Podcast Summary
In this episode, Dr. Amy Proal, microbiologist, delves into the mechanisms of Long COVID, exploring how SARS-CoV-2 impacts immune function, viral persistence, and ongoing symptoms. Gain crucial insights into the complex nature of post-viral illness from a leading expert.
Guest – Dr Amy Proal
Note: The podcast has no bias. All conflicts of interest are highlighted with individual guests.
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Podcast Overview:
Summary
Amy Proal discusses how SARS-CoV-2 can interfere with the immune system, specifically interferon signaling, potentially reactivating latent viruses like Epstein-Barr. She highlights viral persistence in tissues, particularly the gut, which may cause chronic symptoms in Long COVID through inflammation, clotting, and immune dysregulation.
Highlights
- Interferon Signaling and Viral Latency
- Role of interferons in keeping viruses like Epstein-Barr latent
- SARS-CoV-2’s impact on interferon signaling, reactivating latent viruses
- Viral Persistence in the Gut
- SARS-CoV-2 found in the gut up to 600 days after infection
- Connection to gut inflammation, leaky gut, and systemic effects
- Spike Protein and Long COVID
- Spike protein causing clotting, blood vessel damage, and small fiber neuropathy
- Presence of spike protein in Long COVID blood linked to persistent reservoirs
- Impact on Mitochondria and Metabolism
- Viruses hijacking human mitochondria, depleting energy, and causing inflammation
- Immune Dysregulation
- SARS-CoV-2 disrupting adaptive immune responses (T cells, B cells)
- Reactivation of latent viruses complicating the immune system’s response
- Post-Infection Syndromes and Chronic Symptoms
- Chronic symptoms in Long COVID varying between patients
- Combination of viral persistence and immune dysregulation
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Podcast Transcript:
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Episode 12 – Long COVID and other Viral Illnesses that lead to Chronic Post-Viral Illness ft. Dr. Amy Proal
[00:00:00] Funmi Okunola: The information in this podcast is provided for informational purposes only. You should not use any information discussed in this podcast and related materials to make medical or healthcare related decisions. Always consult your physician or other qualified healthcare providers with regards to diagnosing and managing your medical condition. Any medications or treatments, including any discussed in this podcast, should be initiated and managed by a qualified healthcare professional
Funmi Okunola: Welcome to Long Covid – The Answers. Today’s Episode is entitled “Long COVID and Other Viral Illnesses That Lead to Chronic Post-Viral Illness”. I’d like to introduce Dr. Amy Proal. Dr. Proal is a microbiologist who studies how bacterial, fungal, and viral infections disrupt human gene expression, immunity, and metabolism.
Her research also examines how human microbiome disturbance can cause Chronic Inflammatory Illness. Dr. Proal is the President and [00:01:00] Chief Scientific Officer of PolyBio. Welcome, Amy.
Amy Proal: Thank you so much for having me.
Funmi Okunola: Amy, do you have any conflicts of interest to declare? No? Okay good. Amy, what is PolyBio?
Amy Proal: PolyBio is a non-profit research organization that I founded with my collaborator, Mike Van Elsinger, who is a neuroscientist at Harvard Medical School, and we founded PolyBio about five years ago to study what we’ve been calling “Infection Associated Chronic Disease”, but which sometimes we now even call “Post-Acute Infection Syndromes”. Basically, what we’re looking at is we’re trying to understand the chronic consequences of infection, viral infection, bacterial infection and fungal infection, and that’s because nearly all major pathogens that are studied in this capacity, whether it’s viruses or bacteria, are connected to a [00:02:00] Chronic Syndrome in which a portion of infected patients don’t recover and develop chronic symptoms that can last a lifetime. So, we were trying to better study those patients.
There are millions of patients across the globe right now who are in many cases even bedridden from these conditions – these Post-Acute Infectious Syndromes, and we wanted to better understand what was wrong with them and how to treat them. So, we’ve founded PolyBio, and we’re scientists, and what we do is we reach out to other colleagues in our space, other scientists and other people now even capable of running clinical trials. We help them understand that these chronic conditions are tied to infection. Then we build projects with them. We build new teams to understand the root cause drivers of what’s making patients sick, and then we actually seek private funding to try to make those projects happen. That’s what we do via our foundation.
Funmi Okunola: Oh, that’s [00:03:00] amazing. One of the main reasons why I invited Dr. Proal to be interviewed today is because of her extensive experience in researching the link between viruses and chronic illnesses. I wanted her to show the audience, the medical profession, and skeptics that Long COVID is a legitimate disease process.
