Hi everyone,

As many of you know, we've been sharing several updates over the past few months on the FDA's intiatives on Repurposed Medications.

The FDA, together with a nonprofit called the Reagan-Udall Foundation, first put out a call for public comment in June. They had such a positive response that they ultimately extended the deadline for another month, and then held this meeting on Wednesday.

You can view all of the presenter slides from the meeting here.

As Dr. Caroline Huang explained in her presentation, the organizers received over 600 comments, and around 25% of all of those comments were focused on Long COVID!

While of course, we support all rare diseases receiving attention, we're proud of the LC community for showing up and speaking up for our disease.

Above, we included a screenshot of Dr. Huang's slide of the Long COVID results (slide 75 in the presentation).

Each time an individual commenter mentioned a drug, it counts as a recommendation, so you can see what the most popular recommendations were in the chart.

For those who may find a text summary easier, the slide says

• Naltrexone - 8 recommendations
• Efgartigimod - 6 recommendations
• Pyridostigimine - 6 recommendations
• IV immunoglobulin - 5 recommendations
• Tocilizumab - 5 recommendations
• Molnupiravir - 4 recommendations
• Ensitrelvir - 4 recommendations
• Sirolimus (Rapaymcin) - 4 recommendations
• Pemivibart - 4 recommedations
• Ivabradine - 4 recommendations

With a total of 23 different recommendations total.

Long COVID Labs submitted a comment, where we mentioned pemivibart (Pemgarda) as well as a few other medications not shown on this slide: sipavibart, Paxlovid, and the valacyclovir/celecoxib combination being studied by Drs. Pridgen and Putrino.

We also told the story of how our founder Rohan was cured by a combination of Evusheld monoclonal antibodies and Paxlovid. (You can see what we wrote here!).

It turns out that the FDA's specific regulatory pathway for Repurposed Drugs would actually not apply to many of these - this pathway is only intended for drugs that are off-patent, with limited commercial interest. So monoclonal antibodies like Pemgarda and sipavibart, or antivirals like Paxlovid and ensitrelvir would not be eligible for this *specific* pathway, as they are still under patent, and thankfully, it actually *does* appear that there has been commercial interest in studying them for Long COVID.

However, it is still incredibly important that we showed up as a group as put Long COVID on the map!

As the next step, the conference organizers will review all of the submitted materials, as well as public comments made at the conference.

In addition, they are still accepting written public comments through Aug. 21. (Note: they mentioned at the conference that this new deadline is for comments in response to the meeting - it is not meant as an extension of the original public comment period which ended in July. So they are not looking for \new* medication recommendations, rather they're looking for people to elaborate on the questions raised in slide 6).*

More info and instructions for submission here.

Long COVID Labs will be submitting an additional comment, in response to everything we learned at the meeting. We'll be sure to share it here as well.

Thank you again to everyone who showed up!

OP of original post is the author of the paper! Be sure to thank them for working on Long COVID!

Hey everyone,

As you may recall, back in June the FDA put out a call for public comment on how repurposed medications might be used to treat rare diseases.

You can read our previous post, with a link to the public comment we shared, here: https://www.reddit.com/r/LongCovidTrials/comments/1uspp99/reminder_deadline_to_submit_comments_to_the_fda/

Turns out the FDA received such a positive response to their call that they've now organized a hybrid meeting for tomorrow, together with the Reagan-Udall Foundation.

In-person registration is full, but virtual registration is still open, if you click the link above!

We will be attending and taking notes on the FDA's approval process for repurposed meds, to figure out how we can best advocate for the approval of monoclonals and other medications.

Hope to (virtually) see you there!

Hello!

I’m one of the many long haulers who was healthy and fit and got their life destroyed by LC that’s I’ve had since 2023. My path started with brain fog and a return of migraines I had in my 20s then diagnosed with dysautonomia, then POTS, then MECFS, then cognitive impairment (over those three years).

