Haylie Pomroy
Haylie Pomroy is the Founder and CEO of The Haylie Pomroy Group and a New York Times bestselling author of The Fast Metabolism Diet. A leading health strategist with over 25 years of experience, she has worked with top medical institutions and high-profile clients to develop targeted wellness programs rooted in the philosophy that food is medicine. Her own autoimmune journey is at the heart of her work — she brings both clinical knowledge and deeply personal understanding to every conversation.
If you or someone you love is navigating long COVID, this episode is essential listening. Tune in to Fast Metabolism Matters — available wherever you listen to podcasts.
Learn more and connect with Haylie:
Transcript
Haylie Pomroy: Welcome to the podcast, where we talk about science and science-based tools for fatigue and chronic illness. I'm Haylie Pomroy, your host, number one New York Times bestselling author of The Fast Metabolism Diet. And that's right, guys, I am back in school — I am working on my PhD in neuroimmunology. As always, I'm a fierce advocate for those in need of a little bit of help and definitely a whole lot of hope.
Today we're going to talk about long COVID, and specifically we're going to talk about spike protein. So of course I asked our most favorite immunologist, Dr. Nancy Klimas, to come join us today. Dr. Klimas is the director here at the Institute for Neuroimmune Medicine. She's a professor and just a massive, massive advocate for individuals that are struggling to find answers and solutions and how we can just pull it all together and get you guys better each and every day. Dr. Klimas, thank you so much for coming again today. We love it when you join us.
Okay, we're going to tackle a tough subject. I want to talk about long COVID. Can you just bring us up to speed? I always say, talk to me like a third grader. What are we seeing? What does it mean to have long COVID?
Dr. Nancy Klimas: So long COVID is an illness that is triggered initially by having an acute COVID infection. Interestingly, you don't have to be super, super sick with it — it's not like the sickest COVID you ever had, and now I have long COVID. You can have pretty mild COVID, even asymptomatic COVID, and then end up with an illness that looks remarkably like an illness we've been studying for almost 30 years: myalgic encephalomyelitis, or chronic fatigue syndrome.
What they have in common is that both are post-viral illnesses that trigger neuroinflammation and then a chronic neuroinflammatory state. So what's going on in these illnesses has a lot of commonality. We don't know all of it — in fact, we're doing that study and doing those analytics right now. You can ask me back in about six months and I can tell you more about that. But they do have a lot in common. There's a lot of inflammation in the body as well as in the brain. There's mitochondrial dysfunction, which is where your body makes energy — so low energy states, because at the cellular level there's a low energy state. There are problems with blood flow and perfusing the tissues correctly, so it's really, really hard to move around if you're not getting a lot of oxygen to your tissues. There's a lot of fatigue related to that, and related to this post-exertional fatigue, or malaise, or pain.
Haylie Pomroy: So when you talk about post-exertional malaise or post-exertional fatigue, help us understand what that means. Does that mean that after you do something you're more tired, or you're tired coming in?
Dr. Nancy Klimas: You probably are tired coming in, but you feel a whole lot worse afterwards. And maybe not immediately afterwards, but hours later or the next day. So essentially you feel like you're having a mini relapse. It can feel like the flu, or like COVID. Because you did okay yesterday, you felt a little better, you did more than you should have, and then boom — you crashed. The next day you crashed, and that's what it is: a crash.
Haylie Pomroy: So when you talk about neuroinflammation, I'm just helping us all define this. What is neuroinflammation? Everybody's talking about inflammation as it relates to the heart, as it relates to the joints. When you bring in that first part of the word, what are we looking at?
Dr. Nancy Klimas: So inflammation is something your body naturally makes to help you get rid of an infection. It helps destroy the invading organism. So your body's all primed to make an inflammatory reaction at the site — so it's a good thing, mostly. Except when it persists after the infection is over and you still feel like you've got the flu or something all the time, because you still have all those same chemicals circulating in your blood that made you feel lousy when you had the flu.
Haylie Pomroy: So with long COVID, do they still have the COVID virus in their body? Do they still have an active infection?
Dr. Nancy Klimas: That's such a perfect question. And I'm going to say — because I don't know when you're watching this — this is July 2025, and the knowledge is changing every single day. So I'm going to tell you July 2025 knowledge, which has transformed a lot in the last six months. There's been just so much new knowledge.
This is what we know: 40% of people with long COVID have spike protein that you can measure with the most sensitive assays. The sensitivity of the blood test we use isn't perfect, so we don't know if that's everybody or if that's the best we're going to get — but 40% of people with long COVID have this spike protein still in their body. And it's puzzling, because the COVID virus is a coronavirus, in the same family as common colds. You're not supposed to keep it after it's done. There are some viruses, like chronic active hepatitis or HIV, that are famous for persisting — until you get rid of them, you're sick. But this virus, COVID, is in a family of viruses that was not supposed to persist. You're supposed to kick it all the way out of the system when you're done. A week, ten days — as soon as COVID's over, the virus should be over. You shouldn't be able to measure it a week after the infection.
Haylie Pomroy: So is the spike protein a part of the virus, or is it your body's immune response to the virus?
Dr. Nancy Klimas: It is a part of the virus. But just to make things more complicated — viruses have lots of bits and pieces. When you're infected with a virus, the RNA or DNA that codes for it gets into a coding system, and you make all these different parts of the virus, and then they assemble into a whole virus. But it's quite possible for a little chunk of DNA or RNA that codes for the spike protein to just keep coding for spike protein — and that's what you're left with.
So part of the puzzle is: what do we mean by spike protein? Is this evidence that the virus is a replicative, persisting infection that could be treated with an antiviral? Or is it more of a remnant that's just gone a little nuts and continues to be made after the infection is over? In that case, your own body is making one of the most inflammation-triggering parts of the virus. And it's the part that binds to something called the ACE2 receptor, which is on your blood vessels and all over the body. So now the immune system sees this foreign protein stuck on a blood vessel wall and creates inflammation there trying to clear it — a low-grade vasculitis.
Haylie Pomroy: Is spike protein only from native coronavirus, or can it come from the coronavirus vaccine?
Dr. Nancy Klimas: What a great question. The mRNA vaccine essentially codes for spike protein, but it is designed in a way that you only see spike protein for two weeks and then it's gone. So you're not supposed to be able to persistently make spike protein after you've had an mRNA vaccine. And to be clear — we don't have data to suggest that mRNA vaccines cause persistent spike protein. The data on persistence is after COVID infection. The infection.