It’s been understood for centuries that viruses can lead to chronic illness. Today we will explore this and highlight how the coronavirus is causing similar effects in a specific group of people and potentially long-term health issues in possibly all of us who have been infected with this coronavirus.
Much of today’s questions are based on Amy’s 2021 article published in Frontiers in Microbiology, entitled “Long COVID or Post-Acute Sequelae of COVID-19, or PASC, An Overview of Biological Factors that May Contribute to Persistent Symptoms”. The link for this paper will be included in the show notes, and in my opinion, this is a paper that should be read by all medics and medical [00:04:00] students.
Let’s begin. Amy, so to take a quote from your article – “While the development of long-term symptoms following SARS-CoV-2 infection is sometimes framed as novel or mysterious, it is actually an expected phenomenon. Most well studied viral or bacterial pathogens have been connected to the development of Chronic Symptoms in a subset of infected patients”.
Could you please tell us what other viruses can cause Post-Viral Illness and why you feel this is relevant to SARS-CoV-2 and Long COVID?
Amy Proal: Yes. So, some of the more well-documented pathogens that are connected to these Chronic Infectious Syndromes are, for example, Ebola. I guess that’s a good example to start with – in that in the Ebola outbreaks, it’s especially those you know, centralized in Africa, a subset [00:05:00] of patients began to be diagnosed with Post Ebola Syndrome.
Again, these are a proportion of patients who recover actually decently well from the Acute Ebola Infection, but then they start to develop a wide range of chronic health problems. So, some of the key things that people were experiencing ranged from just debilitating pain and joint issues to problems with vision, all kinds of chronic issues.
For a while, and this tends to happen after people develop chronic problems with an infection, it was considered a mystery or people were like “what’s happening? What do we do”? Then a couple of very proactive research teams actually started to collect samples from these patients that went beyond the blood.
They got eye tissue samples. For example, they got semen samples. They even got breast milk samples from some of these survivors with Chronic Symptoms, and in many of those samples they still found [00:06:00] the RNA, the genetic material of Ebola Virus. So, it began to be understood that people who had Chronic Symptoms might still harbor reservoirs or a low level of the Ebola Virus or its genetic material in their tissues especially, or in their what are called in those patients “anatomical sanctuaries”.
In other words, the virus is not,(?) and this is true of many of these conditions in which people develop Chronic Symptoms after an infection. If people still harbor the pathogen, let’s say, which is a very straightforward and one of the most highly researched areas in these conditions, I mean, the straightforward possibility that maybe some people with Chronic Symptoms just didn’t fully clear the infection that made them sick in the first place.
But that infection persists in a low level in their tissue. The key is that it may not be in their blood, and I think that leads to one of the confusions that [00:07:00] can happen with these patients because if these patients go to the doctor, or if they even go to a certain research lab, and they’re just looking for the pathogens, genetic material in their blood, it’s not there.
So, it seems like they’re okay and there’s nothing there, but the issue is that the pathogen may have moved into their tissue, and there it’s persisting in this low- level reservoir and that’s what seems to be happening with the Post-Ebola Syndrome patients. What was interesting is that even then people thought, okay, well then, do these patients just have the genetic material of Ebola?
Does it matter? Does the RNA still do something if they have it in this persistent state? But it’s important to note that actually it’s a couple of years ago now there was a new outbreak, a new Ebola outbreak sparked in Africa, and when they sequenced the strain of the Ebola that was causing that new outbreak, it was almost identical to a strain of Ebola that had caused an outbreak years before. So [00:08:00] several independent teams concluded that the new outbreak must have been sparked by a chronically infected person who had carried Ebola throughout that period. Potentially as part of a Post-Ebola Syndrome case, right? So, you have Ebola that’s now explored in that capacity.
Zika is another virus that we’re familiar with. Post-Zika Syndrome is another one of these chronic conditions. Dengue has been connected to Post-Dengue Syndrome in which a subset of patients develop chronic symptoms after infection with Dengue, and then on the bacterial pathogen side, you have Q Fever, which has been tied to Coxiella Infection and has been tied to Chronic Symptoms and Chronic Syndrome Development.
