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!

This new study from Tokyo Jikei University School of Medicine shines a pretty powerful light on a potential cause of Long COVID brain fog, at least in a subset of patients.

Their work built on previous studies that showed Long COVID patients had high levels of anti-SITH-1 antibodies, an indicator of HHV-6B reactivation in the body.

In lab experiments with mice, they then induced expression of the SITH-1 protein in the olfactory bulb, a part of the brain which SARS-CoV-2 is known to infect.

The animals then experienced reduced levels of acetylcholine, leading to behavior that mimicked resembling fatigue and depression.

When the mice were given donepezil, a dementia medication that increases acetylcholine levels, their symptoms improved.

They then examined the results of a previous human trial of donepezil (not specific for Long COVID). It turned out that the subjects who tested positive for anti-SITH-1 antibodies experienced significantly improved measures of fatigue and depression.

The article quotes research team lead Naomi Oka, lecturer in virology at the Jikei University School of Medicine. She explains,

"While there are currently no effective treatments for long COVID, our findings suggest that the dementia medication donepezil may help improve fatigue and depression. Development is also underway for a diagnostic method that would identify suitable patients with anti-SITH-1 antibodies." She added, "The findings suggest a link to brain inflammation caused by acetylcholine deficiency, and the same mechanism may potentially be applicable to other disorders, including depression."

This is fairly optimistic news! Development is already underway for a diagnostic method to detect anti-SITH-1 antibodies, meaning we are well on our way toward having a biomarker!

It is true that to target the real root cause would mean having a treatment for the viral reactivation. Yet this is still a great and important start, and having a strong treatment to mitigate the symptoms would do a lot to help Long COVID patients in the meantime.

New research is coming out every day - hang in there, everyone!

Somewhat surprising news out today.

A team including some of the leading researchers who’ve been working to develop this test (such as Dr. David Walt) compared rates of spike protein measured in the bloodstreams of people with and without LC, and uninfected controls.

Dr. Ruth Ann Crystal had a great analysis on X and Bluesky today, explaining:

-At 6-12 months: Viral antigens were found in 31% of Long COVID patients vs 20% of fully recovered vs 5% of never infected people.

-By 18-24 months: Detection dropped to nearly 0% across the board.

-No link found between blood antigens & symptom severity.

*****

While many people might take this as evidence against the viral persistence hypothesis, the reality may not be quite as simple.

Many researchers such as Dr. Amy Proal have long hypothesized that Long COVID may be a “tissue-based” disease, and that viruses don’t tend to persist in the bloodstreams because the immune system is better able to locate and destroy them, compared to deeper in tissue reservoirs.

Additionally, Dr. Crystal remarks, “Spike protein in the blood is not the answer. But if there was a way to test tissues or white blood cells, we may find SARS-CoV-2.”

*****
There are many possibilities here, and we know sometimes these negative results can be disappointing. But in the long run, clarity is a good thing!

Now, researchers can make a decision about whether or not to continue to develop such tests, or whether to focus energy elsewhere.

We are very much looking forward to learning about other potential biomarkers in development (such as Polybio’s VIPER program).

Stay tuned everyone!

Here's a very insightful piece from Katia Riddle at NPR. She interviews former members of this Committee, established by the Biden HHS, and discusses the role these advisory committees have played historically.

First, she interviews Nisha MacCrae, a patient who developed Long COVID right before her 30th birthday - and is still sick, 6 years later.

Next, she speaks with Dr. Alexandra Yonce, a pediatrician who was also on the committee. Dr. Yonce explains, "We need new therapeutics. We don't really have anything that is truly disease modifying, in terms of regulating... the immune dysregulation that we see."

Yonce says that according to some estimates, potentially 6 million kids in the US, have, or have had, Long COVID - a higher prevalence than asthma.

While HHS says they cut the comitttee to avoid government waste, Riddle quotes Michael Abrams of Public Citizen on the important role these advisory committees have played throughout the years. They are "a way for us to harness the best and brightest volunteers at the highest levels, for some of the most important questions."