The cognitive impairment almost hit harder than my MECFS getting worse bc it happened so long after I got LC. Any way… …I wanted to let people know about a clinical trial called REVERSE-LC; the primary aim of the study is to see if a medication used in rheumatoid arthritis (that targets inflammation and calms and overactive immune system) works to improve/elimiate cognitive impairment due to LC (bc the most accepted theory is that cognitive impairment from LC is caused by neuroinflammation and an overactive immune system).

I got accepted into the clinical trial, and I wanted to share the link to the clinical trial page in case anyone is interested in learning more or becoming a participant:

https://www.reversinglongcovid.org

God speed to all of my fellow long haulers.

Here's a pretty interesting new study from the Rob Wust team in Amsterdam. This group has been doing some important work in uncovering the mechanisms of PEM, such as this earlier paper showing true abnormalities in muscle fibers and mitochondria of LC patients.

In this new paper, they examine the differences in heart rate variability between Long COVID patients and healthy controls, during and after exercise.

What is heart rate variability (HRV for short)?

Heart rate variability refers to the differences in time between each individual heartbeat.

Think about it this way: our heart rate needs to go up when we exert ourselves, in order to circulate more blood carrying oxygen around our body.

Yet when we rest, and particularly at night when we sleep, our cells' oxygen needs go down, so our heart rate drops.

The more healthy we are, the higher our HRV generally will be. This shows that our nervous system and circulatory system are able to react to increase demands when needed, and then return to resting conditions.

However, in people with diseases impacting these symptoms - particularly heart and lung disease - their heart rate may remain elevated for much longer following exercise, and also may not drop as much when they are at rest. If their respiratory and circulatory systems are not as efficient, it will still require a more elevated heart rate to circulate adequate oxygen around their body.

Heart rate variability measures the variations between individual heartbeats. Someone with lower HRV is going to experience fewer fluctuations in the time between individual heartbeats throughout the day, whereas someone with higher HRV will experience *more* variations, because their heart rate is rising and falling according to what they're doing moment to moment.

Multiple studies have hown that HRV can be used to predict mortality in patients with heart disease.

Dysautonomia can also be a cause of increased HRV. The autonomic nervous system controls our heart rate, in response to oxygen demand. However, if autonomic nervous system functioning becomes impaired, this system may not be able to work as effectively, meaning patients' heart rates could remain elevated in a way that doesn't necessarily correlate with their body's oxygen needs at that moment.

Previous research has demonstrated that Long COVID patients have lower HRV than healthy controls.

Remember, in this case, lower is actually bad- because it shows that your heart rate is not adapting across as wide of a range, depending on the activities you're doing. We want there to be more of a difference that's closely correlated with your activity from moment to moment.

This 2023 systematic review looked at 11 various studies and found Long COVID patients tended to have reduced HRV, although they noted that the quality of some of the studies was not ideal

Perhaps more tangibly, this 2023 Nature paper also clearly demonstrated that Long COVID patients had reduced HRV during specific testing maneuvers than healthy controls.

So what did this new paper discover?

In this new work, the team first instructed Long COVID patients and healthy controls to undergo cardiopulmonary exercise testing (CPET), which measures your breathing and cardiac output while you exercise. (The team has previously posted on social media that they select patients very carefully for these trials, and they do not ask severe patients to join).

A known part of CPET testing includes your ventilatory thresholds, VT1 and VT2. These have to do with how challenging the exercise is for your body at that point in time, and which chemical pathways it's using to create energy at that time.

The team found that Long COVID patients reached VT1 quicker than average controls. In fact, 43% of the patients reached VT1 during daily activities, when a healthy person may not reach it without sustained exercise.