Then the tick-borne or vector-borne pathogens, which are really understudied like Borrelia, Bartonella, Babesia, Rickettsia, are all also tied to Chronic Symptoms in a [00:09:00] number of people. So, the truth is that if you actually start to study a pathogen and labs go ahead and track people after an infection and begin to potentially collect their samples, especially tissue samples and to dig deeper into these patients, it does seem like most pathogens are connected to Chronic Symptom Development in at least a small subset of patients who get that infection.
I should add, you know, that the Herpes Viruses like Epstein Barr Virus, HHV-6, Cytomegalovirus, those are persistent viruses by definition. They’re persistent DNA viruses, and yet most of us harbor Herpes Viruses, and they’re kept in a latent state. They’re kept in check by our immune systems.
But in some patients, it clearly seems that the Herpes Viruses are able to emerge from a state of latency and drive more Chronic [00:10:00] Symptoms and more types of chronic disease. So technically, the Herpes Viruses are also players in these infection-associated or chronic conditions in which people are not recovering or doing okay after an infection.
Funmi Okunola: Thank you. Scary. Yeah. What is viral persistence?
Amy Proal: That’s exactly what I was talking about before. It really is the very straightforward possibility that at least part, and again there are a number of different possibilities for why people develop chronic symptoms after an infection. But one that is increasingly studied, especially after COVID now where we’re studying Long COVID patients who have Chronic Symptoms after COVID, is that it’s a possibility that the virus clears from their blood or potentially from other body fluids where it’s easily identified, and it’s no longer going to be found by a standard nasal swab test.
It’s not going to be identified in [00:11:00] those forms of testing, but maybe some virus a small amount of virus still persists in the patient’s tissue – in the tissue of their gut, in the tissue of their lung and their lymph node, in that reservoir that persistent reservoir of the virus, and is still able to drive a number of immune, genetic and even metabolic abnormalities in the patient, and so that’s persistence, viral persistence in those reservoirs.
Funmi Okunola: Thank you. To again take a quote from your same 2021 research article “It is well understood that humans accumulate persistent viruses over the course of a lifespan time”. Could you please give examples and discuss the role of the immune system in keeping those viruses in check, including the involvement of interferons?
Amy Proal: Yes. So that’s where especially the Herpes Viruses that I mentioned before, those DNA viruses, are some of the most commonly studied pathogens that are just [00:12:00] understood to be accumulated and picked up by people over the course of their life. So, most people acquire, for example, Epstein Barr Virus. In some cases, they get Mononucleosis. For example, the kissing disease that sometimes people get in college when they get Mono. Well, that’s Epstein Barr Virus that drives it, and the thing is once you have gotten Mono or Epstein Barr Virus, it now stays in your system. You have that virus for the rest of your life. So, you know, for better or worse, it’s now in your body.
The thing though is that in people who don’t develop symptoms, the virus is kept in a state of latency. It’s kept in check. So, the immune system is monitoring and saying, “Hmm, the virus could potentially create more proteins and begin to cause more problems”. Immune system says “no, I’m not going to let you”, and it keeps it in check in a state of latency. As you mentioned – interferons. Our signaling molecules that are part [00:13:00] of the immune response, part of what’s called the innate immune response, which is a basic important part of just control of most organisms in the human body, and the interferons have a particular viral signaling effect that keeps viruses in check.
If you have a robust interferon signaling, which is part of this innate immune response, those interferons are going to be circling and keeping, let’s say a virus like Epstein Virus in that state of latency. But the problem is if you have another issue that depletes or interferes with interferon signaling, and for example that could be a new infection, so SARS-CoV-2, for example, that creates a number of SARS-CoV-2 proteins downregulate or disable interferon signaling.
It’s a really potent disruptor of interferon signaling. So, let’s say you get SARS- CoV-2. Now your interferon signaling that was keeping that herpes virus in check [00:14:00] goes down or gets dysregulated. That can create an opportunity for the virus that was in a latent state to activate and now potentially infect a new site, infect a new nerve, or create proteins that start to cause problems.
Then again, now it becomes more of an active virus. So, we have this constant dynamic where we acquire these viral pathogens throughout our lives, and we hope that our immune systems are strong enough to keep them in check, and yet the other infections and other exposures that we get, or simply stressful events or other things that can impact the immune response, are always shifting the way that we might be able to manage those viral infections that we acquire over time.
The thing to consider is that some of these infections can be acquired in the womb. So, it’s still an area of study, but it’s possible to pass a Herpes Virus to a fetus in the womb. For example, if the mother’s infected, the infant [00:15:00] as it’s growing in the womb may also just acquire that virus.
