Could ME/CFS be next?
T-cells fight off pathogens. Even after 2 years they were surprisingly activated in both recovered and long-COVID patients.
There’s nothing like a pandemic to open new doors on post-infectious diseases, and it’s no surprise that the Henrich/Peluso team at the University of California at San Francisco would be the ones to do that. With their LIINC project, they have embraced long COVID like no other group.
Leave it to them to do the first whole-body positron emission imagining (PET) study in long COVID. In a preprint, “Multimodal Molecular Imaging Reveals Tissue-Based T Cell Activation and Viral RNA Persistence for Up to 2 Years Following COVID-19“, Henrich and Peluso et al. keyed a radio-tracer on activated T-cells to see what happened with one of the big guns of the immune response.
THE GIST
- Once again, long COVID prompts investigations that researchers in ME/CFS have wanted to do for years but lacked the funding for.
- In this study, UCSF combined a whole-body PET scan with a radio-tracer keyed on activated T-cells to see what happened with the T-cells – one of the big guns of the immune response, over two years.
- Theoretically, the T-cells should have ramped up to knock down the virus and once they did that, quieted down – but that’s not what happened at all.
- Even in the recovered group, the T-cells remained abnormally activated in a whole slew of tissues. Finding so much T-cell activation suggested that the coronavirus infection had resulted in “a new immunologic steady state”.
- T-cells were particularly activated in in the long-COVID cohort just where you might expect it to be – the brainstem, spinal cord, gut, and lungs (in people with pulmonary symptoms).
- The brainstem stood out. Located at the bottom of the brain, the brainstem regulates very basic functions – like breathing, heart rate, blood pressure, digestion, alertness, and sleep – the fundamental stuff you really don’t want to go wrong – and much of which has gone haywire in ME/CFS.
- Henrich, the senior author of the study, reported, “You really shouldn’t have activated T cells in the spinal cord or the brainstem. We are seeing evidence of this immune response in areas we don’t typically see in the setting of an acute viral infection.”
- The study also zeroes in on activated immune cells called macrophages which have recently been of interest in ME/CFS, and found evidence of pieces of the coronavirus in gut cells.
- All in all, the study suggested that a widespread attempt to continue to fight off the infection, or an autoimmune response, was present. It provided more weight to the idea that pathogen persistence may be driving post-infectious diseases.
- Because it focused on immune activation instead of targeting a specific pathogen, this is the kind of study that could easily be done in ME/CFS.
The Study
The question was – what was happening to the T-cells over 2 years in long-COVID and recovered COVID patients? Theoretically, the T-cells should have ramped up to knock down the virus, and once they did that, quieted down – but that’s not what happened at all – not even in the recovered group.
Even in the recovered group, the T-cells remained abnormally activated in a whole slew of tissues – the brain stem, spinal cord, bone marrow, nasopharyngeal and hilar lymphoid tissue, cardiopulmonary vasculature, lung parenchyma, and gut wall. Finding so much remaining T-cell activation in the recovered patients suggested that the coronavirus infection had resulted in “a new immunologic steady state”.
The T-cells could still be trying to cleanse the body of the coronavirus or they could reflect an autoimmune response. Whatever is happening it’s clear that infections – even infections that seem to have been fought off – have consequences. It will be interesting to see what happens to the recovered patients over time given the unexpectedly high rate of T-cell activation still present.
While T-cell activation was increased in tissues across the body in the recovered patients, it was particularly increased in the long-COVID cohort just where you might expect it to be – the brainstem, spinal cord, gut, and lungs (in people with pulmonary symptoms).
Back to the Brainstem
The brainstem stood out. Located at the bottom of the brain, the brainstem regulates very basic functions – like breathing, heart rate, blood pressure, digestion, alertness, sleep – the fundamental stuff you really don’t want to go wrong – and much of which has gone wrong in ME/CFS. Because it also filters the sensory and “motor” signals from the spinal cord, it also seems like a good place to produce problems with stimuli. It’s also densely packed with mast cells – a clear problem in ME/CFS.
Problems in the brainstem would be a darn good way to dysregulate a bunch of systems. We know that, in part, from Jeff and Jen Brea’s experiences with craniocervical instability, which caused their skull to contact their brainstem – producing virtually all the symptoms of ME/CFS. Down in Australia, Barnden has been charting brainstem dysfunction in ME/CFS for years.