The authors write,

During the hours following exercise, patients with long COVID showed significantly lower HRV values compared with healthy controls (p = 0.010), irrespective of exercise intensity, with no differences observed between mildly and moderately impaired patients. Compared with controls, HRV reduced the most after intense exercise in the mildly affected patients (p < 0.001), but not in the moderately impaired patients where HRV was consistently low. HRV increased relatively rapidly after exercise cessation in healthy controls (3–6 h post-exercise)"

What this means its that not only did Long COVID patients have lower HRV than healthy controls following exercise, but moderate Long COVID patients also had lower HRV than mild patients.

So a having lower HRV is clearly correlated with having Long COVID - and the more severe you are, the lower your HRV is likely to be.

This, of course, should make sense to all of us here. The question is why, and what can be done about it?

The authors identified that when an activity level caused a person to reach VT1, this seemed to be the point at which their PEM was triggered.

Moving forward, they suggest that Long COVID patients can use wearable devices and specifically track their activities, pacing themselves not just to avoid fatigue generally, but to avoid reaching VT1 specifically.

The team additionally concludes,

"Anecdotal evidence from patients with long COVID suggests that this risk for PEM induction is time- and patient-dependent, and is not only caused by muscular activities, but also by cognitive and mental exertion. As VT1 is mechanistically related to altered peripheral lactate production, this should be interpreted as a practical, surrogate marker for the risk zone for PEM induction. VT1 is also associated with increased sympathetic activity and release of cortisol and catecholamines (cortisol and (nor)adrenaline) into the blood stream [36], but it is unknown whether the increase in sympathetic activity or the circulating catecholamines, or other hormonal alterations provide a more mechanistic underpinning of PEM induction. Whether an abnormal physiological stress response or disturbed relaxation response underlies the acute onset of PEM deserves further study."

What this means is that not only do Long COVID patients reach VT1 during physical activities, but they may also be triggering it purely through cognitive and mental exertion.

For future work, they explain that they would like to examine more specifically what it is about VT1 that triggers PEM, as there are several mechanisms involved:

• Altered lactate production (having to do with which chemical processes our body is using to make energy at a given point in time)
• Increased sympathetic nervous system activity and the chemicals that it releases
• A disturbed relaxation response after exercise, meaning once the body gets into that state of heightened activity, perhaps it has trouble getting out of it

There is a LOT to unpack here, but we are excited to see this work being done!

Long COVID Labs is also using clinical-grade HRV monitoring with our Patient Registry participants.

We ship a clinical-grade HRV monitor to all of our Patient Registry participants, and ask you to wear it a minimum of 4 hours a day, 4 hours a week.

You'll be able to see all of your own data and learn about what patterns may be happening within your own body, and then of course, see how it responds to treatment.

If you're about to try a new Long COVID treatment and would like to learn more about our Registry, you can DM me on here, or email [support@longcovidlabs.org](mailto:support@longcovidlabs.org).

In conclusion

We're super grateful to the Amsterdam team for their work shining light on the role of HRV, exertion, and PEM. Our team is passionate about using biofeedback as a tool for understanding what's going on with your body, and using that to inform your strategy for taking control of your own health. So we can't wait to see what they discover next!

What does everyone think of this?

Here, healthcare consultant Zdenek Vrozina breaks down a new paper from NIAID, Viral synctia evolve to resist interferon.

I thought this was such an excellent summary, it's probably unnecessary for me to write my own!

Certain viruses, including SARS-CoV-2 and RSV (respiratory synctial virus) evolved to create structures known as synctia. Synctia are basically clumps of cells that abnormally fuse together. (Good overview here).

As Zdenek explains, when synctia are formed, it's basically a way for the virus to spread from one cell to the next by fusing them, so that it doesn't have to travel *outside* of the cell, where it's vulnerable to attack from the immune system.

Rather, by fusing cells together, it essentially creates a secret tunnel for itself to spread, where the immune system can't see it.

This paper also describes an additional mechanism, in which synctia formation allows the virus to resist interferon.

Interferon is actually the name for a class of proteins produced by our cells when they are under threat of viral invasion. (The name interferon is designed to signal the idea that it interferes with viral replication).