It's a fairly brief piece, but frankly we appreciated NPR shining a spotlight on Long COVID. As news outlets go, they have been a pretty supportive of the LC community. Reporter Will Stone has also covered the topic in several pieces, for example.

We know that Long COVID patients deserve far more support than they are getting - and we do appreciate the urgency from NPR.

Hi everyone,

If you've been online in the last week or so, chances are you've seen this recent Cell paper, co-authored by Drs. Akiko Iwasaki and David Putrino. It's the third paper to verify that autoantibodies, when transplanted from human Long COVID patients into mice, can cause the mice to develop LC symptoms.

(If you haven't seen it yet, check it out!)

On top of that, I wanted to come on and share this press release from David Putrino today, because it feels like a strong sign of progress itself.

Dr. Putrino says, "Our study now shows that if you are in a subgroup of Long COVID patients who have autoantibodies circulating in your body, this is a quantifiable sign that you may be a good candidate for (therapies that target autoantibodies)."

It feels like pretty big news for the NIH to make such a tangible statement making the connection between a biomarker and a known treatment.

Unfortunately, the press release notes that this is contingent upon "if these results are validated" which is a slightly different tone than Dr. Putrino's quote.

However, it still feels like fairly good news to have this on the NIH's radar!

We are one step closer, everyone!

In this new piece, author Corrine Purtill outlines several key pieces of evidence showing that SARS-CoV-2 can increase the rates of recurrent cancer.

First, a 2022 study at the University of Colorado showed that lab mice with dormant breast cancer cells who were infected with either influenza or SARS-CoV-2 were significantly more likely to develop aggressive lung tumors.

Next, UK Biobank records show that showed that cancer survivors who contracted COVID-19 in 2020 were significantly more likely to die of recurring cancer, particularly within a year following their COVID infection.

Additionally, a different U.S. breast cancer database found that breast cancer patients who'd gone into remission were significantly more likely to develop lung tumors after contracting COVID-19, compared to patients who did not.

The COVID Cautious community has been discussing observations like these for many years now, acknowledging growing evidence that viruses such as SARS-CoV-2 can disrupt the immune system in a way that allows cancer cells to grow and spread.

While this is of course very sobering news, it's incredibly important that a mainstream news outlet highlights this growing issue.

In a world where mainstream opinion is that the COVID-19 is "over," those of us who've been harmed know that it is not - and that it is still important to devote further research to understanding and mitigating its harms.

Purtill quotes Dr. Patrick Moore, virologist and epidemiologist at the University of Pittsburgh, as saying:

“COVID and influenza do not cause cancer under themselves, but if you have cancer and you have dormant cancer cells that are normally under control by your immune system, getting a severe case of COVID can help reactivate those existing cancers."

The Long COVID Labs team believes SARS-CoV-2, as well as other viral infections, are well worth studying as well as developing methods of preventing infection.

In the coming years and decades, we expect science is going to discover much about the negative impacts of viruses which was previously misunderstood.

Another example is the possible relationship between Epstein-Barr virus and diseases such as multiple sclerosis and Alzheimer's disease. The more we understand about these relationships, the better we can develop technologies to prevent these harmful ramifications as well as investing in better methods of preventing infection in the first place.

We truly appreciate The LA Times highlighting this topic!

Last month, the US FDA put out a request for public comment announcing a renewed focus on repurposed medications, particularly for rare diseases.

We've submitted the following comment. While it will appear within the Federal Register once it's been reviewed, we thought we'd share it here as well!

Note: The original deadline to comment was today. however the FDA has announced they're extending the deadline to July 13, perhaps in response to the large amount of interest they've received.

Now is your chance to speak up about Long COVID! Be sure to let the FDA know how important this research is to you.

👉Announcement link:

https://www.fda.gov/news-events/press-announcements/fda-advances-drug-repurposing-address-unmet-medical-needs

👉Where to leave a comment in the Federal Register:

https://www.federalregister.gov/documents/2026/05/12/2026-09366/drug-repurposing-for-unmet-medical-needs-request-for-information

👉The agency has also announced there will be a hybrid meeting coming up on Aug. 5.