Stating “We saw some very unexpected findings”, Henrich, the senior author of the study, told National Public Radio (NPR) “You really shouldn’t have activated T cells in the spinal cord or the brainstem. We are seeing evidence of this immune response in areas we don’t typically see in the setting of an acute viral infection.”
Pathogen Persistence
The question was what was causing the T-cells to go off? Since cytotoxic T-cells are pathogen hunters – the obvious answer was that either a lingering virus, or parts of a virus, were still present. Of all the tissues, the colon was apparently the easiest to biopsy and search for the virus, and so they did – and there it was – SARS-CoV-2 RNA was found in virtually all of the long haulers’ gut samples – providing more evidence that pathogen persistence – whether as a whole virus or as bits of it – could be driving the disease.
Next, the UCSF group examined different cells in an attempt to determine where the SARS-CoV-2 virus (the coronavirus), or pieces of it, might still be hanging out two years later, and found them in another immune cell pathogen hunter – the macrophages. Macrophages get rid of pathogens by ingesting them and breaking them up.
Infected macrophages nestled in the tissues could draw more immune cells after them, potentially causing chronic inflammation. The macrophage finding is particularly interesting given Andrew Grimson’s fascinating gene expression finding pegging monocytes (which turn into macrophages when activated) as the center of the immune dysfunction in ME/CFS.
Avindra Nath also found macrophages in the brain tissue of long-COVID patients and Bruce Patterson’s long-COVID protocol focuses on stopping monocytes from reaching the blood vessels.
Not everything was clear. Perhaps because the study was small they did not find correlations between the T-cell activation and symptoms. Still, the study was novel in is ability to find evidence – the authors called it “provocative evidence” – of long-term immune system activation in the tissues.
The tissues have been like a black box in ME/CFS, but then again we’ve never had studies like this. The big question has been whether bits of enterovirus, or other viruses that we don’t see evidence of in the blood, are tweaking the immune system and causing symptoms.
Takeaways
There were several takeaways from the study. Whether you have long COVID or not, the coronavirus appears to be having a dramatic long-term effect on the immune system. Even recovered patients still exhibited a striking immune activation several years after they’ve recovered from the virus.
Secondly, immune activation is particularly increased in long-COVID patients in some intriguing areas. The brainstem, the spinal cord (cerebral spinal fluid leaks, spinal fluid hypertension), and the gut (IBS) are all areas of interest in ME/CFS.
Thirdly, the pathogen persistence hypothesis – which seems to get stronger and stronger as time goes on – was strengthened by finding activated pathogen hunters – the T-cells – in areas across the body – and by finding pieces of the coronavirus in gut tissues. With the pathogen findings ratcheting up, and the Long COVID Research Initiative plowing money into pathogen persistence, we should be hearing much more about this vital issue.
Finally, the whole body PET scan /T-cell study is yet another example of long-COVID sparking research into potentially important areas that the small ME/CFS field always wanted to explore but never got a chance to do so. Because it focused in immune activation, and not on a specific pathogen, this is the kind of study that could be easily done in ME/CFS if the funds were present.
On that note, we should hopefully soon know from Jarred Younger and his fascinating MERUK-funded study whether immune cells from the body are invading the brain in ME/CFS.
Questions remain. The study was small (24 people). We don’t know if the T-cell activation is a real problem or is it a kind of add-on. Is the immune system targeting coronavirus RNA across the body or is an autoimmune reaction present? Whatever is causing it, another door has been opened. The finding is striking enough that it will surely lead to more studies.
Dear Cort, I consider you a hero in this universe of what we now call ME/CFS. I am constantly impressed by your ability to stay on top of all this information and even more digest it and write it up so that most anyone can get the gist of the issue covered.
You really deserve enormous props and any and all possible awards. I don’t come to Health Rising as much as I should for reasons having to do with over half a century of suffering from this syndrome/disease. . .I have to step away for long periods and concentrate on the work I was meant to do in the world as best I can.
My illness began when I was 22 after mono. By my late 20s I was visiting as many sophisticated doctors as I could find. One tested my T cells. I still have the results of that test buried somewhere in my papers. My T cells were off the charts. He told me that my results in an AIDS patient would be considered dire. I actually had another doctor tell me the results meant nothing. Needless to say, I knew that doctor was incompetent and cruel.
I am not sure what this study terms activated T cells means. Mine were elevated and, of course, not tested in situ.
Today’s Washington Post article about WASF3 and mitochondrial respiration lead me back here to check on what you might have posted. I am a month late catching up.
