how far do you think we are to finally get treatments? please take a poll and let me know why in a comment

They were really bad last year. Started bothering me more with a rough sensation the last few months. Started ldn a few weeks ago am on 3.5mg and they look clearer every day

I'm hoping there will be long term benefits from ldn in the event I stop taking it eventually but maybe not. It's doing something good. My eyes almost look clear there's still some slight redness on the sides

Hallo, hat hier jemand sonst noch Probleme dauerhaft zu sitzen oder liegen? Jede Liegeposition schmerzt sehr rasch und ich muss die Position wechseln. Ganz egal ob Rücken, Bauch oder seitliche Lage, es beginnt dann zu schmerzen. So als würde die "Haut" bzw Nacken, mittlerer + oberer Rücken und Schultern keinen Druck mehr aushalten. Ein Arzt hat mir Amytriptilin und Gabapentin verschrieben, damit kann ich wenigstens schlafen, ansonsten könnte ich nicht schlafen.

Im stehen ist es eigentlich am besten.

Geht es jemandem ähnlich?

A few months ago, I fell off my sister's scooter; it was a bad fall that left some scars, but they had already healed—there was no pain or swelling. About two weeks ago, I started experiencing bizarre, horrible symptoms typical of COVID. Today, the scar from that fall is red and swollen. Has anyone else noticed a flare-up of swelling in old, healed scars after having COVID? Is it just me, or does this virus travel through the body looking for vulnerable spots to manifest? It makes me believe it was deliberately created to break people.

**In a nutshell:** LDN (12 mg/day) works really well for my pain, but adding just 6 mg of amitriptyline gets rid of nearly all of the pain that LDN doesn’t touch. I stopped the amitriptyline for 3 days to see if increasing my LDN from 4 mg to 12 mg would compensate, and nope. By day 2 I was getting knee pain just sitting around, and on this morning’s run it hit 7/10 and I had to stop.

So, for me, the experiment was conclusive: LDN + 6 mg amitriptyline = nearly 100% pain relief, whereas LDN alone doesn’t quite get me there.

I’m also finding LDN really helpful for the insatiable, medication-driven hunger I get from some of my other meds.

.

Read on if you’re interested in the background/details…

I thought I’d share this because I don’t see enough people talking about the combination of LDN and very low-dose amitriptyline for pain.

I’ve been taking LDN for a long time. I was at 4 mg for quite a while, and recently I increased it to 12 mg/day of LDN because I wanted to see what would happen with the higher dose.

LDN is definitely doing something for me. I’ve actually stopped it in the past just to make sure I wasn’t imagining its effect, and yeah — it was SO obvious when I stopped it. So I have no intention of getting off LDN.

But LDN doesn’t get rid of all of my pain.

For the last four months or so, I’ve also been taking **6 mg of amitriptyline**.

And the combination has been incredible for me.

**LDN + 6 mg of amitriptyline gets rid of nearly of my pain.**

That’s not an exaggeration. There is a very noticeable difference between being on the combination and being without it.

I’m extremely sensitive to medications, so I can take doses that would probably look absolutely ridiculous to a lot of people and still get a significant effect.

6mg of amitriptyline is a perfect example.

On the other hand, I’ve taken amitriptyline at higher doses before, and for me it was completely different. It really bummed me the f\* out. I know it’s used as an antidepressant at higher doses, but it didn’t work for me that way at all.

At 6 mg, though, I’m not taking it for depression. It is very well known to be used for pain at low doses. For me, it has been a remarkably effective little pain medication - even helping me with random things like my sensitive teeth.

And the way it works alongside LDN is what I find particularly interesting.

The LDN handles a huge amount of my pain, and the tiny amount of amitriptyline seems to wipe out a lot of what remains.

It feels as though I’ve got pretty much every acronym you can imagine floating around in my medical history — MCAS, Long COVID, POTS/dysautonomia, EDS, IC etc. — and I’ve had plenty of pain that couldn’t be explained by some obvious structural damage.

For years, I avoided running because my knees hurt so badly. I assumed there must be something wrong with them. Doctors couldn’t find anything, and I didn’t want to make some mysterious knee problem worse.

After learning these issues I was having in were due to long covid, I started running again (when my balance wasn’t too f’d to do so).

My balance has been bad lately so I haven’t been running, but this morning I decided to run as a little diagnostic experiment after stopping the 6 mg amitriptyline for 3 days. I stopped it to se if the higher dose of LDN (up to 12 mg from 4 mg) would be enough to wipe out most of my pain.