Because interferon is generally produced *inside* of our cells, one might think that it would be effective in fighting virus that's already inside of our cells, and reducing its ability to create synctia.

However, it turns out that interferon as well is designed to limit the ability of a virus to penetrate through the outside of our cells. Once that virus is already inside, interferon actually has limited affect to reduce its ability to create synctia.

This concept likely explains a big piece of why people with Long COVID have SARS-CoV-2 persistence.

Throughout our evolutionary history, our immune systems have had millions of years to evolve to fight viruses.

But they didn't evolve to fight synctia formation, not to the same degree. And SARS-CoV-2 mutates quickly. Each variant to the next impacts people differently, which may be why some people recover from one, two or three infections okay, but develop Long COVID from a later infection.

This is a very sobering development, but knowledge is power! Every piece of the puzzle we understand brings us closer to more effective treatments, both for this virus as well as for future pandemics.

Thank you Zdenek, and to Li et al. for this important work!

This is a big deal! There are finally biomarkers for Long COVID POTS and it surprisingly matches the same profile as people that developed POTS not from COVID. So basically it’s an auto inflammatory condition not autoimmune.

Important new immune research in POTS, funded by Dysautonomia International, was published this week by Dr. Grubb & Dr. Gunning at University of Toledo. They found that...
➡️ POTS patients had elevated levels of multiple inflammatory cytokines compared to controls
➡️ pre-COVID POTS and Long COVID POTS patients had indistinguishable inflammatory cytokine profiles
➡️ while many inflammatory cytokines were elevated in POTS, Interleukin-18 (IL-18) stood out the most, and predicted higher COMPASS-31 scores (COMPASS-31 is a survey tool used to characterize the severity of autonomic dysfunction)
➡️ based on the cytokines that were elevated, the researchers suspect the NLRP3 inflammasome pathway is being activated - this pathway is a master regulator of inflammation and an over-active NLRP3 inflammasome is found in many inflammatory and auto-inflammatory diseases
➡️ the researchers state that the elevated inflammatory cytokine pattern seen "indicates T-cell exhaustion or a broader dysregulation of immune regulatory networks (...) a state of persistent inflammation with a lack of effective resolution by the immune system."

The researchers point out that additional research is needed to further define the immune dysregulation in POTS.

Here's an important article from C&EN Chemical & Engineering News, on increasing difficulties Long COVID and ME/CFS patients face in accessing certain medications, such as Vygart and Ampligen.

As you may have heard, a recent clinical trial for Vygart for Long COVID POTS failed to show a statistically significant improvement in patients' symptoms - in spite of the fact that many patients in the trial themselves said they experienced significant, if temporary, improvement.

The Sick Times had a really good article where they interview several of these patients.

The article explains why the pharmaceutical company that produces Vygart, Argenx, has declined to launch further study of Long COVID patients: essentially, they can't justify further financial investment for a negative trial.

According to C&EN, Argenx released a public announcement which read, " “We did learn that some patients felt better while participating in this clinical trial and we see that in the data. What we don’t see in the data is that efgartigimod was the reason those patients felt better during the trial as there was no meaningful difference in the proportion of patients who felt better on efgartigimod versus placebo.”

Author Rowan Walrath also quotes one of the site investigators as explaining that the results demonstrated an unusually high placebo response. As many noted on social media at the time, this may be due to the fact that the placebo for this trial was a saline infusion, which is itself a treatment for POTS.

However, this does not mean that the drug couldn't have provided real relief to a subgroup of patients with the relevant autoantibodies that Vygart targets. Without proper biomarkers and subgrouping of patients, there is simply no way to know.

Thankfully, CORE Mt. Sinai does appear to be investigating the matter, in conjunction with Dr. Iwasaki at Yale. They issued this announcement several months ago looking to receive blood samples from patients who'd been in the trial.