Haylie Pomroy: When we were together at Cambridge this year, there were large population studies being presented. And what was surprising to me was how, if you took the title or diagnosis away from a person with long COVID versus a person with ME/CFS, the profiles were almost identical.
Dr. Nancy Klimas: That's true. That's part of the reason why our group jumped in to try to help the long COVID problem — we have 30 years of experience with ME/CFS, and it would seem wrong to leave that experience on the table and act like long COVID is something new.
Haylie Pomroy: Is that because this was the instigator of a cascade of responses in the body, like maybe Epstein-Barr virus or an environmental toxin?
Dr. Nancy Klimas: So if you just flip your brain to ME/CFS for a moment and say, here is an illness that's the consequence of something acute that was highly inflammatory — it could have been a toxic exposure, a mold exposure. But more often than not, it's a viral exposure, almost always, actually, and way more often than any other reason. Some virus, maybe not well defined, because we don't go to the doctor when we have viruses and we don't do big tests to find out what it is. But it's clearly able to follow mononucleosis, which is a common one. It's also after the flu or something that really triggers the on button.
I can also say there's a sex bias here. Women get chronic inflammatory conditions far more often than men. There's a reason for that — most of the inflammation coding is on the X chromosome, and women have two of them. So there's a reason women tend to be more prone to chronic inflammatory conditions like autoimmunity. More common in women, absolutely. More common post-acute infection, absolutely. And then you look at the whole list — post-exertional malaise is a uniquely neuroinflammatory event. You don't see it in very many illnesses.
Haylie Pomroy: Because you're supposed to get energy from working out. Working out excites your mitochondria, increases blood flow, increases nutrient delivery, increases oxygen delivery and metabolism. And then in these patients, when we're running VO2 maxes or looking at blood gases, they crash after exercise.
Dr. Nancy Klimas: There's so much to this — it's a whole other episode. But neuroinflammation is part of it, and also perfusion. If your body can't recruit more blood flow when it needs it, like to a muscle or to your brain, then you're going to create a lot of oxidative stress in that space, cause a lot of inflammation downstream of that, and then you're going to have a crash.
Haylie Pomroy: And is that why, even on a basic level, we do things like compression stockings, raising your legs up, adding fluids, giving IV fluids?
Dr. Nancy Klimas: Part of it, yes. Because people with ME/CFS and people with long COVID have the part of your body that regulates your blood pressure, your pulse, and how constricted your vessels are — called the autonomic nervous system — and that is not working correctly.
I'm going to put it back to the brain for a moment, because brain fog is probably one of the most concerning symptoms that all of these patients have. It's also what takes them out of work. People will drag their tired, exhausted bodies to their jobs, but if they can't think when they get there, they're not going to keep that job.
Haylie Pomroy: And from our community's perspective, it's the most gaslit symptom.
Dr. Nancy Klimas: Oh, absolutely. But it's so real. Brain fog — it sounds like nothing. But think about this: when I do math in my head, my resting blood flow in my brain is 90 cc's a minute. When I do math, I double it — 180. And that's to deliver oxygen and glucose to the area where I need it. I have such a sensitive autonomic nervous system that it recognizes where I need more blood and delivers it.
But in ME/CFS — and now we know in long COVID — there's no ramp up. They just get that resting, as-if-you're-still-asleep level of blood flow in their brain. No way to call for more. That's true in their muscles as well. This system that was meant to deliver oxygen and glucose to your mitochondria to make energy — it's just not effective. So essentially you're trying to do a lot of work as if your body was asleep. It's like hibernation.
How does a bear hibernate? It reduces its blood flow, its metabolic levels drop, and it sits there through a whole season not needing food or movement. But we're supposed to keep the organism alive and functioning — just right.
Haylie Pomroy: And I've seen so many young people — really driven, inspired individuals — and I think because of who they are, they push themselves through probably 70% of the symptoms until it becomes too much. I wish they were coming to us earlier, from a preventative standpoint, or when something just feels off. They come a little late.
Dr. Nancy Klimas: And the other thing is that pushing through makes people sicker. That's why it's really important to come early. Pushing through will absolutely cause crash after crash after crash.
Haylie Pomroy: You don't get better by ignoring the symptoms, and you don't get better by toughening up. These are already tough people.
I want to pull back for a second into spike protein, because I want to make sure we all understand the immune system's response to this. And I'm going to go there — there are some good things that have come out of COVID. I wish it didn't happen. But there were very few doctors looking at ME/CFS before. Most of our patients had seen five, ten, fifteen, twenty doctors before they landed in our clinic — whether their symptoms were mysterious, or weren't believed, or they were gaslit into thinking it was all in their mind. With COVID, whether it's a primary care physician or an OB-GYN, they were seeing these patients having long COVID and they couldn't deny it anymore.
Dr. Nancy Klimas: There's just a lot more of it. There's an illness called Postural Orthostatic Tachycardia Syndrome — POTS. It's one of the diagnoses you might get when you have long COVID or ME/CFS, because it's one of the more severe ends of the autonomic problem I was talking about. We went from one million cases of diagnosed POTS pre-pandemic to four million post-pandemic. That's just long COVID, in a very short window of time. No one knew what POTS was before. Now all the doctors know what POTS is, because everyone has patients with it.
Haylie Pomroy: And it's interesting because with ME/CFS, the chronic fatigue label was so reductionistic, in my opinion — there was so much more complexity in the inflammatory cascade happening in the body. And I love that we're seeing new biomarkers, new testing, and hopefully new treatments.
Dr. Nancy Klimas: And the big difference between ME/CFS and long COVID science-wise is the investment. We went from an average investment of $12 million a year for the whole country for ME/CFS to $1.15 billion for long COVID. The difference is doing studies with 30 people and doing studies with 30,000 people — and then you have definitive data you can't ignore. This is real science. Here's your hard data. Follow it. And we are getting some really good science.
I know for the long COVID community this feels like a long time. But you can't begin to understand what the ME/CFS community has been going through for 30 long years, waiting for big answers while doing science on a trickle of investment.
Haylie Pomroy: We had a community member write in the other day saying she went to see her physician to get diagnostics run to see if she had long COVID — and the doctor told her that long COVID is just another made-up syndrome. We're hearing a lot of that. But from a science perspective, you cannot look at the science and say this is made up. Someone cannot fake mitochondrial insufficiency.