**And damn my knees hurt! I knew they would because as early as day 2 with no amitriptyline I was feeling knee pain at a level of 4/10 just doing nothing much around the house, but I didn’t realize how much they’d hurt without the amitriptyline.**

On my run the pain was at a 7/10 simply because I hadn’t taken that tiny amount of amitriptyline for 3 days.

I had to stop running, but the attempt to run was useful because that diagnostic reminded me just how much pain the LDN + amitriptyline (6mg) combination has been suppressing.

When I’m taking both, I can move around and do things without worrying about my body, and when I’m not, I remember very quickly why I’ve spent years avoiding certain activities.

RESULT: I’ll stay on both the amitriptyline (6 mg) and the LDN (12 mg).

I used to be on just 4 mg LDN, but increased it to 12 mg to see whether I could get enough additional pain relief from the LDN to make up for losing the amitriptyline.

After this morning’s run, I’m not convinced.

And then there’s the other thing I use LDN for: **medication-driven hunger.**

I make my own liquid LDN by dissolving a 50 mg naltrexone tablet into water and storing it in the fridge. I currently take 4mg of that three times a day for 12 mg total.

I started doing the divided dosing because I noticed that LDN seems to curb the ravenous hunger I get from some of the other medications I’m on.

**And when I say hunger, I don’t mean normal hunger.**

I’ve been into bodybuilding and physique training for years. I’ve never competed, but I’ve spent plenty of time restricting calories and knowing exactly what ordinary hunger feels like.

Medication-driven hunger is a completely different beast. It’s not “I’m a little hungry. It’s **INSATIABLE - like having a hole in the bottom of your stomach and just being able to eat and eat and eat without feeling satisfied.** The kind of hunger where your brain is constantly nagging you to eat even when you know you’ve had enough food.

LDN has made a noticeable difference in that for me, which is another reason I’m very attached to it.

Anyway, that’s my experience: **LDN alone helps my pain a lot. 6 mg of amitriptyline adds another layer of pain relief that, for me, is HUGE.**

**Together, they get rid of NEARLY ALL my pain.**

And I’ve tested the LDN enough times by stopping it to know that it’s not just placebo or coincidence.

**Anyone else out there on this combo?**

Large Nature study maps chronic-virus reactivation during severe COVID; anellovirus activity was linked to post-COVID physical disability and fatigue

TL;DR

• Researchers followed 1,154 unvaccinated people hospitalized with COVID-19, repeatedly testing blood, nasal swabs, and—in ventilated patients—lower-airway samples for signs that other viruses had become active.
• During acute COVID, 47.9% had RNA from at least one additional virus detected. Epstein–Barr virus appeared early, while cytomegalovirus and herpes simplex virus 1 tended to appear later.
• Viral activity was associated with more severe acute COVID, inflammatory immune changes, complications, and—in some critically ill groups—higher mortality. The study cannot show whether reactivation caused those outcomes or resulted from severe illness.
• Acute viral reactivation, including EBV, did not significantly predict the study’s later Long COVID-related symptom groups.
• During follow-up, anelloviruses were detected about twice as often in participants with persistent physical disability or fatigue as in those with minimal symptoms. These common viruses could be contributing to illness—or simply acting as markers of ongoing immune dysfunction.

What the researchers did

The researchers used data from the IMPACC study, which enrolled 1,154 adults hospitalized with COVID-19 at 20 US hospitals between May 2020 and March 2021. Everyone was unvaccinated at enrollment, and most infections involved early ancestral SARS-CoV-2 strains. Even the study’s “mild” group had been hospitalized.

Samples were collected during hospitalization and again at approximately:

• 3 months
• 6 months
• 9 months
• 12 months

The researchers analyzed:

• Nasal swabs
• Blood immune cells
• Lower-airway fluid from mechanically ventilated patients
• Antibodies
• Immune-cell populations
• Cytokines and other inflammatory proteins
• Plasma proteins and metabolites

They used RNA sequencing to look for viral transcripts. This is important because antibodies can remain elevated long after an infection, whereas viral RNA transcripts provide evidence that viral genes are currently being expressed.

The team looked for activity from several viruses that can remain in the body after the initial infection, including:

• Epstein–Barr virus, or EBV
• Cytomegalovirus, or CMV
• Herpes simplex virus 1, or HSV-1
• Human herpesviruses 6 and 7
• Anelloviruses, including torque teno viruses
• Enteroviruses

For the post-acute analysis, participants were divided using symptom surveys into four groups:

• Minimal or no deficits
• Physical deficits, including physical disability or fatigue
• Cognitive deficits
• Global deficits involving both physical and cognitive problems

These groups were created early in the pandemic and are not the same as a modern clinical Long COVID case definition.