It’s actually possible to even be born already with some of these viral passengers, which means that it’s interesting to think about the fact that the diseases that these viruses are capable of causing may run in families in a sense, because we’re passing viruses, technically, especially down the maternal line.
So sometimes if we see illnesses or chronic conditions run in families, it doesn’t only have to be because of the human genome and our human genetics, which also do dictate chronic disease, but it could also be in some instances because of the passing of pathogens that we pass amongst families as well.
Funmi Okunola: Beautiful explanation, you know, great clarity there. How might viral persistence cause Long COVID?
Amy Proal: Yeah, that’s a good question. So again, if someone, let’s [00:16:00] say doesn’t fully clear the virus from their tissue, there’s a number of things that could potentially happen.
A lot of which are under study right now. In fact, that’s a lot of what the teams were working with through PolyBio and are studying at the moment. But I’ll just use the gut as an example. So, one of the sites that we see growing evidence for as a highly likely reservoir site for SARS-CoV-2 and patients with Long COVID or other symptoms is the gut, the intestinal tissue.
One of the reasons for that is likely because the virus gets into the gut in a lot of patients. So, we all know that despite early thoughts that SARS-CoV-2 was just a respiratory virus, it can actually infect pretty much every tissue of the human body, and in many people, it does get into the gut. I mean, many people have GI symptoms and actually just know this.
The gut lining is also really dense. In fact, it’s the area of the body that most expresses the ACE2 receptors that SARS-CoV-2 uses for cell entry. So, this is just this really ripe area for [00:17:00] infection, the intestinal lining, and the gut is a known reservoir site for other viruses, even for example for HIV.
Let’s say SARS-CoV-2 persists in the intestinal tissue which we’ve seen now in a couple of studies. We’ve found, for example, there’s a team at University of California, San Francisco, that got gut or intestinal tissue via a biopsy procedure from patients with Long COVID and found SARS-CoV-2 spike RNA in that gut tissue up to 600 days after initial infection.
Let’s say you have that persistent virus or RNA antigen there. The virus may continue, and this is what we’re still trying to figure out. It may continue to make proteins because what’s important is that the proteins that any pathogen makes, and they all make them, are somewhat like the weapons they use to drive disease.
So, SARS-CoV-2 makes the spike protein. I’m sure we’re all pretty familiar with this. If the RNA of the virus is there, but it’s going through periods where it’s making even in this chronic [00:18:00] form, more spike protein, and maybe that only happens during certain periods or every now and then, but if more spike protein is being created, the inflammation associated with that spike protein release can potentially wear down the lining of the gut. Maybe you’re familiar with intestinal permeability where a number of inflammatory or infectious issues can drive what’s sometimes called leaky gut or intestinal permeability where the lining of the gut becomes more permeable due to inflammation, and that can allow the products from the gut to leak into the bloodstream where they can be highly pro-inflammatory. So, we find first in Long COVID blood that there’s a number of teams now that have found spike protein in the blood of Long COVID patients, and it’s not every patient, but a good number of patients with Long COVID.
It’s possible that some of that spike protein may be derived from reservoirs of the virus in the gut, where it’s wearing down the gut lining and then leaking [00:19:00] into the blood. Once the spike protein gets in the gut it activates platelets, which are blood cells, and then the platelets which we see in Long COVID, we see a lot of activation of these platelet blood cells.
Once the platelets become active, that can lead to signaling that causes clotting and coagulation. So, we actually also see it in Long COVID blood fibre and amyloid deposits that are causing coagulation in blood. All of that can cause inflammation that might damage the blood vessels, the endothelium, and the blood vessels themselves.
Now you have problems with the blood vessels and the vasculature, which is something seen in Acute COVID as well. Then from there you might have problems where when the blood vessels are in trouble, and there’s more clotting in the blood. The blood has trouble reaching the peripheral nerves which are the smaller nerves of the body that are very energetically demanding.
Those nerves might not get the oxygen they need, and they might die off or diminish. That can lead to small fiber neuropathy, which is another thing we see often in [00:20:00] Long COVID patients. So, you can get this real flow on effect where virus in a site like gut via leakage of spike or even other bacterial products in the blood can really catalyze a whole series of pro-inflammatory, pro- thrombotic, or clotting, pro-inflammatory vascular events that can cause a huge problem to the body. That’s just one way.