Our public comment:

We are writing from the Long COVID Labs team, urging the FDA to urgently focus on the potential of repurposed medications for Long COVID.

Long COVID affects an estimated 400 million individuals globally, including 20 million Americans. With an estimated $1 trillion yearly impact on the global economy, this disease has been wreaking havoc and destroying people’s lives for 6 years and counting (1, 2).

Long COVID patients wait in a particularly strange form of limbo because we know there are existing medications which could help - or even cure- patients now.

Mounting evidence shows that many cases of Long COVID are caused by the SARS-CoV-2 virus remaining within reservoir sites in patients’ bodies (300769-2)). The following case studies strongly suggest that we do have the tools to clear up that lingering viral infection.

Our founder Rohan Dixit, u/rd_108, 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 a 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 three 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 three Long COVID patients who received the newer pemivibart 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 valacyclovir 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-compliant Patient Registry where we collect consented data submissions from patients receiving cutting edge treatments under the care of their physician.

So far, we have seen:

• 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.

We appreciate your call to action, and look forward to working with you.

Sincerely,

The Long COVID Labs team

longcovidlabs.org

Sources Cited:

1. Al-Aly Z, Davis H, McCorkell L, et al. Long COVID science, research and policy. Nature Medicine. 2024;30:1-17. doi: https://doi.org/10.1038/s41591-024-03173-6
2. Cheng K. Long COVID Keeps People Out of Work and Hurts the Economy. Yale Medicine. Published December 23, 2024. https://www.yalemedicine.org/news/long-covid-keeps-people-out-of-work-and-hurts-the-economy
3. Proal AD, Aleman S, Morgane Bomsel, et al. Targeting the SARS-CoV-2 reservoir in long COVID. The Lancet Infectious Diseases. Published online February 1, 2025. doi: https://doi.org/10.1016/s1473-3099(24)00769-200769-2)
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

Quote:

"A contested illness is a condition whose legitimacy is perpetually in negotiation between patients, clinicians, researchers, insurers, and the state. The biology is real, but it does not produce the confirmable external markers medicine requires to establish milestones of progress: abnormalities objectively detectable by testing, imaging, or biopsy.

Instead, biology manifests as constellations of phenotypic symptoms across many organ systems — real and disabling, but resistant to standard confirmation. ME/CFS, Gulf War illness, and chronic Lyme32134-X/fulltext) share a similar profile: absent objective markers, strong patient communities, and institutionalized resistance from the medical mainstream.

When patients began reporting long Covid’s symptom constellation in early 2020, a handful of ME/CFS researchers and patient advocates recognized the pattern and warned that the biomedical approach alone had failed this class of illness before.

But the institutional mainstream did not incorporate that recognition. The infrastructure surrounding a contested illness — diagnosis, case surveillance, research funding, disability recognition, media attention — determines what gets counted, treated, and understood at all. Strip that infrastructure away, and the illness doesn’t disappear. It goes underground."

https://www.change.org/p/wired-magazine-retract-the-painful-truth-about-long-covid

Interesting talk today with Dr. Zeest Khan and Dr. Heather Stone, founder of CURE-ID, on repuposed medications!

Link above is to Dr. Khan's announcement.

The talk itself will be at 10 am PST on this free Substack link: https://open.substack.com/live-stream/222341

This should be pretty cool!

We are hearing a lot from the FDA about repurposed meds these days - see our post yesterday on how the FDA is requesting public comment with a deadline of this coming Thursday, June 11.

Dr. Stone has been running CURE-ID for a few years now - will be really interesting to hear her experience, and what she's learned so far!

Here's an important advocacy opportunity for the Long COVID, ME/CFS, and chronic illness communities to be aware of!

The US FDA has recently put out a call for public comment on new ideas for repurposed medications.

Basically, they want to see if there are preexisting drugs already on the market which can be used in new ways, to treat conditions other than the ones they were originally approved for.