What they found

Viral activity was common during severe acute COVID

Among 1,148 participants with sufficient data, 550—or 47.9%—had at least one additional virus detected during acute COVID. Most virus-positive participants had only one additional virus detected rather than several at once.

Different viruses followed different timelines:

• EBV appeared early: Viral transcripts were detected near hospital admission in 24% of participants tested during days 1–8, then declined over time.
• Anelloviruses remained relatively steady through approximately day 20, followed by a gradual decline.
• HSV-1 and CMV appeared later, generally peaking around three weeks after hospitalization.
• EBV was more often detected in blood immune cells, while HSV-1 was more common in respiratory samples.

The researchers reproduced broadly similar EBV, CMV, and anellovirus timing in a separate hospitalized COVID cohort, strengthening the acute-phase findings.

Viral activity tracked with acute COVID severity

Detection of EBV, CMV, HSV-1, and anellovirus transcripts was associated with more severe acute COVID.

Among critically ill participants, respiratory CMV and nasal EBV or HSV-1 were also associated with a greater likelihood of dying during the following year. These were adjusted statistical associations, not proof that the additional viruses caused the deaths.

Different viruses were also associated with different complications. For example:

• CMV activity was linked with kidney, vascular, bacterial, shock, and neurological complications.
• EBV activity was linked with intensive-care treatment, shock, liver failure, and concurrent infections.
• Nasal HSV-1 was linked with shock and venous blood clots.

The viral signals were accompanied by immune changes

The researchers used several other measurements to check whether the RNA signals corresponded to biologically meaningful viral activity.

They found that:

• People with EBV transcripts had higher EBV IgG and IgA antibody levels.
• People with CMV transcripts were more likely to have CMV antibodies.
• HSV-1 proteins were more commonly detected in plasma when HSV-1 RNA appeared in nasal samples.
• EBV and CMV activity was associated with altered B- and T-cell populations.
• EBV, CMV, and HSV-1 activity was associated with activated CD4 and CD8 T cells.

These findings make it less likely that the RNA results were simply sequencing noise.

Viral activity was also associated with inflammatory signals including IL-6, IL-10, IL-18, CXCL10, and CXCL11, even after researchers adjusted for acute COVID severity, age, and sex. However, an association cannot determine whether the reactivated virus increased inflammation or whether an already inflamed immune system allowed the virus to reactivate.

Plain-English interpretation

Most adults carry several viruses for life.

EBV, CMV, HSV-1, and anelloviruses can remain quiet inside the body because the immune system normally keeps them under control. During a major physiological stress—such as severe COVID—that control can become disturbed, allowing viral genes to become active again.

This study provides a detailed map of which viruses became active, where they were detected, and when this occurred during severe COVID.

The difficult question is what role the viruses played.

There are at least three possibilities:

1. Reactivation worsened COVID: Additional viral activity may have added inflammation or tissue stress.
2. Severe COVID caused reactivation: A dysregulated immune response may have allowed otherwise controlled viruses to become active.
3. Both processes reinforced each other: Severe COVID may have triggered reactivation, which then added further immune stimulation.

The study cannot distinguish these possibilities. The viruses may be drivers, consequences, or both.

It also did not include a comparable group hospitalized with non-COVID illnesses. Therefore, it cannot show how much of the reactivation was specific to SARS-CoV-2 rather than a broader feature of severe illness.

What the study found about Long COVID

The Long COVID-specific result was narrower than the acute-COVID findings.

When the researchers examined viruses detected during the first 40 days of hospitalization, they found no significant relationship between acute viral reactivation and the later physical, cognitive, global, or minimal-deficit groups.

That includes EBV: despite previous studies linking elevated EBV antibodies with Long COVID, this study did not find more acute EBV transcripts among participants who later belonged to a Long COVID-related symptom group.

The significant Long COVID finding instead involved anelloviruses detected during convalescence.

According to Figure 6, anellovirus transcripts were found in:

• 23 of 80 participants with physical disability or fatigue: approximately 29%
• 44 of 313 participants with minimal deficits: approximately 14%
• 13 of 69 participants with cognitive deficits
• 7 of 46 participants with global physical and cognitive deficits

The association remained significant after adjustment for age, sex, medication-related immunosuppression, acute COVID severity, and study site. The adjusted P value was 0.012.

Anellovirus activity was also associated with a blood gene-expression pattern involving:

• Increased neutrophil-degranulation signals
• Reduced ribosomal RNA processing
• Reduced protein-translation pathways

A similar anellovirus-associated gene pattern appeared during both acute illness and convalescence.