Dr. Nancy Klimas: Seriously — did you walk into the doctor's office and say, 'I think today I will fake cardiovascular inflammatory biomarkers'? Here's my D-dimer. Here's my pulse going up to 110 beats when I stand. I'm just pretending. All the diagnostic devices would have to be false and irrelevant for that to be true.
But I want to say one thing before I go further — and this is to my fellow clinicians, very clearly. We did a study after a major hurricane in the ME/CFS community, and we measured for PTSD. Our control group was in an area that had no hurricane. Both the ME/CFS patients who were hit by the hurricane and those in the control group had very high PTSD levels. So don't jump to say this is a psychiatric condition — that is not the point. When you do a PTSD assessment, you ask about recurring nightmares. And the recurring nightmare was the way they were treated by their physicians. We gave them PTSD by saying things like 'it's all in your head.' The most dismissive, patronizing treatment you can imagine. Most patients walk out of those appointments hopeless — sometimes battered and beaten up after waiting six months for an appointment with a specialist who totally dismissed them.
We swear, first do no harm, the day we graduate from medical school. And part of doing no harm is being willing to say, 'I don't know. I believe you. This isn't the right place for you because I don't know. But that doesn't mean it's not real.' If you haven't gotten some education about long COVID and ME/CFS, the CDC and NIH both have webpages you can go to right now and learn simple things that will tell you whether or not these patients have this illness.
But one of the most important things is this: post-exertional malaise is an extremely rare symptom. You see it in multiple sclerosis. You see it in myasthenia gravis — two autoimmune diseases that cause neuroinflammation in the brain. And then you see it in ME/CFS and long COVID. That's your list. There's not a hard differential diagnosis when someone walks in with that symptom. Your obligation is to make sure they don't have the other two, and then do some further listening. If you see dysautonomia symptoms — tachycardia when standing, palpitations, dizziness — or cognitive fog, brain fog, generalized systemic pain, sometimes fibromyalgia, these are all comorbid conditions and symptoms that go along with these illnesses.
Haylie Pomroy: I like post-exertional malaise as a litmus test. And so many people in our community have been told by their doctors, 'You need to get out and get some exercise. I don't want you back here until you're doing cardio three days a week. I want you to hire a trainer.'
Dr. Nancy Klimas: How many times have we seen that. I've had so many patients with such sad stories — people that were really improving, and then they went and got a personal trainer, and they were all the way back to ground zero. After scrambling up for a year or two years to get to the point where they felt like they could do a little something more.
The rule of thumb with exercise is: don't do very much of it. You can do a little. If you think you can do three minutes of exercise — even just walking or something gentle — then do three minutes and see how you do. If the next day you're okay, you can do that every day, and then add another three minutes in a separate episode — not all at once. The worst thing you can do is try to get to 20 or 25 or 30 minutes of cardio; that will always put you down. But you could conceivably work up to 30 minutes by doing ten three-minute episodes over three months of gradually working your way back to that level of fitness.
Haylie Pomroy: Even though it's become common, it's not normal. I don't want people to think that because we're seeing so many people with POTS and post-exertional malaise, that's just the new norm. It's not normal.
What are you most excited about in terms of what's coming — both in long COVID and in how it's going to bridge into ME/CFS?
Dr. Nancy Klimas: They have so much more in common than they have apart. Frankly, COVID itself is the thing that's apart — the trigger and that ACE2 receptor binding that makes their vascular system more at risk for inflammation. That's going to be the big difference when we line up all the pathophysiology of these two illnesses. Otherwise they're going to align. We've got people whose immune systems don't work well. Specifically, their natural killer cells — their innate immune system, their ancient immune system that can rid you of chronic viruses and cancer — are not working well. That's a really important feature of both illnesses, and they're very, very close to identical on that.
Haylie Pomroy: Which is odd, because they're designed to bounce back after insults.
Dr. Nancy Klimas: Yes. But there is this thing called immune exhaustion — and that's what we're seeing with these NK cells, and also with the rest of the immune system that deals with viruses. Immune exhaustion, or immune senescence, is what happens to an immune system when it's under constant barrage — constantly activated, constantly working. It uses up all its resources and goes into this sort of save-the-cell, quiet-down mode. It becomes non-adaptive. If you think of long COVID and ME/CFS as essentially going into self-protection mode — hunkering down and dropping all function to a baseline — that's essentially what the immune system is doing.
And here's the other piece: when the immune system doesn't function well, all of us have latent viruses — our childhood viruses that are known to go dormant. One of them is the mononucleosis virus, Epstein-Barr. Another is CMV. EBV is present in about 98% of adults, CMV in about 88% — it's really high. Both of these viruses, when they reactivate, cause a lot of immune noise and signal a lot of inflammation. And they're both known to trigger autoimmunity.
So as you go through this illness over time, you start out with perhaps persisting COVID — maybe for a long, long time, we don't know — and that's driving the immune system into an inflamed, exhausted, non-functional state. Now your latent viruses start to reactivate: EBV, CMV, HHV-6, Coxsackie. All these viruses floating around in different systems and organs start reactivating at a low level, smoldering, noisy, keeping the immune system trying to respond and creating more inflammation. That viral reactivation picture is well documented in both long COVID and ME/CFS — and it's a target for therapy.
Haylie Pomroy: And they were finding leftover COVID in the GI tract?
Dr. Nancy Klimas: They were finding evidence that it wasn't just spike protein — it actually was replicating COVID. That's a huge deal. Because if it's a replicative, persisting infection, we can insert antivirals that mess up replication and clear the virus completely. We can completely cure hepatitis C. HIV — we can completely suppress it and these patients live long, healthy lives. So there are different ways to treat persistent infection than trying to treat a remnant of an old infection that's still making something that's messing up your immune system.
Haylie Pomroy: And is spike protein a protein that our bodies can digest or break down?
Dr. Nancy Klimas: The system is meant to clean the mess up. You have these cells called macrophages — they go around hunting for stuff, suck it inside, take it away from the area, and digest it with enzymes. We have that cleanup system built into our cells, and we have it in the brain as well. It's very unlikely that you have spike protein from something you had three years ago still circulating on its own. You made that spike protein recently — there's something in the system causing continued production.
And when they did organ biopsies in China, they found that 80% of long COVID patients had COVID antigen in solid tissue. So when we say 40% of long COVID patients have spike protein in their bloodstream, we're probably undercounting. We don't really know how many people are dealing with it, because it depends on where you look.