To be honest, you can also have potential issues with virus in a reservoir site where, and I think one of the things that is really important to understand about viruses and other pathogens is that they hijack our mitochondria – the energy powerhouses of our human cells in order to replicate, in order often to gain, in the case of bacteria, the substrates that they need for their own nutrition and their own survival. So, if you don’t fully clear a virus it’s very possible that if it does go through some periods of replication, that it’s going to keep using your own [00:21:00] mitochondria to do that, and it’s going to keep pulling from your own energy powerhouses of your cell, which can obviously deplete your metabolic function, and then of course it can just drive a number of inflammatory issues that can be problematic.
So, there’s really honestly effects that can happen from persistent reservoirs of viruses or other pathogens to the immune response to our human genes signaling, depending if they get into the center of the cell to our metabolism and then to all kinds of effects on blood vessels, neuropathy and function like that.
Funmi Okunola: I’ve heard you interviewed before, and you said that basically viral persistence can probably connect all the other hypotheses as to the cause of Long COVID, and from your explanation that’s what it sounds like.
Amy Proal: That is basically correct, and again, that’s one of the reasons that we’re studying viral persistence in Long COVID [00:22:00] a lot. We’re really doing as many studies as we can in that direction, and we’re studying other things too. But yes, for a number of logical reasons you have all these different findings in Long COVID, depending on the team. Some teams are finding that there’s metabolism problems. Some teams are finding that there’s clotting problems. Some teams are finding the Small Fiber Neuropathy. It is true that if you didn’t clear the virus, and the virus especially was still creating spike protein, even during periods, that that could account for the clotting problems, the metabolic problems, it makes it a very attractive target to keep studying because of the fact that it can exactly account for so many of the other problems that otherwise seem disconnected in the patient.
Funmi Okunola: Great. Thank you. In your 2021 publication, you discuss how SARS-CoV-2-induced Immune Dysregulation could reactivate other latent viruses. What is Immune Disregulation, and how does [00:23:00] SARS-CoV-2 reactivate other latent viruses in this way?
Amy Proal: Yeah, I did allude to that before where I talked about the interferon signaling those very essential molecules that are part of our human innate immune response that are normally keeping viruses and other pathogens in check and keeping them from expressing the proteins that they can use to drive more disease.
So, I mentioned that if interferon signaling is disabled, which can happen under conditions of SARS-CoV-2 infection or other infections, you lose that control and that creates an atmosphere in which other pathogens that were in a latent state could become active and drive problems. But there’s also that interferons are part of the innate immune response which is a very conserved and more basic general part of the immune response.
So, if you think of the human immune response as an army, the innate immune response is like the foot soldiers and the people with the arrows. They [00:24:00] go after everything. They just come out and they make sure they’re checking. So, any kind of infection, anything they’re going to go after, but we have what’s called the adaptive immune response, and those are the B cells and the T cells. Those are more specialized immune cells that go after specific threats. For example, they understand they’re programmed to go after just SARS-CoV-2 or after a specific pathogen, so they’re targeted in their response, and that’s kind of like an army if you had your more specialized soldiers or whatever that have a unique type of fighting mechanism.
You can also have issues with let’s say SARS-CoV-2 and other organisms or pathogens by changes in those adaptive immune cell activity. The activity of those cells, because, for example, it’s possible that if you already have not cleared or are dealing with one infection, so let’s say the Epstein Barr Virus actually activates in a patient, it’s not in latency. It’s not being well kept in [00:25:00] check. There will be T cells that recognize that Epstein Barr Virus and become specific to it and are now similar called SARS-CoV-2 Specific Epstein Barr cells.
Funmi Okunola: Yeah.
Amy Proal: If you have your T cells sort of caught up in the response to Epstein Barr Virus, but you get a new infection like SARS-CoV-2, it may be harder for your T cells and the others to mobilize against the new pathogen because less of them are in what’s called a “naive state” where they can go after the next thing.
So, there can be issues as well with the adaptive immune system where each subsequent infection or hit that a person gets that might contribute to Chronic Symptoms and can tie up parts of the T cell and B cell signaling or modulate them in ways that might make the immune system respond in a more dysregulated or less precise way to the next infection.
So, honestly, the overall takeaway is that it’s important to consider that SARS- CoV-2, and let’s say in [00:26:00] Long COVID as well, that a kind of an infecting pathogen is driving chronic symptoms. The chronic symptoms could be caused by that packaging, let’s say just not clearing and persisting in a reservoir, or maybe that infecting pathogen, like SARS-CoV-2, is doing something to the immune response to interfere on signaling, to B cell signaling, to T cell signaling, that’s causing another latent pathogen to be able to gain more of a foothold.