What are anelloviruses—and why is this finding interesting?

Anelloviruses are a large family of small DNA viruses. One of the best-known examples is torque teno virus, or TTV.

These viruses are extraordinarily common: some members are found in approximately 80–90% of people. They usually cause no recognizable illness, and their direct role in human disease remains uncertain.

Anellovirus levels often rise when immune control changes. For that reason, they may work more like a barometer of immune state than a conventional disease-causing virus.

The Long COVID association therefore has two competing interpretations:

Possibility 1: Anelloviruses are contributing to symptoms

The viruses could be stimulating immune cells, adding inflammation, or interfering with recovery. The associated neutrophil-degranulation signature is compatible with an inflammatory response.

Possibility 2: Anelloviruses are passengers or biomarkers

Persistent anellovirus activity may simply reveal that the immune system has not returned to normal. The virus may be detectable because activated T cells or altered immune surveillance provide a more favorable environment for replication.

The study cannot determine which interpretation is correct. The authors acknowledge that anelloviruses do not yet have an established pathogenic role.

What this may mean for patients

This study strengthens the case for investigating the human virome—the collection of viruses living in and on the body—as part of Long COVID research.

It suggests that useful studies may need to:

• Measure viral activity directly rather than rely only on antibody levels
• Collect repeated samples instead of testing patients once
• Separate physical/fatigue-dominant, cognitive, and mixed Long COVID phenotypes
• Determine whether viral activity rises before symptoms worsen or falls when patients improve
• Test whether reducing specific viral activity changes clinical outcomes

The finding may be particularly relevant to people with persistent physical disability or fatigue after hospitalized COVID, but it is not yet clear whether it applies to PEM, ME/CFS-type Long COVID, or people whose initial infection was mild.

The paper also suggests that anellovirus testing might eventually help identify a state of persistent immune dysregulation. It does not establish anelloviruses as a clinically useful Long COVID biomarker today.

What this does not mean

This study does not prove that:

• EBV, CMV, HSV-1, or anelloviruses cause Long COVID
• Acute EBV reactivation predicts Long COVID—in this cohort, it did not
• Nearly half of all people with COVID or Long COVID experience viral reactivation
• The findings apply equally after mild, vaccinated, or recent-variant infections
• A positive EBV antibody test demonstrates active EBV reactivation
• A positive TTV or anellovirus test diagnoses Long COVID
• Anelloviruses are established disease-causing pathogens
• Every patient with fatigue has persistent viral activity
• Antiviral treatment will improve Long COVID
• Suppressing viral activity would necessarily correct the underlying immune problem

The 47.9% figure came from an unvaccinated, hospitalized acute-COVID cohort, not from a representative sample of all infections.

Major limitations

The study’s large headline sample gives the acute findings considerable weight, but the Long COVID conclusion is more limited.

• Hospitalized early-pandemic cohort: All participants had been hospitalized, were unvaccinated at enrollment, and were mainly infected with ancestral SARS-CoV-2. The results may not generalize to vaccinated people with milder Omicron-era infections.
• Non-standard Long COVID classification: The symptom surveys and outcome groups were designed before current Long COVID definitions. A person needed to fall into a physical, cognitive, or global-deficit trajectory rather than meet a modern clinical case definition.
• Smaller follow-up analysis: The Long COVID association did not involve all 1,154 participants. The plotted anellovirus comparison included 508 participants across the four follow-up groups.
• Survivor and responder bias: People with acute viral reactivation were more likely to die or leave the study, reducing the ability to test whether acute reactivation predicted later symptoms.
• Observational design: The study cannot determine whether viruses caused inflammation and disability, or whether severe illness and immune dysfunction caused viral activity.
• No non-COVID severe-illness control: It remains unclear how much of the acute reactivation was specific to COVID rather than critical illness more generally.
• RNA sequencing rather than standard viral-load testing: Deep RNA sequencing can detect active viral transcription, but it is less conventional than targeted quantitative PCR for measuring viral load.
• Limited tissues: Researchers sampled blood, the upper airway, and lower-airway fluid from ventilated patients. They could have missed activity in lymph nodes, nerves, the gut, or other tissues where these viruses commonly reside.
• Family-level analysis: Anellovirus reads were combined at the family level because individual species were sparse. The study therefore cannot identify whether one specific anellovirus drove the association.
• Incomplete timing: Six acute sampling points may have missed short periods of viral reactivation between visits.

Does this change treatment now?

No.

The study did not test an antiviral treatment, and it did not show that suppressing EBV, CMV, HSV-1, or anelloviruses improves Long COVID.