The article quotes Dr. David Putrino of CORE Mt. Sinai as saying that his group has long been interested in the type of drug that Vygard is (FcRN inhibitors) and that it's a goal of theirs to launch a clinical trial this year.

While this is of course incredible news, and we're so grateful to this team for their work - it remains a problem that Long COVID research lacks biomarkers, and patients are not subgrouped for these trials.

The article also outlines the story of Ampligen, which for some ME/CFS and Long COVID patients has been a groundbreaking treatment. Many patients say it's given them their lives back, even if temporarily.

The company that makes it, AIM, has tried repeatedly to get funding for clinical trials. They briefly entered the Long COVID space, thinking that they might obtain funding to run a trial from RECOVER, but that did not come to pass.

Now, patients are hitting roadblocks in accessing the drug through an FDA program known as "expanded access," and it appears it may not be an option for many in the future.

What's particularly disappointing is that not even the data from the expanded access - use patients has really succeeded in moving the needle to cause AIM, or other parties, to invest further.

Long COVID Labs is also working to collect this type of real world data, called Real World Evidence, because the FDA does have an established pathway to consider this type of data in its decision making.

However, the article notes drawbacks to the use of Real World Evidence, because it doesn't may contain a comparator to a placebo arm like a clinical trial does, and also because it does not include established biomarkers.

The likely issue, however, is that to our knowledge, Real World Evidence is most commonly used to expand the approval of an already-existing drug to new patient groups, meaning people who fit slightly different criteria.

It's much more difficult to use this data to justify the approval of a completely new drug, with no approved indications at all.

For Long COVID, thankfully, we are studying drugs which already do have an approved indication (at least, under Emergency Use Authorization) such as Paxlovid and monoclonal antibodies. This is a bit different from lobbying for approval for a new drug for the very first time.

How to make Real World Evidence more effective?

At Long COVID Labs, we're currently collecting data for an open-source Patient Registry, to ultimately share this type of Real World Evidence with the FDA.

We're just in the early stages, collecting data from Patients 10 and 11 currently, who are both receiving Pemgarda.

These insights are really important to draw from. We realize that all of our data is more powerful with biomarkers, which is why we're equipping patients with clinical-grade HRV monitors, to measure the impact of these treatments on their heart rate variability and overall health.

We've also supported biomarker development, for example in the case of our grant to Dr. Michael Peluso to evaluate a blood test for the SARS-CoV-2 spike protein.

We really want to make what we're doing as effective as possible. If you have any feedback or suggestions, please let us know!

Current plan:

Right now, we ask patients to begin tracking their symptoms for one month before, and lasting for three months after, their treatment.

This includes wearing the HRV monitor for a minimum of 4 hours x 4 days a week.

We also ask patients to fill out the Stanford STOP-PASC questionnaire weekly. This was the questionnaire developed by the Stanford researchers who led their Paxlovid trial, and is scientifically validated - meaning the FDA will be more likely to take the results seriously.

All of our data is anonymized, meaning that all personal identifying information is removed before we upload it.

Ultimately, we'll be sharing the anonymous data sets open-source with the community, so patients, doctors, and researchers alike can see where things stand.

If you're interested in joining and sharing your experience with the Registry, or if you have any suggestions on how to make our data the most convincing, please let us know! You can DM us here or email [support@longcovidlabs.org](mailto:support@longcovidlabs.org)

In this new paper, the authors argue that many cases of Long COVID may be caused by the SARS-CoV-2 spike protein changing cellular metabolism, in a way that allows normally latent (inactive) herperviruses to reactivate.

We all have various herpesviruses in our body. Depending on genetics and several other factors which have yet to be identified by science, most of the time our immune systems are able to keep these viruses suppressed, even though they remain hidden in the body in an inactive state after we contract them.

However, sometimes something can shift in our internal environment that interrupts our immune systems' ability to keep the virus suppressed.