The best therapies for me have always included Dr. Myhill’s suggested protocol for addressing mitochondrial dysfunction, especially B12 injections. My current doctor won’t even consider prescribing them, sigh.
I have also found a Keto diet to help as have many others. Staying on it requires much discipline.
I have leaky gut which I believe abates with a Keto diet.
The brainstem connection really surprised me when I first read about it, but because I believe ME/CFS is the result of some process distributed throughout the body, there is no reason why the brainstem would not have a specific response.
I also believe that the immune system is intertwined with the nervous system and that the mind/body dualism which rules our culture prevents the medical establishment from understanding the totality that is the body/mind.
Today’s WP article sent me off in a tizzy because it, once again, gave me hope that something might be done about this century long travesty of willful ignorance regarding ME/CFS. That tizzy lead me here where I just had to add my two cents.
AND
a thank you, ramona
Thanks Ramona and thanks for mentioning Brian Vastag’s great article.
https://www.healthrising.org/blog/2023/08/16/nih-mitochondria-chronic-fatigue-syndrome/
Health Rising actually covered it a couple of weeks ago but Brian’s article fleshes things out more 🙂
Lots of things are happening – be sure to stay tuned! 🙂
Cort is definitely a hero!!
Well said! Ramona
Fascinating! I am interested in how the vaccines and boosters fit into this picture… What was the status of those tested? I have been advised not to get vaccines for medical reasons, but I have natural immunity from Covid Feb 2020. I have long covid.
That would have been an interesting study! At some point they’re going to to have to include that. I imagine that most of the people were not vaccinated in the beginning as the vaccines may not have been available but later on I’m sure some were. Interesting question!
If you click the link to the study and look at Table 1 they show the days from vaccine and the days from covid to when they had the PET scan. The study shows that all but one participant was vaccinated and two patients were hospitalized.
Nice! Thanks James 🙂
Allow me to use this comment forum to communicate the following. Today’s Washington Post has an article about NIH scientist’s breakthrough in finding the cause of ME/CFS – ramping up WASF3 in mitochondria. Hope the link is accessible.
https://wapo.st/3Pem0G4
thanks for link!
Interesting article Guang, thanks!
Great article from Brian!
We covered this in a blog a couple of weeks ago but it was great to see Brian flesh it out more – and good for WAPO to feature it 🙂 Fingers crossed!
https://www.healthrising.org/blog/2023/08/16/nih-mitochondria-chronic-fatigue-syndrome/
Hope scientists could show a statistic distribution of WASF3 level in a group of , say, 200 ME/CFS patients and the same in a group of healthy people. This would indicate WASF3 is a convincing biomarker for ME/CFA. All the biochemical information just goes straight over my head.
I’ve been working with Dr Systrom in Boston and when I saw this article, I naively asked if I could get muscle tested for WASF3. His pa explained few places do this and even if they did it would cost 10s of thousands of dollars not covered by insurance.
So we do indeed need larger studies on this.
Thankyou Cort. Another fantastic article. My worst symptom has always been severe pain in the back of my head and neck. It is interesting that “pathogen persistence may be driving post-infectious diseases”. As someone with chronic reactivating Epstein Barr virus, this makes a lot of sense. For this reason, subgroups like mine really need some type of treatment to address the EBV infection. The treatments exist now (for Multiple sclerosis) but it is as though PWME are invisible to these researchers.
Wish I could have been in this study bc of my 2 PET scans which showed hyperactive mediastinal lymph nodes along w the c-spine inflammatory lesion. My dx of possible neurosarcodosis which followed came even though I had atypical symptoms. 8 years later, I still believe it is all related to my 30years of ME/CFS.
Right – T-cell activation in the spinal cord! That could tweak so many nerves and cause so many problems.
Your case was very atypical indeed. If I remember correctly, one doctor was surprised you were still walking…
Interesting! But not sure about this. People who recovered from covid also had high levels of T cell activation, right? So potentially it is an ‘add on’ (secondary factor) rather than a causal factor in illness.
I have long been interested in peripheral versus central inflammation / immune activation. Perhaps this study is suggestive of the theory I favour that in ME/CFS (and long covid?) we have peripheral inflammation, but for us this crosses over, if you like, in to the central system (CNS), with resulting fatigue etc. The study seems to suggest that the T cell activation in the brain, if not the periphery, was greater in the long covid patients?