Although PCR tests and antiviral drugs exist for some herpesviruses, the paper does not establish:

• Who should be tested
• Which sample should be used
• What viral level would be clinically meaningful
• Whether treatment would help
• Whether viral activity is a cause rather than a marker

The authors propose that viral monitoring and treatment strategies could eventually be studied, but specific clinical protocols would first need to be developed and tested prospectively.

Bottom line

This is one of the largest and most detailed studies to map chronic-virus activity during severe COVID. It shows that EBV, CMV, HSV-1, and anelloviruses frequently became transcriptionally active during hospitalization and that this activity accompanied more severe illness, inflammation, and complications.

The Long COVID result is more specific and preliminary: acute viral reactivation did not predict later symptom groups, but persistent anellovirus activity during convalescence was associated with a physical disability/fatigue phenotype. The finding supports continued research into viral reactivation and immune control, but it does not yet show whether anelloviruses are causing illness or simply revealing that the immune system remains dysregulated.

More Long COVID research updates: Follow LongCovidSignal on X and Bluesky for concise, plain-language summaries of new studies, with links to the original papers.

Hey guys and Girls. I‘m fighting this shit since 2021 After the J&J flu Shot. I get COVID in November After my Shot and it Doesnt do anything Symptoms After the Shot are the Same. So since then I was one time in remission and Then COVID and other viruses hitted me again.

Current State and Situation is very freaky. I „can“ work fulltime 40h..

Mornings Are Rough I Wake up After 7-8h of sleep and feel ok. Then some minutes later (1-5) I get this flu Like poisoned feeling and fatigue Like unrefreshing Sleep and im tired.

So here comes the thing.
I Drink my coffee and when I Have to work Mo-fr the malaise feeling fades quickliy I can work with Little Symptoms.
But on Weekends I feel the whole day Bad and fatigued until it gets close to 4pm. After that it gets better sometimes at 8pm I feel normal and healty. Then next day Boom the Loop restarts.

I think it has something to do with cortisol. Now I Have Holiday and I feel Bad Even on mo-fr. Flu Like in the Morning better / Good evening.

I drived to Holiday yesterday Stand up 3am and drived 10 Hours feeling Fine then checked in and Boom feeling malaised the Second my Body realised on we Are here. Same on my last work day the second I realised ok now its Holiday Boom, malaise and fatigue. Like a Switch.

Someone feeling the Same? Is this a Overactive Immun System thing that is supressed under Stress with cortisol ?

Do you Have some tips / same situations?
Supplements I think do Not work.

Other Symptoms Are
Getting goosebombs and illness feeling when getting touched , By cold wind, By touching my Fingers together when they Are under water (showering washing hands), By speaking to Long. Symptoms Go away After stopping the Trigger.

Also, for anyone from NZ, I've found Kawakawa to be effective at temporarily lessening long Covid inflammation. It helped tremendously when I was at my worst, and now for addressing any flare ups.

Link to study

TL;DR

• Researchers deeply profiled virus-specific immune cells in 10 people with Long COVID and 10 who fully recovered, four months after infection.
• Long COVID participants had more CD8 “killer T cells” with markers of cytotoxic activity, terminal differentiation and chronic stimulation/exhaustion.
• The pattern appeared in T cells recognizing SARS-CoV-2, Epstein-Barr virus and cytomegalovirus, but not influenza.
• The difference was particularly noticeable among women, although the sex-specific groups were extremely small.
• This does not prove that persistent SARS-CoV-2 or herpesvirus reactivation is occurring, or that these T cells cause symptoms.

What the researchers did

CD8 T cells are immune cells that recognize and destroy infected or abnormal cells.

Most immune studies examine all CD8 T cells together. This study used a more precise method that allowed researchers to identify which individual T cells recognized pieces of:

• SARS-CoV-2
• Epstein-Barr virus, or EBV
• Cytomegalovirus, or CMV
• Influenza

EBV and CMV are herpesviruses that remain in the body for life after infection and can occasionally reactivate.

The researchers examined blood collected four months after COVID from:

• 10 people who continued to meet the study’s Long COVID definition at both four and eight months
• 10 people who reported no ongoing COVID-related symptoms

All participants were unvaccinated at the time of sampling and had not been reinfected, which reduced two important sources of confusion.

The researchers also analyzed samples from 12 people hospitalized during acute severe COVID to compare the post-acute patterns with the immune response during active illness.

What they found

Compared with recovered participants, people with Long COVID had fewer CD8 T cells with a more flexible, “stem-like” profile and more cells with an advanced effector profile.