Haylie Pomroy: I always tell clients who maybe fall in that 60% who test negative for spike protein: our labs are so good that it's like getting in a helicopter and looking at the freeway system of downtown LA. It's better than just sitting in a car and looking left and right, but there's also a freeway system in New York and in Chicago. Just because there wasn't a blue car on the 405 freeway at the exact moment they drew your blood doesn't mean you don't have it. It just means that one box has been kind of checked off.
Dr. Nancy Klimas: It's all about compartments — did you look in the right place? And can you look in that place? There's a virus called Coxsackie that's a plague to ME/CFS, and increasingly I think we understand it to be true of long COVID as well. It hangs out in muscle and gut — you don't find it in the bloodstream. John Chia did amazing work biopsying intestine and gut in 300-plus patients. And he found the actual replicating virus — not the antibody signature, but the actual virus — along with replicating EBV and replicating CMV in the gut, where we weren't looking at all. We were just pulling blood.
Haylie Pomroy: We're currently doing a trial with monoclonal antibodies. Can you help us understand that? And is it accessible to people in our community?
Dr. Nancy Klimas: Depending on when you're watching this — as of July 2025, we are recruiting. You can find our webpage, which has a link to register for any of our long COVID studies through a general registry, and then we reach out to tell you more about the studies we're doing right now.
That antibody study is trying to mop up spike protein — that's its target. We're using the AstraZeneca product. It's a long-acting, six-month, single-injection monoclonal antibody that targets spike protein. It's a placebo-controlled study. It's just off the ground. We don't know if it's going to work yet.
The theory is this: whether spike protein is being made by a replicative virus or by cells that have the machinery to make it, the monoclonal antibody will bind to the spike protein and signal to the immune system to come take care of it. It would immune-complex with circulating spike protein and the liver clears it. If it's coming out of a cell, it would flag that cell as foreign. If there's actually a replicating virus in a cell, it would target that as well, because it would be making spike protein. So it works against active infection, persistent infection, or just antigen itself.
I also recommend everyone go to the Recovery Initiative website — they have great webcasts and resources. They have several silos of interventions they're working on, one of which targets replicative virus and spike protein. They've just finished a short Paxlovid study that didn't show results, but now they're doing a long Paxlovid study. In other viruses that persist, you needed more than one antiviral to get it under control — a cocktail. That's how we managed hepatitis and HIV. So this is an evolving thing. The investment in long COVID is already paying fruit — in three years since late 2022, the mechanisms have been worked out and big, definitive trials are now underway. It's an exciting time. And we do hope that the ME/CFS community will also benefit from the discoveries.
Haylie Pomroy: We've lost good years — ten to twenty — bypassing the step of believing patients. We believe you. We lost so much time in ME/CFS.
Dr. Nancy Klimas: I sat as the only non-psychiatrist on NIH expert panels for years, where every single expert was a psychiatrist except for me. Long COVID people should thank the ME/CFS people who suffered through that, because it was their advocacy that pushed the NIH and other federal agencies to stop encouraging that kind of thinking.
Haylie Pomroy: Dr. Klimas, it is always such an honor and a privilege to have you on. I love the other aspect I'll say about going through the pandemic — how empowered people have become to learn about their bodies and their immune systems for the first time. Terms like cytokine storm, spike protein, understanding that viruses are cleared through the liver, that macrophages chomp them up with enzymes — I think the more we learn about this amazing, biodiverse body, and the more scientists like yourself train and teach the next generation, the closer we get to real solutions for people in need. Thank you. Promise me you'll come back.
Dr. Nancy Klimas: I will always be back. You just have to ask me. Thank you for trying to help these patients. I want to underscore hope — the progress in this field is astronomical in the last two years. If you are feeling hopeless because of long COVID or ME/CFS, please hear me say that we are translating the understanding of the underlying causes of these illnesses into clinical trials. Big trials. Definitive trials. And we are seeing patients get well in our practice. Even without the trials, we take care of our patients with the tools we have, which aren't shabby at all. It's just a question of treating the whole thing and not just little bits and pieces. It's very important to be hopeful at this time.
Haylie Pomroy: And it's exciting and inspiring. And as always, you guys, we're here for you. Post your questions, keep commenting — it helps us generate new topics, know what you need, and get you what you deserve. Thank you.
If you've recovered from COVID-19 but still don't feel like yourself — the fatigue, the brain fog, the crashes after even mild exertion — you are not imagining it. And you are not alone.
In this episode of Fast Metabolism Matters, Haylie Pomroy sits down with Dr. Nancy Klimas, Director of the Institute for Neuro-Immune Medicine at Nova Southeastern University, to dig into one of the most pressing and under-addressed questions in medicine right now: why do so many people still feel sick long after COVID is "over"?
What Is Long COVID, Exactly?
Dr. Klimas brings clinical precision to a condition that is often dismissed or misunderstood. Long COVID is not simply "feeling tired after being sick." It is a complex, multi-system illness characterized by persistent symptoms that last weeks, months, or even years after the initial infection — and it involves real, measurable changes in the body.
At the center of it is something called neuroinflammation — inflammation in the brain and nervous system that disrupts everything from energy production to cognitive function to the body's ability to regulate itself.
The Spike Protein Problem
One of the most important things Dr. Klimas explains in this episode is the role of the spike protein in driving ongoing symptoms. For many long COVID patients, fragments of the SARS-CoV-2 spike protein persist in the body long after the active infection has cleared. This persistent spike protein continues to trigger an immune response — keeping the body in a state of low-grade inflammation and immune activation that never fully resolves.
This isn't a theory. It's one of the leading mechanisms being actively researched and treated at Dr. Klimas's institute.
Post-Exertional Malaise: Why "Pushing Through" Makes Things Worse
One of the most misunderstood aspects of long COVID is post-exertional malaise (PEM) — the significant worsening of symptoms that follows physical or mental exertion. For people with long COVID, what would seem like a normal day of activity can trigger a multi-day crash.
Dr. Klimas explains the physiological mechanism behind this, and why the common advice to "just push through it" can actually cause harm. Understanding PEM is essential — not just for patients, but for the doctors, family members, and employers trying to support them.
Long COVID and ME/CFS: A Critical Overlap
Dr. Klimas has spent decades studying ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome), and she draws a striking parallel in this episode: the symptom profiles of long COVID and ME/CFS overlap significantly.