Or, both things could happen in someone, and the thing is every patient may be somewhat different, and I think that’s what’s important to understand. With these Post-Infection Syndromes each patient might have somewhat different manifestations of Chronic Symptoms.
So, some people might harbor the initial pathogen. Some patients may be dealing more with reactivation caused by the initial infection. Some patients may have a combination of those factors, and in each case the latent pathogens that reactivate in each [00:27:00] patient are going to be different just based on what the different types of viruses or bacterial pathogens that someone might be dealing with at the time that they get an infection like SARS-CoV-2.
Every patient might not respond perfectly to the same medicine. We’re probably going to have to do combinations of different antivirals or other medications to get specific patients better.
Funmi Okunola: Again, citing your 2021 paper, you remind us of our Herpes Viruses such as the Epstein-Barr Virus, the Mono, which can cause Leukemia, Cytomegalovirus which is associated with Breast Cancer, and others such as Human Papillo Virus, which cause Cancer and are recognized as Cancer causing Viruses. Can you explain the proposed mechanism by which this takes place?
Amy Proal: Yeah, exactly. So, a number of those Herpes Viruses are known to be oncogenic or potentially Cancer-causing viruses, and many viruses are actually [00:28:00] somewhat studied now for the possibility that they can contribute to Cancer or oncogenesis type processes.
Part of how viruses do that is that they infect tissue, and they infect often the human cells themselves in those tissue samples. They can cause the cells that are infected to lose certain inhibitions. So, most of our cells have what’s called ‘checkpoint inhibition’, where they only replicate a certain number of times because signaling turns on to check and turn down their replication.
But viruses can actually get in the way sometimes of that checkpoint signaling, and that means that the cells don’t get that signal, and then they can keep replicating and replicating. If cells replicate often, that can be, for example, the basis of the formation of a tumor. There’s a number of mechanisms by which viruses do that. But really key there is that they’re taking what our human cells [00:29:00] do and their proteins are interfering with the human programming that should keep those cells from replicating more or from expressing more inflammatory or other signaling molecules that are part of the signaling that drives Cancers, and so really in simple terms they’re hacking our human cells
Funmi Okunola: This makes me not want to go outside. I’m going to have to do a program where we talk about how viruses are positive. Do you think SARS- CoV-2 is causing cancer amongst us now or might have the propensity to do so in the near future?
Amy Proal: It’s something that we should study. There are one or two teams that have published papers showing that, at least in the lab, SARS-CoV-2 might be able to drive some inflammatory or cellular changes that could be consistent with cancer. I think that based on the [00:30:00] fact that we know that other viruses can drive cancer in that in a growing number of studies where teams are using pretty advanced technologies to look for viruses and cancer tissue, they’re finding them so that there’s a number of studies now where teams are collecting tumor tissue from the tumor patients with cancer, and then they take the genetic material out of those samples and sequence them to figure out what pathogens might be in that tissue, and there’s a wider variety of viruses and sometimes even bacteria in those tumor tissue samples than was previously thought. These are not just the Herpes Viruses, other viruses, sometimes RNA Viruses, so in other words, with all this circumstantial evidence, it’s like you were investigating a crime.
You saw that SARS-CoV-2 is the potential perpetrator. Yes, it’s a virus. Other viruses have been known to drive Cancer. Other [00:31:00] viruses have been found in tissue samples. SARS-CoV-2’s proteins are able to cause a lot of changes in human cell signaling in other words that you would consider SARS -CoV-2 a high suspect. I hope that we do more research to figure that out.
Funmi Okunola: Yeah and wear your N95. Thank you.
Thank you, Amy for today’s interview. Please join us next week for part two of this Episode where we will continue our discussion and talk about how Chronic Post-Viral Illness can result from viruses affecting our human microbiome. Thank you.
Funmi Okunola: Some questions for listeners to consider.
What are your top five takeaways from this Episode?
How will this Episode change your practice or perception of this disease?
What will you do to act on what you’ve learned?
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Please rate this Episode.
SHOW NOTES:
Dr Amy Proal, Microbiologist, President and Chief Scientific Officer of Polybio discusses Long COVID in the context of other viral illnesses that lead to Chronic Post Viral Illness. This is part 1 of a 2 part series.
REFERENCES