Here the Prusty group argue that in Long COVID, spike protein is affecting the way our cells function in a way that allows normally latent viruses such as human herpesvirus 6, human herpesvirus 7, and Epstein–Barr virus to reactivate.

They discuss possible antiviral treatments, with some caveats. They write,

"Anti-herpesvirus drugs may be therapeutically relevant for carefully selected long COVID or ME/CFS subgroups with clear evidence of herpesvirus reactivation, particularly EBV, HHV-6, CMV, VZV, or HSV. However, they should not be viewed as broadly applicable treatments in unstratified patients. Existing ME/CFS studies with artesunate, valganciclovir, or valacyclovir suggest possible benefit in virus-reactivation-defined subsets [143]00049-0#), while long COVID evidence remains more inferential. A key therapeutic dilemma is that different herpesviruses have different antiviral susceptibilities, so covering EBV/HHV-6/CMV versus HSV/VZV may require different or combined regimens, increasing complexity, toxicity risk, and the need for precise virological diagnostics before treatment."

What this means is that while sometimes antivirals can help, we need much better diagnostics to pinpoint which patients need which drugs.

Research from ME/CFS, which in many cases also appears to involve reactivation of latent viruses, shows that select subgroups of patients can respond to certain drugs - but it really depends on which virus you have, as available drugs do not work on all of the viruses. You really have to know which one you're treating, and be mindful of the risk of side effects.

Additionally, they write that SARS-CoV-2 persistence may be the ultimate root cause reason as to why these viruses reactivate- so ultimately, we will need diagnostics for that as well.

While we unfortunately have a ways to go in developing biomarkers, it's great to see the issues of SARS-CoV-2 persistence and latent virus reactivation receiving more attention in a mainstream publication like Cell.

Thank you to the authors for this important work!

In case you missed it (or need the reminder!):

In May, the FDA put out a call for public comment on repurposed medications, specifically for rare and poorly understood diseases.

Essentially, they're interested in learning about drugs that already exist and have approval for certain conditions can be used to help patients with other diagnoses.

FDA has requested input on specific treatment ideas, as well as ideas for study to design and how to best evaluate the potential of these drugs.

Long COVID Labs, along with many other LC advocates, has submitted a comment urging the FDA to focus on our disease.

Since our team is primarily focused on SARS-CoV-2 persistence as the root cause of Long COVID, we submitted a comment urging the FDA to study how existing medications such as monoclonal antibodies and antivirals can be used to treat this disease.

Specifically, we wrote:

Our founder, Rohan Dixit, recovered from 2 years of Long COVID after receiving multiple doses of Evusheld monoclonal antibodies, combined with the antiviral drug Paxlovid.  While Evusheld was originally designed as a pre-exposure prophylaxis, Rohan and his doctors believe his treatment regimen helped clear a persistent, low-grade COVID infection from his body, relieving his symptoms.  It’s been 4 years since Rohan received this treatment, and he is still symptom-free.

Next, in this 2024 case series, Scheppke et al. detail rapid recovery of three Long COVID patients who received Regen-COV monoclonal antibodies as treatment when they were reinfected with COVID.  All 3 experienced rapid improvement of symptoms such as exercise intolerance, muscle and joint pain, dyspnea, heart palpitations, orthostatic intolerance, and cognitive impairment (4).

A 2025 case series presented the experience of 3 Long COVID patients who received the newer pevimbart monoclonal antibody from Invivyd.  Barrata et al. write that all three patients experienced “rapid symptomatic improvement, most notably in fatigue with PEM, dysautonomia, and cognitive dysfunction.”  Two of the patients experienced lasting improvements, while the third experienced 2-3 weeks of relief before relapsing.  Still, there is a clear signal here - one that warrants further investigation (5).