Personally, with myself as guinea pig (!), I have found significant value in reducing both peripheral and central inflammation. Address the former and you should get less of the latter. But addressing the latter directly is also important.
And it sounds like Younger’s study might help answer this question.
Yes, it’s potentially an add-on, and T-cell activation in the brainstem, spinal cord, gut, and lungs was significantly higher in the long COVID patients. I would not be surprised if you’re right that reducing peripheral inflammation should help. That was put less stress on the central nervous system which may be having trouble coping with all the signals hitting it.
I have had real success with curcumin over the years. Allows me to do mild-moderate exercise.
Thank you for all you do to keep us updated on the latest research. Your article today and the link from the Washington Post article supplied by Guang Rong are keeping me hopeful.
I was diagnosed with CFS in 1990 after a serious case of EBV. In 2008, I had a bout of H1N1 which really flared my CFS and I also experienced a Takotsubo Syndrome event (acute stress cardiomyopathy). My POTS symptoms worsened and I was usually housebound and was now at a new level of illness that did not improve but waxed and waned.
Last year in august 2022, I had Covid and two more viruses (flu) in rapid succession within 4 months into early 2023. I was not surprised that now I was even more ill with either a bad CFS flare or long Covid. Then in August of this year, I experienced another more serious Takotsubo event which is technically a heart attack without blockage caused by either physical or emotional stress. If caused by emotional stress, this is usually a one off event but if caused by a virus the prognosis isn’t as good. I now have another unexplained and under researched mostly female illness diagnosis. It seems the rates of Takotsubo Syndrome have gone up exponentially since Covid. This illness affects primarily women and usually over the age of 50. It is very under researched and usually represents about 2% of the heart attacks but now after Covid , the rates have almost tripled. This diagnosis is frightening because it can be fatal and/or reoccur. I was in the ICU with my heart functioning at 10%. Fortunately, to the doctors surprise my heart function improved and I was discharged after a week as now a bedbound CFS sufferer.
What I have found from research and patient su-port groups is that the doctors are as puzzled about this problem as they are with CFS and Long Covid. I believe this heart syndrome is related to post viral syndromes and I so hope that all the new research helps all of us who have ongoing CFS and/or long Covid syndromes.
I have always known heart issues are a problem with CFS but this heart issue is under reported so that even the greater CFS community never mentions it. They do in the Takotsubo groups of where there are people with CFS
Fascinating, Renee – interesting that the microvascular circulation is implicated.
“Impaired microvascular function is seen in a vast majority, if not all, of patients with TTS and is currently one of the most supported theories.”
It “is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the muscular portion of the heart.”
“Excess catecholamines, when released directly by nerves that stimulate cardiac muscle cells, have a toxic effect and can lead to decreased cardiac muscular function or “stunning”. Further, this adrenaline surge triggers the arteries to tighten, thereby raising blood pressure and placing more stress on the heart, and may lead to spasm of the coronary arteries that supply blood to the heart muscle. This impairs the arteries from delivering adequate blood flow and oxygen to the heart muscle. Together, these events can lead to congestive heart failure and decrease the heart’s output of blood with each squeeze.”
Cort, any thoughts on approximately when Younger’s research results might be out?
I think we could hear something about his preliminary findings by the end of the year.
Thanks! Look forward to it
As someone with a PhD in immunology I find these results sort of shocking if it is the case the T cell activation is persisting 2 years after COVID infection – that is just not normal after an acute infection/viral clearance and the T cells can’t stay persistently activated like that without causing major issues (yes, could be autoimmunity or T-cell exhaustion like you see with persistent activation from cancer). Either way, it begs the question why those “recovered” patients don’t have more problems resembling long COVID if their immune system is really that out of whack?
I just glanced at the actual study – it is a preprint, not peer reviewed, so a bit more skeptical of it. Also the PET tracer they are using is not validated or widely used from what I can tell and doesn’t tell you anything about the type of T-cell activation or WHICH T cells are activated (can’t say it would be CD8 or cytotoxic T cells rather then CD4 T helper cells or Tregs which actually dampen inflammation). They do flow cytometric analysis and see higher CD8 and CD4 effector memory T cells but then go on to say the T cell phenotypes weren’t correlated at all with the PET uptake or long COVID symptoms?? Also they used pre-pandemic controls from before 2020 that had this PET tracer used and there could have easily been differences in the signals generated in that much earlier timeframe than when this study was done, so not a good comparison and also not specified why those controls had this imaging to begin with. I think the overall premise makes sense but requires a lot more investigation – like, say, look at the PET uptake over time in the same long COVID patient or recovered patient to see if uptake wanes or not within one patient?