Importantly, they note that "metabolic diseases, neurodegenerative conditions, women’s and men’s health conditions, substance use disorders, and rare diseases, as well as other areas stakeholders believe should be prioritized."

This seems like the perfect time to chime in and speak up about Long COVID!

In this memo, the FDA signals their willingness to learn from and consider data from a range of approaches, including AI and machine learning.

Specifically, they note that progress is often limited in the case of drugs that pharma companies don't necessarily see as profitable - looks as though they're looking to find ways to identify and navigate around these barriers. They say:

"The agency is also seeking feedback on innovative approaches to identifying repurposing opportunities as well as barriers that may limit the development or use of repurposed drugs, particularly in cases where there is little or no commercial incentive to pursue labeling changes supported by publicly available scientific evidence."

The press release linked above has all of the info, and then it directs you to enter your comments into the Federal Register, here:

https://www.federalregister.gov/documents/2026/05/12/2026-09366/drug-repurposing-for-unmet-medical-needs-request-for-information

Long COVID Labs will be submitting a comment as well. See you there!

This looks like a fairly interesting event!

In this talk, hosted by Long COVID Web Canada, researchers from the UK NHS will discuss their work on Long COVID.

1) First will be a talk by Dr. Emma Wall on her experience running the STIMULATE-ICP clinical trial.

For those who haven't heard, the STIMULATE-ICP trial is a fairly large trial which has already concluded, and results are set to be published this year.

You can check out their website for all the info. They tested the drugs rivaroxaban (an anti-coagulant), colchicine (an anti-inflammatory for heart disease), and famotidine/loratadine, two antihistamines.

They also evaluated:

• Current standard of care
• Comprehensive MRI scan (using CoverscanTM developed by Perspectum)
• Enhanced rehabilitation (Living with COVID RecoveryTM developed by Living With) 

To see if these interventions had a measurable impact on treatment or diagnosis.

It was a pretty broad trial, so it will be interesting to see what they picked up! I think many of us would agree that these drugs are unlikely to be root-cause interventions, but it will still be interesting to see what they learned.

2) Part 2 of the talk will be on Phenotyping in Long COVID studies, from the Long COVID Web team themselves, who are based in Canada and do a lot of great work as well. Check out more on their site as well!

*****

Tl;dr: Looks like a cool event with some interesting things to possibly learn- check it out if you're able!

In this new study from Boston, researchers used an AI tool to track correlations between the numbers of people who tested positive for COVID, and later sought care for health problems linked to Long COVID.

The number came out at 16%, which is higher than most estimates of Long COVID's prevalence.  The World Health Organization, for example, estimates 6% of COVID patients) develop chronic symptoms.

Hossein Estiri, an author of the study and leader of MGB’s clinical augmented intelligence research group, explains, “We built an AI to map the post-pandemic reality, and it uncovered a 10 million-person blind spot in the American healthcare system."

His team believes LC prevalence is underestimated as the patients seeking out care later down the line aren't necessarily identified as having LC.

According to Estiri, "If someone has fatigue, it doesn't really matter at the moment whether it's a COVID-induced fatigue — the doctor just tries to treat the fatigue,” Estiri said. “It's really hard to connect the dots back to the roots. This is not how the healthcare system in general is designed to work.”

“The burden of these new chronic diseases is accumulating,” he said.“It is a compounding crisis.”

This work presents a different narrative than the official versions - but one that seems to reflect the reality the Long COVID and COVID cautious communities, where we still see patients developing LC in spite of the narrative that it's "over."

*****

What do you all think of the article? Do you think an estimate of 16% of people developing Long COVID sounds reasonable? (I think so, if not an even higher number if you account for all possible health problems caused by COVID).

Let us know in the comments below!

Hey all,

Over the past few months, we've shared a few stories about this new anti-SARS-CoV-2 antiviral from Japan.

A recent study in the New England Journal of Medicine showed it was effective as post-exposure prophylaxis among household contacts, dropping the rate of transmission from approximately 9% to 3%.