This matters because ME/CFS research — though historically underfunded — has produced real insights into how these illnesses work at a biological level. The long COVID surge has brought new attention and funding to this area, and Dr. Klimas explains how that research is now accelerating treatment options for both conditions.
The Rise of POTS After COVID
Postural Orthostatic Tachycardia Syndrome (POTS) — a condition affecting the autonomic nervous system that causes heart rate spikes, dizziness, and fainting upon standing — has seen a significant increase since the pandemic began. Dr. Klimas discusses why COVID appears to trigger POTS in some patients, what it looks and feels like, and how it fits into the broader picture of post-COVID dysautonomia.
How to Talk to Your Doctor About Your Symptoms
One of the most practical parts of this conversation is Dr. Klimas's guidance on how to advocate for yourself in a medical setting. Many long COVID patients report being dismissed, misdiagnosed, or told their symptoms are anxiety or stress. Dr. Klimas offers specific language and framing that can help patients be taken seriously and get the care they need.
What's Coming: Monoclonal Antibody Trials
Dr. Klimas also shares exciting updates on monoclonal antibody trials currently underway at the Institute for Neuro-Immune Medicine. These therapies are being studied for their potential to target and clear persistent spike protein from the body — a direct intervention into one of the root mechanisms driving long COVID symptoms.
This is leading-edge research that could represent a real turning point for patients who have been struggling without answers.
About Dr. Nancy Klimas
Dr. Nancy Klimas is a clinical immunologist and one of the world's leading experts in complex, chronic immune-mediated illnesses. As Director of the Institute for Neuro-Immune Medicine and Professor and Chair of the Department of Clinical Immunology at Nova Southeastern University, she has dedicated her career to patients whose conditions have historically been dismissed by mainstream medicine.
She also serves as Director of Environmental Medicine Research at the Miami VA Medical Center GRECC, where her work extends to veterans dealing with Gulf War illness and related conditions.
Connect with Dr. Klimas:
About Haylie Pomroy
Haylie Pomroy is the Founder and CEO of The Haylie Pomroy Group and a New York Times bestselling author of The Fast Metabolism Diet. A leading health strategist with over 25 years of experience, she has worked with top medical institutions and high-profile clients to develop targeted wellness programs rooted in the philosophy that food is medicine. Her own autoimmune journey is at the heart of her work — she brings both clinical knowledge and deeply personal understanding to every conversation.
If you or someone you love is navigating long COVID, this episode is essential listening. Tune in to Fast Metabolism Matters — available wherever you listen to podcasts.
Learn more and connect with Haylie:
Transcript
Haylie Pomroy: Welcome to the podcast, where we talk about science and science-based tools for fatigue and chronic illness. I'm Haylie Pomroy, your host, number one New York Times bestselling author of The Fast Metabolism Diet. And that's right, guys, I am back in school — I am working on my PhD in neuroimmunology. As always, I'm a fierce advocate for those in need of a little bit of help and definitely a whole lot of hope.
Today we're going to talk about long COVID, and specifically we're going to talk about spike protein. So of course I asked our most favorite immunologist, Dr. Nancy Klimas, to come join us today. Dr. Klimas is the director here at the Institute for Neuroimmune Medicine. She's a professor and just a massive, massive advocate for individuals that are struggling to find answers and solutions and how we can just pull it all together and get you guys better each and every day. Dr. Klimas, thank you so much for coming again today. We love it when you join us.
Okay, we're going to tackle a tough subject. I want to talk about long COVID. Can you just bring us up to speed? I always say, talk to me like a third grader. What are we seeing? What does it mean to have long COVID?
Dr. Nancy Klimas: So long COVID is an illness that is triggered initially by having an acute COVID infection. Interestingly, you don't have to be super, super sick with it — it's not like the sickest COVID you ever had, and now I have long COVID. You can have pretty mild COVID, even asymptomatic COVID, and then end up with an illness that looks remarkably like an illness we've been studying for almost 30 years: myalgic encephalomyelitis, or chronic fatigue syndrome.
What they have in common is that both are post-viral illnesses that trigger neuroinflammation and then a chronic neuroinflammatory state. So what's going on in these illnesses has a lot of commonality. We don't know all of it — in fact, we're doing that study and doing those analytics right now. You can ask me back in about six months and I can tell you more about that. But they do have a lot in common. There's a lot of inflammation in the body as well as in the brain. There's mitochondrial dysfunction, which is where your body makes energy — so low energy states, because at the cellular level there's a low energy state. There are problems with blood flow and perfusing the tissues correctly, so it's really, really hard to move around if you're not getting a lot of oxygen to your tissues. There's a lot of fatigue related to that, and related to this post-exertional fatigue, or malaise, or pain.
Haylie Pomroy: So when you talk about post-exertional malaise or post-exertional fatigue, help us understand what that means. Does that mean that after you do something you're more tired, or you're tired coming in?
Dr. Nancy Klimas: You probably are tired coming in, but you feel a whole lot worse afterwards. And maybe not immediately afterwards, but hours later or the next day. So essentially you feel like you're having a mini relapse. It can feel like the flu, or like COVID. Because you did okay yesterday, you felt a little better, you did more than you should have, and then boom — you crashed. The next day you crashed, and that's what it is: a crash.
Haylie Pomroy: So when you talk about neuroinflammation, I'm just helping us all define this. What is neuroinflammation? Everybody's talking about inflammation as it relates to the heart, as it relates to the joints. When you bring in that first part of the word, what are we looking at?
Dr. Nancy Klimas: So inflammation is something your body naturally makes to help you get rid of an infection. It helps destroy the invading organism. So your body's all primed to make an inflammatory reaction at the site — so it's a good thing, mostly. Except when it persists after the infection is over and you still feel like you've got the flu or something all the time, because you still have all those same chemicals circulating in your blood that made you feel lousy when you had the flu.
Haylie Pomroy: So with long COVID, do they still have the COVID virus in their body? Do they still have an active infection?
Dr. Nancy Klimas: That's such a perfect question. And I'm going to say — because I don't know when you're watching this — this is July 2025, and the knowledge is changing every single day. So I'm going to tell you July 2025 knowledge, which has transformed a lot in the last six months. There's been just so much new knowledge.