Because the issue with ME/CFS and long covid is inflammation in the brain. The inflammation in those who recovered is confined to the periphery.
The findings related to inflammation of the brainstem in ME/CFS and Long COVID can also be found in the 2023 Griffith University Study in QLD, Australia. Using the world’s strongest MRI machine, they found almost identical brainstem inflammtion in ME/CFS and Long COVID patients.
https://news.griffith.edu.au/2023/03/14/worlds-strongest-mri-investigates-covid-and-myalgic-encephalomyelitis-chronic-fatigue-impacts-on-the-brain/
I wonder how their findings compare to Dr Artur Fedorowski’s recent study of biomarkers in POTS. Sadly I am not fluent enough in biology to read both papers and compare.
Oops, just realised this papre is looking at T-cells, and Dr Fedorowski was looking broadly.
C=ort, when will they do finally big rigourus research in ME/cfs? i am il since ’94. am at the end of my rope. Like so many. I wish long covid patients the best research and treatments. but where are we with ME/cfs, etc? i have the feeling still nowhere because no money. Even nancy klimas, so many promises of research, treatment, still nothing… Many verry severe people simply can no more… And also for the ones alone and verry severe still no adapted homes with adapted care and up to date knowledge.. They can rot in hell…
I posted in an email above about how long and difficult my journey has been also. But, I feel that without Covid and the research money that is going to Long Covid, we in the CFS community would be getting the same attention we have gotten for decades – next to nothing!
We have hopped on their bandwagon or they on ours with the addition of millions of research dollars. We have more hope now than ever because of long Covid research. I am grateful rather than bitter for the participation and feel if long Covid benefits, so will the CFS community.
Given my experience this past summer with heart issues, that is saying a lot. Also, the last couple ER and hospital trips, the medical personnel are so much more accepting and knowledgeable about CFS and POTs. Instead of gas lighting my symptoms, I was treated with respect and sympathy. This was even without a cure – priceless!
If I read correctly you had serious measurable heart problems. How can they not take that seriously? That doesn’t mean they take CFS/ME/POTS and Long Covid seriously. These conditions are still considered psychosomatic by the medical community.
I have had several serious medical issues in the 30 plus years that I have had CFS. Quite often the medical community treated me as you alleged and I often tried not to mention CFS because it would change the doctors attitude and they would treat me differently . I only started noticing a change 6 months ago when I had an ER visit and I mentioned POTS and this time most of the medical staff knew what I was talking about and were surprisingly supportive.
With my first Takotsubo event in 2008, I mentioned CFS and the cardiologists had the typical reaction of disdain. Now this time in aug 2023, they knew what CFS was and that it was a post viral illness. They were not aware of the connection with Takotsubo and Covid but were aware of the connection between Covid and CFS which surprised me. I am sure this varies by specialty and cardiology uses the POTS diagnosis to add CFS people to its fold so,they have a better understanding of,this illness. Being that Takotsubo cardiomyopathy is relatively rare, more nurses etc. recognized a POTS diagnosis than Takotsubo. That doesn’t make me feel better either! In the last 3 months I have been to the ER four times in all and I have seen quite a few doctors and staff. So in my experience, things are looking up for recognition. As far as me getting healed , there isn’t anything anyone can do for CFS and Takotsubo is take a blood thinner, a beta blocker and hope your heart heals. This is still all disease management not healing. But ,
for me recognition is important too and the research possibilities are promising.
That POTS is being recognized and treated seriously is a huge step forward. I was amazed to learn that even with its biological underpinnings POTS was always accepted! Glad to hear things are changing.
in my country not, it is still cfs, GET and CBT or rot in hell. In many countrys.
I guess you are from the US where healthcareworkers get educated?
here no education in any way….No POTS, nothing… ill since ’94, 99% bedridden. declining further. Could for so long not even go to specialist…
Konijn. I do believe the medical community is being educated about CFS because of long covid and therefore taking it more seriously.
More literature is showing that long covid is in fact CFS. I think Cort may have mentioned these articles before.
https://www.statnews.com/2023/09/14/long-covid-me-cfs-myalgic-encephalomyelitis-chronic-fatigue/
https://www.frontiersin.org/articles/10.3389/fmed.2023.1187163/full
here in my country not. I think you are also from the US?
in my country it is still cfs, GET and CBT or rot in hell. In many countrys.