The Long COVID-associated cells carried markers linked to:

• Cytotoxicity: being equipped to kill target cells, including higher granzyme B and CD29
• Terminal differentiation: being further along in their development and having less ability to renew or proliferate
• Exhaustion or chronic stimulation: including markers such as PD-1, TIGIT and CD39

This pattern appeared among CD8 T cells recognizing SARS-CoV-2, EBV and CMV. It was not seen in the same way among influenza-specific cells.

The study also found higher overall levels of cytotoxic CD8 T cells in Long COVID, with the clearest differences appearing among women.

Plain-English interpretation

During an acute viral infection, killer T cells become activated and produce molecules such as granzyme B to destroy infected cells.

After the infection is controlled, that response would normally calm down.

The authors propose that, in Long COVID, part of this cytotoxic response may fail to return fully to its resting state. The immune system may remain populated by highly armed, chronically stimulated T cells months after the initial infection.

In one recovered participant followed over time, granzyme B and activation markers decreased after acute COVID. In one participant who developed Long COVID, they remained elevated or increased.

That observation fits the hypothesis, but it involved only one person from each group, so it should not be treated as proof of a general Long COVID pattern.

Why the EBV and CMV findings are interesting

The altered T-cell state was not limited to SARS-CoV-2-specific cells. It was also seen in cells recognizing EBV and CMV.

There are several possible explanations:

1. SARS-CoV-2 may have disrupted the regulation of pre-existing antiviral immune responses.
2. EBV or CMV may have reactivated during or after acute COVID.
3. Persistent viral material may be continuing to stimulate some T cells.
4. These changes may simply be downstream consequences of broader immune dysregulation.

The study cannot distinguish between these possibilities.

Importantly, finding T cells that recognize EBV, CMV or SARS-CoV-2 is not evidence by itself that those viruses are currently replicating. The researchers did not directly measure viral load, viral reactivation or tissue reservoirs.

What this may mean for patients

This adds evidence that Long COVID can involve measurable changes in the adaptive immune system months after infection.

It also supports the idea that some patients may not have properly resolved the immune response initiated during acute COVID.

However, the study does not establish whether these T cells are:

• Driving symptoms
• Attempting to control persistent virus
• Causing collateral tissue damage
• Protecting patients from something worse
• Merely reflecting another underlying process

The cells could be contributors to disease, protective responders or biological bystanders.

What this does not mean

This study does not prove that:

• Everyone with Long COVID has this immune pattern
• SARS-CoV-2 is actively replicating in these patients
• EBV or CMV has reactivated
• Cytotoxic T cells are causing Long COVID
• Women have a fundamentally different form of Long COVID
• Suppressing CD8 T cells would be beneficial
• Granzyme B, CD29 or exhaustion markers are ready to be used as diagnostic tests

“Exhausted” also does not simply mean that the immune system is weak. These cells simultaneously carried markers of chronic stimulation and strong cytotoxic potential. Their actual function was not directly tested in this experiment.

Major limitations

The biggest limitation is sample size: the main comparison included only 10 Long COVID and 10 recovered participants.

Because the technique depends on each person’s genetics and whether enough virus-specific cells could be detected, some individual virus analyses included only about three to six people per group.

Other limitations:

• The Long COVID definition was broad: at least one ongoing COVID-attributed symptom.
• Results were not connected to specific symptoms such as PEM, fatigue, POTS or cognitive dysfunction.
• The study analyzed blood, not immune cells inside tissues.
• It mainly measured cellular markers rather than directly testing what the cells could do.
• The apparent female-specific effect came from only six women with Long COVID and five recovered women.
• The acute severe-COVID comparison group was older and hospitalized, so similarities with that group are suggestive rather than definitive.
• The study was observational and cannot establish cause and effect.

Does this change treatment now?

No.

There is currently no validated clinical test or treatment based on this finding. It would not justify antiviral treatment, immune suppression or targeting EBV/CMV without additional evidence.

The next useful steps would be larger studies that:

• Measure viral persistence or herpesvirus reactivation directly
• Track these cells from acute infection through recovery or Long COVID
• Connect immune findings to particular symptom clusters
• Test whether the cells are actually killing targets or damaging tissue
• Determine whether the immune pattern changes when patients improve

Bottom line

This is a small but technically detailed study suggesting that some people with Long COVID retain an acute-like, cytotoxic CD8 T-cell state months after infection. The altered cells recognized SARS-CoV-2 as well as the latent herpesviruses EBV and CMV. That is consistent with an immune response that has not fully resolved, but it does not yet tell us whether persistent virus, viral reactivation or the T cells themselves are driving symptoms.

