r/LongCovidTrials

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!

TLDR: My first pemgarda (pemivibart) didn't do anything (besides its great prophylactic work of course) but my second has made a big step of improvement for me in terms of severity and PEM. I don't know how permanent or temporary that improvement will be. I also have been spending all of 2026 in a rest regimen with a single goal of not getting PEM, which may be helping provide support. I will be getting a third infusion and will continue to provide updates as I am able. It makes me nervous to rely on something that is so difficult to access and could be taken away so quickly and easily. But I'm trying to not worry in advance.

LONG VERSION - no AI was used in the writing of this post SO it is longer than needed cause I have no editor lol but I hope it helps and answers all your questions about my improvement on Pemgarda bc I know people are going ask all this stuff in the comments if I don't include it:

History cause I know y'all will ask in the comments:

- original infection in May 2022. Had GI symptoms occasionally since then but didn't get really sick, still GI, until Jan 2024 (no known reinfection but totally possible there was asymptomatic exposure or something, I really have no idea and never will). Developed MECFS around July 2024 and MCAS around a year later. I was basically mild in 2024, moderate in 2025, and had rolling PEM the last few months of 2025 that made me severe.

- first pemgarda details here: https://www.reddit.com/r/covidlonghaulers/comments/1qeoa8m/update_my_experience_with_pemgarda/ second pemgarda I had same basic response - a few great days afterwards, then back to feeling like crap garbage all the time, but within my usual rules about energy expenditure

It's Not All In My Head/How I know what helped and that it helped (most skippable section):

- As you can see from above post, I was completely convinced I was going to be a case pemgarda didn't work for. After my first infusion I started a rest-ish regimen with the main goal being no PEM. And I still got PEM from once, reading an article that was too long and another time, doing slightly too much PT (which is all gentle movement done laying in bed given to me by a covid OT). So I'm not just like, maybe it did work and I missed it. I obviously didn't think that the article was too long or the exercises were anywhere close to too much, I wouldn't have done it. I simply was still severe.

- So I was expecting no progress from the infusion when I went to a wedding and I was expecting a 1 week or longer PEM crash from the wedding. These were deeply held beliefs psychologically so that's where I'm like this is CONCRETE EVIDENCE that it is NOT IN MY HEAD

- first sign something had changed after my second infusion was I got a haircut in a salon and didn't have any PEM... suspicious, but I was just like wow my resting and pacing, hydrating, nervous system regulation, etc must really have worked because I took almost a week before and after that for rest. To repeat, I still feel like garbageeeeee day in and day out so I had no real idea anything had changed (now I know the horrible feelings are attributable to the GI issues)

- I went to the wedding (which I had to also travel for by car) and paced very carefully, missed out on a lot, but still used 3-7x my usual exertion by pacepoints three days in a row whereas in my rest-ish regimen I only did one thing for two hours per week. I DID NOT HAVE ANY PEM. I repeat I DID NOT! HAVE ANY! PEM! Usually for me doing things in a row without the rest in between is the biggest problem. But THERE CAME NO CRASH. NO PEM. if belief was enough, I freaking would have

- Only explanation to me is that the pemgarda must be working. It's been almost two months since last infusion, two weeks since wedding. Rest obviously huge factor but no way it could have done this much in just five months, right??? No idea if this improvement is temporary but I have also done a very loud very hot very bright few hours outside with no PEM since.

Looking forward:

- As mentioned, I feel horrible all the time due to how severe my GI issues and dysautonomia still are. I hope that I can find ways to improve this because I worry the level of inflammation will just make me worse again and this improvement I am seeing from Pemgarda will be fleeting. I plan to keep updating after future infusions.

- I plan to mostly maintain the rest-ish regimen but with slightly more physical activity to help my GI issues and dysautonomia.

- IF pemgarda is causing improvements, that indicates a likely issue with viral persistence so I'm going to explore other anti-viral options to try to support the progress and give my body the best leg up I can through this. I don't know what that looks like yet until I talk to my doctor but if you all have suggestions I'll take them!!

Other factors:

- I do have a supplement stack. I don't really think any of them are doing much for me other than melatonin, magnesium, and my multivitamin

- I do take meds that help - LDN, pepcid, allergy meds, nasal sprays, Ketotifen, Cromolyn, and for my uterus havers I also take continuous pill to avoid hormone swings and periods. I was on all of those things (some for long years prior to LC) by ~October of last year so I do not think any of the improvement on PEM/baseline is contributable to them but they help me in other ways.

- for the mold warriors, please do not comment about that. I have a lifelong history of allergies, allergy doctors, and allergy treatment and there is nothing you have to say to meeeeee thanks :)

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.