This is what we know: 40% of people with long COVID have spike protein that you can measure with the most sensitive assays. The sensitivity of the blood test we use isn't perfect, so we don't know if that's everybody or if that's the best we're going to get — but 40% of people with long COVID have this spike protein still in their body. And it's puzzling, because the COVID virus is a coronavirus, in the same family as common colds. You're not supposed to keep it after it's done. There are some viruses, like chronic active hepatitis or HIV, that are famous for persisting — until you get rid of them, you're sick. But this virus, COVID, is in a family of viruses that was not supposed to persist. You're supposed to kick it all the way out of the system when you're done. A week, ten days — as soon as COVID's over, the virus should be over. You shouldn't be able to measure it a week after the infection.
Haylie Pomroy: So is the spike protein a part of the virus, or is it your body's immune response to the virus?
Dr. Nancy Klimas: It is a part of the virus. But just to make things more complicated — viruses have lots of bits and pieces. When you're infected with a virus, the RNA or DNA that codes for it gets into a coding system, and you make all these different parts of the virus, and then they assemble into a whole virus. But it's quite possible for a little chunk of DNA or RNA that codes for the spike protein to just keep coding for spike protein — and that's what you're left with.
So part of the puzzle is: what do we mean by spike protein? Is this evidence that the virus is a replicative, persisting infection that could be treated with an antiviral? Or is it more of a remnant that's just gone a little nuts and continues to be made after the infection is over? In that case, your own body is making one of the most inflammation-triggering parts of the virus. And it's the part that binds to something called the ACE2 receptor, which is on your blood vessels and all over the body. So now the immune system sees this foreign protein stuck on a blood vessel wall and creates inflammation there trying to clear it — a low-grade vasculitis.
Haylie Pomroy: Is spike protein only from native coronavirus, or can it come from the coronavirus vaccine?
Dr. Nancy Klimas: What a great question. The mRNA vaccine essentially codes for spike protein, but it is designed in a way that you only see spike protein for two weeks and then it's gone. So you're not supposed to be able to persistently make spike protein after you've had an mRNA vaccine. And to be clear — we don't have data to suggest that mRNA vaccines cause persistent spike protein. The data on persistence is after COVID infection. The infection.
Haylie Pomroy: When we were together at Cambridge this year, there were large population studies being presented. And what was surprising to me was how, if you took the title or diagnosis away from a person with long COVID versus a person with ME/CFS, the profiles were almost identical.
Dr. Nancy Klimas: That's true. That's part of the reason why our group jumped in to try to help the long COVID problem — we have 30 years of experience with ME/CFS, and it would seem wrong to leave that experience on the table and act like long COVID is something new.
Haylie Pomroy: Is that because this was the instigator of a cascade of responses in the body, like maybe Epstein-Barr virus or an environmental toxin?
Dr. Nancy Klimas: So if you just flip your brain to ME/CFS for a moment and say, here is an illness that's the consequence of something acute that was highly inflammatory — it could have been a toxic exposure, a mold exposure. But more often than not, it's a viral exposure, almost always, actually, and way more often than any other reason. Some virus, maybe not well defined, because we don't go to the doctor when we have viruses and we don't do big tests to find out what it is. But it's clearly able to follow mononucleosis, which is a common one. It's also after the flu or something that really triggers the on button.
I can also say there's a sex bias here. Women get chronic inflammatory conditions far more often than men. There's a reason for that — most of the inflammation coding is on the X chromosome, and women have two of them. So there's a reason women tend to be more prone to chronic inflammatory conditions like autoimmunity. More common in women, absolutely. More common post-acute infection, absolutely. And then you look at the whole list — post-exertional malaise is a uniquely neuroinflammatory event. You don't see it in very many illnesses.
Haylie Pomroy: Because you're supposed to get energy from working out. Working out excites your mitochondria, increases blood flow, increases nutrient delivery, increases oxygen delivery and metabolism. And then in these patients, when we're running VO2 maxes or looking at blood gases, they crash after exercise.
Dr. Nancy Klimas: There's so much to this — it's a whole other episode. But neuroinflammation is part of it, and also perfusion. If your body can't recruit more blood flow when it needs it, like to a muscle or to your brain, then you're going to create a lot of oxidative stress in that space, cause a lot of inflammation downstream of that, and then you're going to have a crash.
Haylie Pomroy: And is that why, even on a basic level, we do things like compression stockings, raising your legs up, adding fluids, giving IV fluids?
Dr. Nancy Klimas: Part of it, yes. Because people with ME/CFS and people with long COVID have the part of your body that regulates your blood pressure, your pulse, and how constricted your vessels are — called the autonomic nervous system — and that is not working correctly.
I'm going to put it back to the brain for a moment, because brain fog is probably one of the most concerning symptoms that all of these patients have. It's also what takes them out of work. People will drag their tired, exhausted bodies to their jobs, but if they can't think when they get there, they're not going to keep that job.
Haylie Pomroy: And from our community's perspective, it's the most gaslit symptom.
Dr. Nancy Klimas: Oh, absolutely. But it's so real. Brain fog — it sounds like nothing. But think about this: when I do math in my head, my resting blood flow in my brain is 90 cc's a minute. When I do math, I double it — 180. And that's to deliver oxygen and glucose to the area where I need it. I have such a sensitive autonomic nervous system that it recognizes where I need more blood and delivers it.
But in ME/CFS — and now we know in long COVID — there's no ramp up. They just get that resting, as-if-you're-still-asleep level of blood flow in their brain. No way to call for more. That's true in their muscles as well. This system that was meant to deliver oxygen and glucose to your mitochondria to make energy — it's just not effective. So essentially you're trying to do a lot of work as if your body was asleep. It's like hibernation.
How does a bear hibernate? It reduces its blood flow, its metabolic levels drop, and it sits there through a whole season not needing food or movement. But we're supposed to keep the organism alive and functioning — just right.
Haylie Pomroy: And I've seen so many young people — really driven, inspired individuals — and I think because of who they are, they push themselves through probably 70% of the symptoms until it becomes too much. I wish they were coming to us earlier, from a preventative standpoint, or when something just feels off. They come a little late.
Dr. Nancy Klimas: And the other thing is that pushing through makes people sicker. That's why it's really important to come early. Pushing through will absolutely cause crash after crash after crash.
Haylie Pomroy: You don't get better by ignoring the symptoms, and you don't get better by toughening up. These are already tough people.