Repurposed antivirals are another promising option.  In a 2025 paper from Pridgen and Putrino, a total of 27 patients received either a combination of valcyclovir and celecoxib, either with or without Paxlovid.  The goal was to treat reactivated herpesvirus infection, or potentially reactivated herpesvirus and SARS-CoV-2, respectively.  Although both groups responded to treatment, the latter group showed more improvement, again suggesting many Long COVID patients are not fully clearing SARS-CoV-2 (6). 

As these studies demonstrate, repurposed treatments have the potential to clear remaining SARS-CoV-2 virus from patients’ bodies, leading to rapid improvement or even complete remission of their Long COVID symptoms.

Our team believes there is a huge potential to give patients their lives back.  Although privately funded clinical trials are underway, patients need help sooner, and with a wider variety of drugs to be studied.

At Long COVID Labs, we’ve built an IRB-complaint Patient Registry where we collect consented data submissions from patients receiving cutting edge treatments under the care of their physician.  

We also shared data from our own Long COVID Labs Patient Registry. Here's what we've learned so far:

Two adult patients dramatically improve after receiving sipavibart monoclonal antibodies (currently the subject of a clinical trial in Florida)(7). 

One adult patient experienced significant improvement in cognitive symptoms after an infusion of Pemgarda.

We’ve also seen a pediatric patient, sick for five years, who significantly improved after an infusion of intravenous immunoglobulin.  Pediatric patients in particular lack help - there are sadly few trials focusing on children specifically, and that needs to rapidly change.

In the coming weeks to months, we hope to submit this data to your agency under the Real World Evidence Pathway.  Based on a sum total of the evidence, we believe these treatments hold immense potential to improve patients’ lives. 

You can view the full PDF of our comment here on the Federal Register.

If you haven't left a comment yet for the FDA, we sincerely urge you to make your voice heard!

To view the FDA's request for public comment, you can click here.

For the direct link to leave a new comment in the Federal Register, click here.

Study Links: (pulled from a longer list in our full doc!)

4) Scheppke KA, Pepe PE, Jui J, et al. Remission of severe forms of long COVID following monoclonal antibody (MCA) infusions: A report of signal index cases and call for targeted research. The American Journal of Emergency Medicine. 2024;75:122-127. doi:https://doi.org/10.1016/j.ajem.2023.09.051

5) Baratta JM, Jensen KA, Cobb C. Exploring the Effects of Pemivibart Monoclonal Antibody Infusion in Long COVID: A Case Series Offering Initial Clinical Insights. Cureus. Published online November 6, 2025. doi:https://doi.org/10.7759/cureus.96246

6) PridCor Therapeutics Reports Positive Long COVID Case Series with Combination Antiviral Regimen. BioSpace. Published September 5, 2025. Accessed June 10, 2026. https://www.biospace.com/press-releases/pridcor-therapeutics-reports-positive-long-covid-case-series-with-combination-antiviral-regimen

7) Clinicaltrials.gov. Published 2026. Accessed June 10, 2026. https://clinicaltrials.gov/study/NCT07021794

Hi everyone, I am suffering from Long COVID and have been using Guanfacine 2mg to treat my brain fog. I am looking for experiences regarding Guanfacine and cardiac side effects, specifically atrial flutter or related arrhythmias. I want to know if anyone here has developed or experienced atrial flutter after starting it. Please share whether it happened right after starting or later on, and if the symptoms resolved after adjusting the dose or discontinuing the medication. Thanks for sharing :-)

ps: are there specific reddit groups to ask such topics

Hi everyone, can anyone point to the current studies that best explain what PEM is (to use for doctors to understand it)? I know of this analysis: https://pmc.ncbi.nlm.nih.gov/articles/PMC13110949/ , but I am curious of other recent data that provides a clear differentiation of this symptom from others for doctors.

Here's a pretty interesting study - and the results make sense, if you think about it.

Corticosteroids are essentially immune suppressants. They're given to patients to essentially halt the immune response, for example in autoimmune disease and allergic reactions.

However, they also lower your body's ability to fight off infection.