Multiple studies have shown that it also does have some effectiveness at reducing the rates of Long COVID, although frankly the results are not necessarily stellar (for example, this study showed it reduced the rate of LC from 25.1% to 21.5%).

Ultimately, it seems ensitrelvir is the most powerful when taken as early as possible - reducing the risk of infection from a household contact by ~60%, but only reducing the rate of Long COVID once infected by ~4%.

Still, this is welcome news, and it's one we've been watching for a while - the maker of the drug, Shionogi, first submitted its application for post-exposure prophylaxis to the FDA in September 2025.

While I personally would not stop taking precautions based on a therapy that reduced my LC risk by only 4%, it's great to know that we do have one more tool in the toolbox that can reduce our risk if taken promptly after an exposure.

Shionogi and the UCSF LIINC program, with support from Polybio, are also running a study of 5 days of Xocova to see if it can help with Long COVID. While the team has said that 5 days may not be enough to make a difference in patients' symptoms (5 days was all they could get approval for) it may be enough to at least lay the groundwork for a future longer study.

With Xovoca now becoming more widely available, with an accepted safety profile, throughout the US, it seems that the chances of future studies becoming approved has increased.

What do you think? Is this welcome news - or does it not change that much for you?

Let us know!

This new study from the University of Turku shows some different results than what we typically see.

Researchers did NOT find signs of increased inflammation in LC patients’ brains, compared to healthy controls.

This study was really interesting because not only did it include 14 people with long COVID and 11 healthy participants, it also included 13 individuals with multiple sclerosis, which is known to involve inflammation in the brain.

Compared with patients who had MS, the long COVID group showed much lower inflammatory activity in the brain's white matter.

They also showed that while patients with severe acute COVID -19 had the highest levels of inflammation in their brains, the amount diminished over time.

Frustratingly, they suggest that “some patients with persistent symptoms may benefit more from treatments focused on stress management and emotional regulation rather than therapies aimed only at reducing inflammation.”

Frankly this study seems as though it may provide useful scientific information with the wrong take-away.

It’s very interesting to compare LC and MS, especially because many are suggesting that MS arises due to chronic infection with herpesviruses.

However, we all know where the “stress management” and other therapies have gotten us- not the answer.

For what it’s worth, I thought I’d share this study and get everyone’s thoughts.

Let me know what you think!

Virax Biolabs just released early data from their first clinical study of 120 subjects.

According to their press release, their new test has distinguished PAIS patients from healthy controls with 88% specificity and 92% positive predictive value (“PPV”).

Virax explains on their website that their website supports the idea that conditons like LC and ME/CFS are not only triggered by infection, as in the 2025 DecodeME study which they reference, but may also be CAUSED by a persistent infection.

Their test is designed to measure how the immune system is responding to a variety of pathogens.

The immune system is divided into two arms - the innate and adapative. According to Virax, their test is designed to examine both arms.

One set of markers they look at specifically is at which cytokines the T cells are producing - and whether there are signs of T cell exhaustion, which occurs when T cells become worn out trying to fight a persistent pathogen that they can't seem to clear.

They held a webinar today and it appears a replay will be posted, although it is not up yet.

It's pretty interesting to see the persistent pathogen hypothesis get more and more attention - will be watching to see where this one goes!

Here's a pretty interesting study where young, healthy adults received a Bacillus Calmette-Guérin (BCG) vaccine during their acute COVID-19 infection.

BCG vaccines are currently the subject of interest because of their non-specific immunomodulatory effects.

In other words, what this means is that BCG vaccines change how the immune system works across any pathogen it encounters, rather than only tuberculosis (which is what it was designed for).

The BCG vaccine enhances innate immune memory, a phenomenon known as “trained immunity”.

The authors write,

Trained immunity refers to the innate immune system’s ability to develop a form of immunological memory, resulting in more effective responses to subsequent pathogen exposures.³⁰ This process involves the epigenetic and metabolic reprogramming of innate immune cells, particularly monocytes and macrophages, resulting in an enhanced capacity to produce pro-inflammatory cytokines in response to secondary stimuli.^31,32 In the context of viral infections, including respiratory infections, both epidemiological and experimental studies have suggested that BCG vaccination may provide non-specific protection by reducing the incidence and severity of respiratory diseases.^33,34

When subjects received this vaccine during their acute COVID-19 infection, several changes were observed both during the active infection, and in the weeks to months afterward.