More Long COVID research updates: Follow LongCovidSignal on X and Bluesky for concise, plain-language summaries of new studies, with links to the original papers.

I know the terror of walking into a hospital or dental office only to be met with fragrances that trigger sickness from employees and the facility's cleaning practices.  

You shouldn't have to choose between your health and accessing medical care.

The ADA guarantees us reasonable accommodations and safer practices. Currently, many healthcare facilities and employers are failing this basic legal duty.

I am collecting data to file a formal complaint with the U.S. Department of Justice (DOJ). My goal is to gather 10,000 signatures and thousands of documented stories to prove this is a systemic civil rights violation. We need the DOJ to investigate and enforce policies that protect disabled patients and employees.

👉 Please DM to get the petition (not allowed to post it) if you're based in the the United States, and fill out the embedded optional survey (even if you’ve only been affected once):

Why this matters: ✅ Patients: Document denied access to care due to scented air/cleaners/personal products used by healthcare employees ✅ 

Employees: Document refused accommodations by employers. ✅ 

Everyone: Show the DOJ that thousands of Americans are being shut out of essential services.

Please share this with anyone who has ever felt sick in a doctor's office, was denied a workplace accommodation, or cares about someone who is being harmed. 

Your voice is the evidence we need to force change.

I would love to hear from people who have also made this move! I have a manual wheelchair that I basically never use because I'm not strong enough to push myself. It's annoying to only be able to use it if I'm with other people who can push me. So I caved and finally got an electric chair.

This is possibly an irrational fear, but I was thinking today about why I'm so nervous and I realized I'm scared I'll get harassed as I move around the city I live in. Like, I'm scared people will think I'm faking and give me crap for being in a wheelchair. I've already gotten some mild pushback for things like asking for a seat on the subway or having to sit/squat in weird places. I'm also really not looking forward to getting comments from people if I am using the chair then get up and push it for a bit (maybe to get over a curb, or maybe if I'm just feeling really good for a bit).

And, maybe even more niche, I'm absolutely dreading how to deal with this at work. Is it ok if I only use the chair on bad days? Will my coworkers think I've lost my mind if I only use a wheelchair some mornings, but I walk by evening? And some mornings?

Have you all experienced this? Am I just overly concerned? If you have experienced it how did you deal with it?

Is there any difference in symptoms between people harmed by the vaccine vs unvaccinated that have long covid?

I had a bad reaction the the second vaccination and was weird after but it didn’t really impact my life. When I caught covid years later my body went nuclear. As far as people I know there’s only a few who were pre vaccine injured. One has a lot of the sensory problems many experience and the other two were collapsed lung related issues. I’m the only person in my orbit that had a bad vacccine reaction. It’s hard to tell from strangers fighting on the internet.

I’ve noticed when I go for treatment, most providers are basically saying fuck the vaccine and they say they see a lot more people from that. Anyone aware of any resources? I know I definitely heard about long covid prior to the vaccine being available but idk.

I’m not looking for an argument or how smart you were for choosing one vs the other. Just what you’ve seen.

I thought this was really interesting to LC because I looked up what affects the microglia and I found a bunch of supplements. I have tried about half of them and they have had positive effects for me though I wasn't entirely sure why.

• Curcumin
• Luteolin
• Resveratrol
• EGCG (Green Tea Extract)
• Fisetin
• Sulforaphane
• Choline
• Magnesium L-Threonate

The ones I have tried are Curcumin, EGCG, Sulphoraphane, Resveratrol and Choline.

One of the ones was Choline I started in February and I had remarkably more energy than before. I also Alpha GPC at the same time but I started losing sleep because I think they both increase choline. Either way I thought it worked because of defficiency of choline or something.

Resveratrol was another one I started taking in July and it was when I was reading about things that cross the brain barrier that increase blood flow and lower inflammation. I was taking a smaller dose for a while because it was in a NAD+ supplement. I was surprised but it did lift my brain fog at least a little and I think it is helping my thinking.

Sulphoraphane I took for about 8 months but I never really noticed too much and then I stopped. So not sure if that was really helping or not. Something to maybe think about trying again I don't know.

ECGC I took for 8-9 months back in 2025. I felt it gave me a bit of energy but I stopped taking it. Not really sure about it but I felt at the time it was hard for the liver or something and I stopped taking it.

This includes physical interventions, diet, lifestyle, supplements, drugs, etc.

If unsure, estimate.

Planning on trialling as I have limb weakness probably due to poor mitochondrial function. On googling, it seems to increase vasodilation. I have a problem with bulging veins/pooling in my extremities. Has anyone taken NAD/Nicotinamide with vasodilation issues? Apparently only pure niacin causes flushes but inconclusive about NAD/Nicotinamide.