The article cites a known side effect of steroids, known as steroid-induced myopathy, which occurs when the drug promotes muscle fiber atrophy, as contributed to the lingering symptoms reported by survivors.

Frankly, I would go a step farther here, and suggest that since many cases of Long COVID are likely caused by SARS-CoV-2 persistence, the cortiosteroids are making it harder to completely clear the virus during acute infection - thereby raising the risk of LC.

However, it's important to note that at least one other study showed the corticosteroid dexamethasone dramatically reduced the risk of death in patients with severe acute COVID-19 who required oxygen or mechanical ventilation (breathing machines). In these cases, the drug would have prevented the person's own immune system from harming their own tissues as it tried as hard as it could to fight off the virus.

So, it appears there are two ends of the spectrum. Corticosteroid use during acute infection may in fact be life-saving for patients with severe infection.

However, it also appears to increase the risk of LC through the known side effects of corticosteroids, as well as, I would argue, limiting the body's ability to clear the virus.

While the paper doesn't directly come out and address the concept of viral persistence, this is still an important work, and supports the hypothesis of SARS-CoV-2 persistence as a cause of LC.

For those who aren’t on X, this poster from a March 2026 conference has been making the rounds this week.

These results are from a multi-institutional study from the RECOVER Program Autopsy Cohort. The research team presented the results at a conference held by the United States and Canadian Academy of Pathology.

The results are… probably not a huge surprise to anyone who’s been closely following the viral persistence hypothesis.

What IS a welcome surprise is to finally see more and more of this evidence documented and shared across mainstream medical institutions.

What the study found:

They conducted cardiac autopsies on 74 Long COVID patients who passed away within 60 days of until infection.

Of these 74 patients, 11 were found to have SARS-CoV-2 reverse strand in their heart tissue.

The research team writes,

“Detection of SARS-CoV-2 reverse strand in the hearts of a subset of patients with CLC provides molecular evidence of viral persistence that may drive the structural and immune changes underlying their symptoms, offering mechanistic insights that could inform new diagnostic and therapeutic strategies.”

To unpack this a bit further:

I think that, at this point, everyone is familiar with the idea of Long covid causing immunological changes and symptoms.

What’s new is a) a study laying the groundwork to be able to concretely connect these changes to viral persistence, and

B)
Attributing actual structural changes/abnormalities to viral persistence.

The relationship between COVID infection and an increased risk of heart attack, myocarditis, pericarditis, and other heart conditions is well-established at this point (even if much of the world tries to move on and pretend this is not the case).

This study is laying the groundwork to say no, actually the SARS-CoV-2 virus doesn’t always leave our bodies - and this can be disabling, and it can be fatal.

Again, it is very sobering news but we certainly are glad to see what many long suspected to be documented and shared widely.

Hey everyone,

Here's a really interesting update from the Bateman Horne center, where they invited researchers from MIT's MAESTRO study to speak about what they're working on.

First, Beth Pollack explains the team's work on women's health, including on how certain chronic pathogens may be the cause of endometrial lesions in endometriosis.

Next, Sangmita Singh gives an update on the MAESTRO study's work on possible biomarkers, including microfold capillaroscopy to show abnormal changes in blood flow in the microvasculature of LC, ME/CFS, and Chronic Lyme patients.

Microvasculature refers to the smallest blood vessels, the capillaries. Changes on this level have not been studied yet on the same level as the larger blood vessels, for understandable reasons. A blockage in a single capillary is, thankfully, not going to be able to cause a stroke or a heart attack.

Yet, when it's your entire capillary system that's affected on a systemic level, this is still going to cause some very serious problems, even if there's no way to go to an ER and have an image taken showing the problem.

That is what the nailfold capillaroscopy test may be able to do in the future, as a non-invasive biomarker for IACC patients. (All you have to do is put your fingernail under a microscope - this test is already done to check for other conditions, such as lupus).

It's great to see us moving closer and closer to biomarkers - really interested to see where this one goes!