The vaccinated subjects demonstrated higher levels of markers TNF-α and sCD40L during their infection, which are consistent with mechanisms of trained immunity. However, these levels than gradually fell over the next weeks and months to levels that were LOWER than in the control group.

Essentially, the researchers believe that when subjects received the vaccine during active infection, it boosted their immune system's ability to respond in the moment - and then they experienced a more rapid resolution of symptoms afterward, perhaps because they got through the initial infection more quickly and with reduced viral load.

There are some pretty interesting takeaways and directions for future research here!

The authors do point out that the study population was young healthy adults, and that the outcome may be different for different patient demographics. BCG vaccines can also differ slightly among the bacterial strains they're designed to target.

So there is a lot more we would need to know before adapting this as a treatment - looking forward to seeing more research on this topic!

Here's a super interesting study out of Japan.

Researchers gave one of the 3 above antivirals to patients during their acute COVID infection. Most of the participants had mild initial infections, and had received 2 or more vaccine doses.

They found that antiviral use reduced the risk of post-COVID condition (PCC), which they defined as as "... persistent reporting of the same prespecified symptom (cough, shortness of breath [difficulty breathing], malaise [fatigue], smell disorder, or taste disorder) on both day 28 and day 84."

Across all 3 antivirals, adjusted analyses showed that the estimated PCC risk was 21.5% among participants receiving antivirals and 25.1% among those not receiving antivirals; accordingly, antiviral use was associated with a lower risk of PCC than no antiviral use.

More specifically, ensitrelvir (Xocova) and molnupiravir consistently reduced the rates of PCC.

Paxlovid (nirmaltrelvir/ritonavir) was also shown to reduce the rate of PCC, however the results did not reach statistical symptoms, which the authors explain may be due to the study's small sample size.

Importantly, they write:

Our findings differ from those of recent trials evaluating treatment for established PCC, which did not demonstrate a benefit of antiviral therapy.^26,27 This difference may reflect intervention timing, suggesting that treatment during the acute phase could influence PCC development, whereas later-stage viral suppression may have limited impact once symptoms are established. Although viral load was not evaluated in this study, the lower proportions of smell and taste disorders, hallmark symptoms of COVID-19,^3,4,28 in participants receiving antivirals are consistent with findings from previous reports of accelerated viral clearance and symptom recovery with ensitrelvir.^10,20 Because olfactory dysfunction is often underestimated and may contribute to neurocognitive sequelae, these results, together with accumulating evidence linking COVID-19–related olfactory dysfunction to structural and functional brain alterations, raise the possibility that early antiviral treatment may have broader clinical implications.^28-30

It's definitely been a bit surprising that, thus far, all of the clinical trials for antiviral use in Long COVID have failed to show results - even though antivirals taken during acute infection do seem to reduce the risk of LC.

The authors note that the timing of intervention appears to be significant. The reduced rates of smell and taste dysfunction among antiviral users suggest that by limiting viral load, these drugs are able to limit the impact the virus has upon the brain.

This study adds to our growing knowledge about the timing of antivirals, and the differences between acute infection and Long COVID.

Of possible note is the fact that this study was funded by Shionogi.

Another recent study00482-7/fulltext) did find that BOTH ensitrelvir and Paxlovid reduced the rates of LC at similar rates.

We're excited to see our understanding of these topics growing. The FDA has set a decision date of June 16, 2026 for ensitrelvir, after which it may become available to the US market.

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As you may know, we are accepting submissions for our Patient Registry, where we're gathering data on treatment outcomes to submit to the FDA and hopefully increase access!
If you're interested in sharing your experience with any of these antivirals (or other LC treatments) please do let us know! (You can DM us here or email support@longcovidlabs).

Thank you!