In the US healthcareworkers get educated…
here no education in any way… No intrest, nothing…
Yes, I’m in the US. I’m so sorry you’re going through this. I have had it 30 years as well. I live alone. I can go out 1-2 days a week, mostly for doctors and running errands. I’m home resting on couch or in bed rest of the time. The frustration is real.
good update.
I have been dreadfully
decapacitated by long covid – 2 years now
and by side effects following the third covid booster jab.
I can no longer work as a nurse or do any other job.
Stayed tuned! Lots more is coming out 🙂
I have a question on my surprising response to Paxlovid treatment for Covid in June this year. For the five days on Paxlovid, a range of FMS & ME symptoms started subsiding. I was shocked and terribly hopeful. Symptoms all returned within days after the Paxlovid. I have had Fibromyalgia since 1981, and an ME/CFS diagnosis since 1993 with the late Dr. Jay Goldstein. Decades of very compromised function, medical testing, money, and pain. IS THIS A Paxlovid response YOU HAVE HEARD OF BEFORE??
Secondly, what antivirals could be tried. I wrote to NIH and they said to see my doctor.
I have been so grateful for your newletter for years now, Cort, and keep holding out hope. Your writing is comprehensive, understandable, and always encouraging. Take good care of yourself…you are so important to so many of us on the receiving end of your remarkable efforts. Thank you, deeply.
Interesting Connie. The Yale Paxlovid study is a 15-day course of treatment. My functional medicine doctor was going to prescribe it for me to see if it would help but my insurance was only going to cover five days. He was going to prescribe the five days but then I got approved for IVIG.
Thank you so much for your information. I was so excited about this and asked my pc at my next visit. He has promise me an antiviral since my amazing response to Paxlovid. As yet, I have no prescription as he has been concentrating on other testing. I have looked at the Yale site and will email them, but wondered how you are doing with your IVIG therapy. Please let me know, and I hope hope hope you have had a good response. Are you a ME or Covid Patient? I’ve had FMS, ME since 1981 and am desperate for some successful treatment. Where do you live – big city, University town??? I’m in Las Cruces NM near El Paso and the border and we don’t have great medical care in LC. Sure hope you have some good news to report :o) .
Fingers crossed that the Yale study has positive outcomes and then maybe our docs will be okay prescribing a longer course of Paxlovid (and insurance companies will approve it!).
I’m a long COVID patient, March 2020, but I’m one of the 50% of long haulers who has the ME/CFS manifestation of it. I live just north of NYC, so I’m fortunate to be near some of the best doctors. I did two rounds of IVIG but have asked my doctor to stop; it seems to have thrown me either into perimenopause or terrible dysautonomia, in the form of very intense hot/cold flashes many times a day and at night. It’s really messing with my sleep – covers on, covers off, repeat several times an hour. My ID doc said the IVIG could be causing this, and she is planning to try switching me to the subcutaneous form of it, which sounds great to me because the infusions mean five hours of a nurse in your house! So, we’ll see what happens. It was no magic bullet in the two months I did it.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4147979/
https://www.researchgate.net/post/LongCovid_PostCovid_syndrome_continued_Erythropoietin_EPO_deficiency_syndrome
https://www.researchgate.net/post/Covid-19_Erythropoietin_EPO_deficiency_syndrome2
Very interesting, Cort. My infectious disease doctor says I have T cell exhaustion; I guess from being overworked for three years now? (although I started having that finding after the first six months).
Also, I just got insurance approval for IVIG and my first drip session was yesterday. I wonder if it could help address any T cell problems?
https://open.substack.com/pub/longcovidandme/p/starting-ivig-intravenous-immunoglobulin?r=o3zsi&utm_medium=ios&utm_campaign=post
Dr. Peter McCullough says the spike protein persists in the body, and he has developed a “Base Spike Protein Detoxification” program (using 3 available supplements–Nattokinase, Bromelain, Curcumin).
The spike may fit the “pathogen persistence hypothesis,” though Medicine isn’t likely to acknowledge that the MRNA Vax ingredients could be detrimental. (There is also a “Spike Support Formula” by the Wellness Company.)
https://petermcculloughmd.substack.com/p/base-spike-protein-detoxification?utm_source=profile&utm_medium=reader2