I want to pull back for a second into spike protein, because I want to make sure we all understand the immune system's response to this. And I'm going to go there — there are some good things that have come out of COVID. I wish it didn't happen. But there were very few doctors looking at ME/CFS before. Most of our patients had seen five, ten, fifteen, twenty doctors before they landed in our clinic — whether their symptoms were mysterious, or weren't believed, or they were gaslit into thinking it was all in their mind. With COVID, whether it's a primary care physician or an OB-GYN, they were seeing these patients having long COVID and they couldn't deny it anymore.
Dr. Nancy Klimas: There's just a lot more of it. There's an illness called Postural Orthostatic Tachycardia Syndrome — POTS. It's one of the diagnoses you might get when you have long COVID or ME/CFS, because it's one of the more severe ends of the autonomic problem I was talking about. We went from one million cases of diagnosed POTS pre-pandemic to four million post-pandemic. That's just long COVID, in a very short window of time. No one knew what POTS was before. Now all the doctors know what POTS is, because everyone has patients with it.
Haylie Pomroy: And it's interesting because with ME/CFS, the chronic fatigue label was so reductionistic, in my opinion — there was so much more complexity in the inflammatory cascade happening in the body. And I love that we're seeing new biomarkers, new testing, and hopefully new treatments.
Dr. Nancy Klimas: And the big difference between ME/CFS and long COVID science-wise is the investment. We went from an average investment of $12 million a year for the whole country for ME/CFS to $1.15 billion for long COVID. The difference is doing studies with 30 people and doing studies with 30,000 people — and then you have definitive data you can't ignore. This is real science. Here's your hard data. Follow it. And we are getting some really good science.
I know for the long COVID community this feels like a long time. But you can't begin to understand what the ME/CFS community has been going through for 30 long years, waiting for big answers while doing science on a trickle of investment.
Haylie Pomroy: We had a community member write in the other day saying she went to see her physician to get diagnostics run to see if she had long COVID — and the doctor told her that long COVID is just another made-up syndrome. We're hearing a lot of that. But from a science perspective, you cannot look at the science and say this is made up. Someone cannot fake mitochondrial insufficiency.
Dr. Nancy Klimas: Seriously — did you walk into the doctor's office and say, 'I think today I will fake cardiovascular inflammatory biomarkers'? Here's my D-dimer. Here's my pulse going up to 110 beats when I stand. I'm just pretending. All the diagnostic devices would have to be false and irrelevant for that to be true.
But I want to say one thing before I go further — and this is to my fellow clinicians, very clearly. We did a study after a major hurricane in the ME/CFS community, and we measured for PTSD. Our control group was in an area that had no hurricane. Both the ME/CFS patients who were hit by the hurricane and those in the control group had very high PTSD levels. So don't jump to say this is a psychiatric condition — that is not the point. When you do a PTSD assessment, you ask about recurring nightmares. And the recurring nightmare was the way they were treated by their physicians. We gave them PTSD by saying things like 'it's all in your head.' The most dismissive, patronizing treatment you can imagine. Most patients walk out of those appointments hopeless — sometimes battered and beaten up after waiting six months for an appointment with a specialist who totally dismissed them.
We swear, first do no harm, the day we graduate from medical school. And part of doing no harm is being willing to say, 'I don't know. I believe you. This isn't the right place for you because I don't know. But that doesn't mean it's not real.' If you haven't gotten some education about long COVID and ME/CFS, the CDC and NIH both have webpages you can go to right now and learn simple things that will tell you whether or not these patients have this illness.
But one of the most important things is this: post-exertional malaise is an extremely rare symptom. You see it in multiple sclerosis. You see it in myasthenia gravis — two autoimmune diseases that cause neuroinflammation in the brain. And then you see it in ME/CFS and long COVID. That's your list. There's not a hard differential diagnosis when someone walks in with that symptom. Your obligation is to make sure they don't have the other two, and then do some further listening. If you see dysautonomia symptoms — tachycardia when standing, palpitations, dizziness — or cognitive fog, brain fog, generalized systemic pain, sometimes fibromyalgia, these are all comorbid conditions and symptoms that go along with these illnesses.
Haylie Pomroy: I like post-exertional malaise as a litmus test. And so many people in our community have been told by their doctors, 'You need to get out and get some exercise. I don't want you back here until you're doing cardio three days a week. I want you to hire a trainer.'
Dr. Nancy Klimas: How many times have we seen that. I've had so many patients with such sad stories — people that were really improving, and then they went and got a personal trainer, and they were all the way back to ground zero. After scrambling up for a year or two years to get to the point where they felt like they could do a little something more.
The rule of thumb with exercise is: don't do very much of it. You can do a little. If you think you can do three minutes of exercise — even just walking or something gentle — then do three minutes and see how you do. If the next day you're okay, you can do that every day, and then add another three minutes in a separate episode — not all at once. The worst thing you can do is try to get to 20 or 25 or 30 minutes of cardio; that will always put you down. But you could conceivably work up to 30 minutes by doing ten three-minute episodes over three months of gradually working your way back to that level of fitness.
Haylie Pomroy: Even though it's become common, it's not normal. I don't want people to think that because we're seeing so many people with POTS and post-exertional malaise, that's just the new norm. It's not normal.
What are you most excited about in terms of what's coming — both in long COVID and in how it's going to bridge into ME/CFS?
Dr. Nancy Klimas: They have so much more in common than they have apart. Frankly, COVID itself is the thing that's apart — the trigger and that ACE2 receptor binding that makes their vascular system more at risk for inflammation. That's going to be the big difference when we line up all the pathophysiology of these two illnesses. Otherwise they're going to align. We've got people whose immune systems don't work well. Specifically, their natural killer cells — their innate immune system, their ancient immune system that can rid you of chronic viruses and cancer — are not working well. That's a really important feature of both illnesses, and they're very, very close to identical on that.
Haylie Pomroy: Which is odd, because they're designed to bounce back after insults.
Dr. Nancy Klimas: Yes. But there is this thing called immune exhaustion — and that's what we're seeing with these NK cells, and also with the rest of the immune system that deals with viruses. Immune exhaustion, or immune senescence, is what happens to an immune system when it's under constant barrage — constantly activated, constantly working. It uses up all its resources and goes into this sort of save-the-cell, quiet-down mode. It becomes non-adaptive. If you think of long COVID and ME/CFS as essentially going into self-protection mode — hunkering down and dropping all function to a baseline — that's essentially what the immune system is doing.