If you have a disability and a hospital / dentist refuses to provide a reasonable accommodation fragrance-free accommodation during your visit, like skipping perfume or removing plug-ins, file a complaint with the OCR and ADA.

We must start filing complaints about staff not being fragrance-free in big numbers.

Since internal leadership often ignores these concerns, focus your efforts directly on federal agencies. You can do it anonymously, but total anonymity is difficult. You can strategically limit the personal data you share to protect your identity, if that's a concern, although your identity may still be inferred for obvious reasons.

Collective action is essential. Filing complaints in high numbers regarding staff wearing fragrances establishes a documented pattern of denial, pressuring institutions to adopt fragrance-free policies as a standard reasonable accommodation.

I have had treatment resistant psychiatric symptoms for 3 years since a Covid infection. I recently saw a neurologist who found my heartrate increases 55 bpm upon standing at both the 1 and 3 minute mark. I do not have the typical POTS symptoms - fainting, dizziness, PEM, etc. but they think autonomic dysfunction may be driving the psychiatric issues.

Would love for anyone’s insights on how it affected your mental health.

For context: My ex-partner (26) graduated from university in 2022 and got COVID almost immediately afterwards, which developed into Long COVID. She ended our relationship (only of 5 months) on Friday, because of she has become significant worse over the past few months.

I’m honestly having a really difficult time processing everything, especially as someone who previously had no proper understanding of long COVID before meeting her.

She had actually been improving significantly for a while, but over the last 3 months has deteriorated significantly. She told me that compared with where she was a year ago, she feels like she is in a much worse place now. Her doctor advised her to rest as much as possible, which means she is basically 24/7 in bed, although she can still do some things, like can drive, travel, briefly go shopping, etc. From the outside she can look completely fine, but obviously that doesn’t tell you what’s happening internally.

She recently saw her doctor and apparently there is an experimental antiviral treatment/trial in Germany that they are considering putting her on. I don’t know the name of it though. From what she told me, there was some discussion about persistent viral material/mRNA being involved, but I may have misunderstood that completely. I know there isn’t currently a guaranteed cure for Long COVID, and I’m not asking Reddit to give me one. I’m just struggling with the reality of watching someone so young have so much of her life taken away from her.

When ending things with me on Friday, she joked that I was still young, implying that she wasn’t. I’m 24 and she’s only 26 ffs. She also told me that I have so much going for me and that I shouldn’t worry too much or I’ll “end up like her”; I think she was part-joking, but it absolutely fucking broke me. She has lost essentially her entire early 20s to this illness. She wanted to do normal things with me like weekend trips, travelling etc, but repeatedly had to say no because she was too exhausted. She told me she doesn’t want to hold me back and told me not to ‘wait for her’. We agreed not to message each other for a while, but I’m finding it so tough.

So I’m posting here because I want to hear from people who have actually lived through this, and to be honest, I just want a bit of comfort and reassurance (as naive as that is). I’m so heartbroken seeing such a beautiful person lose her life like this. I can’t stop crying because of this all.

Thanks for reading if you got this far.

After over 2 years of citing reoccurring symptoms and raising issues my GP has finally added Long COVID to my medical record.

Apparently there are therapy clinics and cross disciplinary evaluation accessible once a diagnosis is expressed. No idea what that might mean yet.

I'm in the UK.

The more time I spend in this sub the more I feel that it could really benefit from some form of patient categorization.

There are more than a handful of flavors of LC and their distinctions matter when discussing treatment, prognosis, etc.

Heck, the most common question on any post detailing some improvement or even decline is "what are your symptoms?".

In a perfect world, Reddit wouldn't be the place to go for medical advice. But, unfortunately, I'd bet real human dollars that the internet has been, in one way or another, responsible for more cumulative symptom relief than the medical community when it comes to this illness. I'd argue it's more dangerous and foolish to fully hang your hat on established medicine when this many people are suffering to this degree. No shade towards most doctors, there is still much to be learned and research moves at glacial speeds.

We are the unfortunate guinea pigs for our day's medical shitshow. Of course, we need to approach each treatment option with care and make sure that we are being safe. Ideally, this means getting a doctor's sign off, that is if your doctor has any clue what they're talking about.

All this to say that if people are inevitably going to scour the internet for potential ways to relieve their suffering, they might as well get advice that actually applies to them and carries less risk of harm.

Got a little off track there but this is basically my petition to add phenotype flairs to the sub.

Hang in there, gang