Advocates are calling on senators and representatives to include the ME/CFS Research Roadmap and new Long COVID funding in the fiscal year 2027 budget as legislators debate appropriations bills in the coming weeks.
Read more at The Sick Times:
https://thesicktimes.org/2026/08/18/congresss-2027-budget-could-include-new-funding-for-long-covid-and-me/
This is huge news.
Various studies have strongly suggested gut viral persistence, but to my knowledge this is the first one that’s truly come out and documented it.
The amazing researchers at UCSF’s LIINC program, who began as HIV researchers and expanded their work to Long COVID, have just published this groundbreaking preprint.
They found single- and double-stranded viral RNA in cells lining the intestine. Because these cells normally turn over within days, this means that the viral RNA is being newly produced- it’s not just leftover from acute infection.
(When scientists use the phrase “turn over” in the context, this means that all of the cells that were present replicated to form new cells and then died off. This means that all of the cells in that cell type are completely replaced by new cells within days).
So they found viral RNA that had been newly produced.
They also found signs that the immune system was struggling to clear the virus. Part of the immune system was trying to fight, yet key parts of the response were also being suppressed by the virus itself - meaning the immune system was locked trying to perpetually fight a battle that it could not win.
This is really huge news. While this research is still only in preprint form, this team has a great reputation and has been published in many high-level journals such as Nature and The Lancet, so we have every reason to believe this work will eventually pass peer-review as well.
The evidence base here also strongly supports the rationale for immunomodulatory treatments which as Antkiva, as this may help to overcome the ways in which the virus is suppressing the immune response.
All in all, this is fantastic work and we’re so glad to see it!
What does everyone think- does this fit with your understanding of what Long COVID is? How do you think the virus might be hiding from the immune response?
Let us know what you think!
Paywall free version: https://archive.is/NIGhp
Hey all,
Thank you so much for all of your insightful comments on our last post.
In case you’re just catching up, this summer the FDA put out a call for public comment on the possibilities of repurposed medications, particularly to treat rare diseases.
They originally put out a call for written comments, and ultimately received such a positive response that they ultimately convened a hybrid meeting on Aug. 5.
You can view the meeting slides here, and we also shared a summary in our last post.
While we of course believe all rare diseases are deserving of attention, we were particularly excited to see that ultimately, 25% of the comments they received were about Long COVID! Our community really showed up, and it’s so important to continue to put LC on the map.
In the next step, the FDA is now accepting additional public comments through Aug. 21st.
Dr. Caroline Huang noted that from this point forward, they are looking for answers to the 3 questions in the slide above (slide 6 in the presentation).
These questions are:
•What are examples of successful prioritization approaches from other programs or jurisdictions that could be adapted?
•What factors should guide repurposing candidates, and how should they be prioritized?
•What evidence gaps or policy/regulatory barriers most hinder promising repurposing opportunities?
*****
**Note: during the presentation, Dr. Caroline Huang noted that they are not looking for additional medication recommendations in this round of comments. Rather, they are specifically focused on these three questions, as the second stage of this initiative.
**Note 2: the FDA’s definition of repurposed medications as a regulatory pathway is slightly different than what we might think in terms of everyday speech. If you check out slides 15-16, they describe the criteria there - they are specifically referring to medications that are off-patent and don’t currently have commercial interest.
Believe it or not, many of the candidates that are being studied for Long COVID wouldn’t fit here, as medications like Pemgarda, Anktiva and Ampligen are all patented, and have companies sponsoring them.
That doesn’t mean you should not speak up- I just share this so you can make the most effective comment with the information at hand.
You can send comments to repurposing@reaganudall.org
Feel free to workshop any comments/request feedback from the community in the space below! We are in this together :)
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
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!
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!
A new study supported by the PolyBio Research Foundation has found that people with Long COVID harbor persistent populations of highly cytolytic CD8+ T cells directed against SARS-CoV-2 but also the herpesviruses Epstein-Barr virus (EBV) and cytomegalovirus (CMV). The findings suggest that Long COVID is characterized by an ongoing immune response to persistent viral proteins, which are most likely produced during the continued persistence or reactivation of these viruses within the body. The study adds to a growing body of research indicating that SARS-CoV-2 persistence and herpesvirus reactivation contribute to Long COVID pathogenesis.
Paper:
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 signals that there's less of a difference between your lowest and your highest heart rate. We want there to be more of a difference across the day.
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 mild Long COVID patients also had lower HRV than moderate patients.
So a having higher HRV is clearly correlated with having Long COVID - and the more severe you are, the higher 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:
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.
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!
This article posted earlier this year outlining the HPC therapy trial being conducted by regenecyte. Great results, no overhype, showing great results at the end of phase 2 and is going into phase 3 soon.
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!