And here's the other piece: when the immune system doesn't function well, all of us have latent viruses — our childhood viruses that are known to go dormant. One of them is the mononucleosis virus, Epstein-Barr. Another is CMV. EBV is present in about 98% of adults, CMV in about 88% — it's really high. Both of these viruses, when they reactivate, cause a lot of immune noise and signal a lot of inflammation. And they're both known to trigger autoimmunity.
So as you go through this illness over time, you start out with perhaps persisting COVID — maybe for a long, long time, we don't know — and that's driving the immune system into an inflamed, exhausted, non-functional state. Now your latent viruses start to reactivate: EBV, CMV, HHV-6, Coxsackie. All these viruses floating around in different systems and organs start reactivating at a low level, smoldering, noisy, keeping the immune system trying to respond and creating more inflammation. That viral reactivation picture is well documented in both long COVID and ME/CFS — and it's a target for therapy.
Haylie Pomroy: And they were finding leftover COVID in the GI tract?
Dr. Nancy Klimas: They were finding evidence that it wasn't just spike protein — it actually was replicating COVID. That's a huge deal. Because if it's a replicative, persisting infection, we can insert antivirals that mess up replication and clear the virus completely. We can completely cure hepatitis C. HIV — we can completely suppress it and these patients live long, healthy lives. So there are different ways to treat persistent infection than trying to treat a remnant of an old infection that's still making something that's messing up your immune system.
Haylie Pomroy: And is spike protein a protein that our bodies can digest or break down?
Dr. Nancy Klimas: The system is meant to clean the mess up. You have these cells called macrophages — they go around hunting for stuff, suck it inside, take it away from the area, and digest it with enzymes. We have that cleanup system built into our cells, and we have it in the brain as well. It's very unlikely that you have spike protein from something you had three years ago still circulating on its own. You made that spike protein recently — there's something in the system causing continued production.
And when they did organ biopsies in China, they found that 80% of long COVID patients had COVID antigen in solid tissue. So when we say 40% of long COVID patients have spike protein in their bloodstream, we're probably undercounting. We don't really know how many people are dealing with it, because it depends on where you look.
Haylie Pomroy: I always tell clients who maybe fall in that 60% who test negative for spike protein: our labs are so good that it's like getting in a helicopter and looking at the freeway system of downtown LA. It's better than just sitting in a car and looking left and right, but there's also a freeway system in New York and in Chicago. Just because there wasn't a blue car on the 405 freeway at the exact moment they drew your blood doesn't mean you don't have it. It just means that one box has been kind of checked off.
Dr. Nancy Klimas: It's all about compartments — did you look in the right place? And can you look in that place? There's a virus called Coxsackie that's a plague to ME/CFS, and increasingly I think we understand it to be true of long COVID as well. It hangs out in muscle and gut — you don't find it in the bloodstream. John Chia did amazing work biopsying intestine and gut in 300-plus patients. And he found the actual replicating virus — not the antibody signature, but the actual virus — along with replicating EBV and replicating CMV in the gut, where we weren't looking at all. We were just pulling blood.
Haylie Pomroy: We're currently doing a trial with monoclonal antibodies. Can you help us understand that? And is it accessible to people in our community?
Dr. Nancy Klimas: Depending on when you're watching this — as of July 2025, we are recruiting. You can find our webpage, which has a link to register for any of our long COVID studies through a general registry, and then we reach out to tell you more about the studies we're doing right now.
That antibody study is trying to mop up spike protein — that's its target. We're using the AstraZeneca product. It's a long-acting, six-month, single-injection monoclonal antibody that targets spike protein. It's a placebo-controlled study. It's just off the ground. We don't know if it's going to work yet.
The theory is this: whether spike protein is being made by a replicative virus or by cells that have the machinery to make it, the monoclonal antibody will bind to the spike protein and signal to the immune system to come take care of it. It would immune-complex with circulating spike protein and the liver clears it. If it's coming out of a cell, it would flag that cell as foreign. If there's actually a replicating virus in a cell, it would target that as well, because it would be making spike protein. So it works against active infection, persistent infection, or just antigen itself.
I also recommend everyone go to the Recovery Initiative website — they have great webcasts and resources. They have several silos of interventions they're working on, one of which targets replicative virus and spike protein. They've just finished a short Paxlovid study that didn't show results, but now they're doing a long Paxlovid study. In other viruses that persist, you needed more than one antiviral to get it under control — a cocktail. That's how we managed hepatitis and HIV. So this is an evolving thing. The investment in long COVID is already paying fruit — in three years since late 2022, the mechanisms have been worked out and big, definitive trials are now underway. It's an exciting time. And we do hope that the ME/CFS community will also benefit from the discoveries.
Haylie Pomroy: We've lost good years — ten to twenty — bypassing the step of believing patients. We believe you. We lost so much time in ME/CFS.
Dr. Nancy Klimas: I sat as the only non-psychiatrist on NIH expert panels for years, where every single expert was a psychiatrist except for me. Long COVID people should thank the ME/CFS people who suffered through that, because it was their advocacy that pushed the NIH and other federal agencies to stop encouraging that kind of thinking.
Haylie Pomroy: Dr. Klimas, it is always such an honor and a privilege to have you on. I love the other aspect I'll say about going through the pandemic — how empowered people have become to learn about their bodies and their immune systems for the first time. Terms like cytokine storm, spike protein, understanding that viruses are cleared through the liver, that macrophages chomp them up with enzymes — I think the more we learn about this amazing, biodiverse body, and the more scientists like yourself train and teach the next generation, the closer we get to real solutions for people in need. Thank you. Promise me you'll come back.
Dr. Nancy Klimas: I will always be back. You just have to ask me. Thank you for trying to help these patients. I want to underscore hope — the progress in this field is astronomical in the last two years. If you are feeling hopeless because of long COVID or ME/CFS, please hear me say that we are translating the understanding of the underlying causes of these illnesses into clinical trials. Big trials. Definitive trials. And we are seeing patients get well in our practice. Even without the trials, we take care of our patients with the tools we have, which aren't shabby at all. It's just a question of treating the whole thing and not just little bits and pieces. It's very important to be hopeful at this time.
Haylie Pomroy: And it's exciting and inspiring. And as always, you guys, we're here for you. Post your questions, keep commenting — it helps us generate new topics, know what you need, and get you what you deserve. Thank you.