Personally, I’m excited to see the results of the trails for the following three interventions:
- Anktiva
- Erase trial (remdesivir)
- Humanity Neurotech head-worn device being investigated by Dr Putrino
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
> Abstract
> Introduction
> Long COVID is an emerging public health concern with heterogeneous prevalence. Evidence on the impact of reinfection and vaccination remains limited, especially in Spain.
> Methods
> We conducted a prospective online cohort survey between January 2024 and April 2025, gathering data on demographics, vaccination, symptoms, comorbidities, and reinfection history from Spanish adults (n = 1018). Long COVID was defined per NICE guidelines as symptoms persisting beyond eight weeks after viral clearance. Multivariate logistic regression identified associated factors.
> Results > Of 972 participants (332 men, 640 women), long COVID prevalence was 14.3% (n = 139). Female sex (OR: 1.70; 95% CI: 1.10–2.57; p = 0.014) and chronic obstructive pulmonary disease (COPD) (OR: 4.14; 95% CI: 1.28–13.42; p = 0.018) increased risk. Mixed vaccination schedules raised risk compared to Pfizer-only regimens (OR: 1.30; 95% CI: 1.04–1.62; p = 0.020). Reinfection, reported by 47.2%, was also a risk factor (OR: 1.64; 95% CI: 1.12–2.42; p = 0.012). Frequent long COVID symptoms included anosmia, dyspnea, pneumonia, and myalgia.
> Conclusions
> This national cohort underscores the persistent burden of long COVID in Spain. Female sex, COPD, reinfection, and mixed vaccination schedules are key associated factors, with implications for targeted prevention strategies and vaccination policies.
https://www.sciencedirect.com/science/article/abs/pii/S0025775326001417?via%3Dihub
Unfortunately the whole paper is paywalled. If anyone knows a way to get it let me know.
Of course self-reporting is thought to be a huge undercount since theres loads of people who have long covid but dont realise it. I personally know many such people. Most of here have had the experiance of someone saying "Ever since I got sick with a fever back in June I've had <list of common long covid symptoms>". Then you say "woah that sounds like long covid" only for them to reply "cant be, covid is a cold".
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], 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!
It’s been 6+ years since the pandemic started. Pretty much everyone who could get COVID has had COVID.
So is anyone new getting long covid in 2026?
(I’ve had long covid since 2022)
This was posted already in r/openmecfs but I figured as it also relates to Covid, it is important to post here too!
Solve M.E. has a helpful guide here:
https://solvecfs.org/how-to-submit-a-public-comment-on-the-proposed-federal-grant-rule/
This proposed federal rule could affect how research grants are awarded, managed, and potentially terminated. That matters for ME/CFS and Long Covid because so much of the progress we are waiting for depends on stable, independent, peer-reviewed biomedical research.
A few of the concerns Solve highlights:
Active research studies could potentially be canceled before completion if political priorities change.
Political appointees could have more influence over which research gets funded.
Small pilot grants, patient registries, biobanks, publication costs, literature access, and conference participation could all become harder to support.
For a disease like ME/CFS, where there are still no FDA-approved treatments and research is already badly underfunded, this kind of instability could really hurt.
The good news: submitting a comment is not hard. Solve provides a template, and you can personalize it with your own story.
I used ChatGPT to help turn the template into a comment based on my own situation, and it took me about 2 minutes. You do not need to be a scientist, lawyer, or policy expert. A short personal comment is still meaningful.
A few tips:
Don’t copy/paste the exact same form letter as everyone else.
Mention that you are a patient, caregiver, family member, or concerned member of the public.
Say why ME/CFS or Long Covid research matters to you.
Ask OMB not to finalize the rule in its current form.
Remember that public comments are public, so don’t include private details you don’t want posted online. You can submit anonymously.
Deadline: July 13 at 11:59 pm ET
If you have the energy, please consider doing this. It’s one of those small advocacy actions that could actually matter, especially if a lot of patients and families submit clear, personal comments.
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.
US-based diagnostics company Visby Medical has been granted US FDA clearance for a new OTC at-home COVID-19 and influenza A/B combo molecular test.
This will become the second molecular test available on the U.S. market — the sole option now being Aptitude Medical’s Metrix platform following the exit of Cue, Lucira, and 3EO in recent years.
This test will be single-use (disposable), and fully integrated, so following the Lucira model instead of the Metrix/Pluslife model with a reusable reader. However, it will be powered via USB-C cable instead of batteries like Lucira. It will be nasal swab only, requires a mobile app, and results will be available in 30 minutes.
The Visby test boasts a much lower Limit of Detection than Metrix’s combo test:
However, the clinical sensitivity still ended up being roughly equivalent to Metrix )actually very slightly lower, but the confidence intervals sort of make that a moot point):
This test has been in development since 2021 when Visby received a $12.3M grant from HHS’s BARDA, and is subsequent to Visby’s OTC STI panel (FDA authorized 2025) and point-of-care PCR COVID-19 test (EUA September 2020).
As far as I’m aware, no information is available yet on distribution channels, availability, or pricing.
FDA documents: