Robert Fusaro

[Kenny Carmody @KennyCarmody]

Almost Five years ago I was a healthy, very active man in the prime of my life.

An artist by heart and soul who had traveled to over 100 countries, maintained peak health and fitness, and ran or hiked miles in nature almost every day. Simple, full, and free.

Then on July 21, 2021, I received the Moderna COVID vaccine.

I felt it the moment it entered my body.

Within days a cytokine storm triggered a rare neuromuscular disease and multi-system damage. I went from the ICU to six brutal weeks in hospital, and nothing has been the same since.

Today I am mostly bedridden, confined to my bedroom. I cannot work. I cannot drive. I cannot grocery shop. I can barely walk more than short distances on my best days. I have not left my house further than a quarter mile in years.

Every single day I endure ischemic stroke-like episodes, a partially paralyzed diaphragm that makes breathing a struggle, severe neuropathic pain, esophagus and larynx spasms, severe swallowing issues that make eating difficult, severe trigeminal and occipital neuralgia, crushing fatigue, dysphagia that turns eating into an hour-long ordeal, neuro degeneration and neuromuscular disease diagnosed as ALS unspecified, and waves of symptoms that force me to be bedridden.

Doctors mostly dismissed me as psychosomatic, anxious, or worse. One diagnosis I had to sue to have removed from my record. I spent over $60,000 chasing every treatment the injured community has tried. Nothing gave lasting relief. I became my own doctor , turning to sunlight, grounding, circadian alignment, nature, and my faith in God, which is what carries me when the body wants to quit.

For three years I have spoken out , documenting my journey, writing on X and Substack, calling for acknowledgment, proper diagnostic codes, real care, and accountability for what was done to us. I stand with every vaccine-injured person who has been denied, dismissed, and abandoned.

Yet suddenly the story has gone silent.

People are no longer talking about the people who became severely disabled after one shot. Support has dwindled. The institutions that told us it was safe have offered no honest accounting. No real acknowledgment. No justice.

The reality is that we did not recover when the headlines ended.

We are still here. I am still here.

Still mostly bedridden.

2026 has been brutal.

Still fighting every single day.

Still waiting for the truth to be told.

Please share this. Not for sympathy, but because thousands of vaccine-injured people deserve to know they have not been forgotten.

My time here in X soon comes to an end and halt, yet I am grateful to have met such wonderful people and the support I have received . I know there is not much you can do for us, but I am very grateful for all the absolutely amazing and wonderful prayers and words I have received. Thank you from my heart.
Prayers is what this worlds needs more than ever.

Please don’t stop believing and dreaming of a better world.

God is not finished with us yet.

May God Bless you and peace be with you.

[Manuel Ruiz @manruipa]

💊‼️Long COVID could be, at least in some patients, an autoimmune disease occurring alongside chronic infection, antigenic persistence, or viral reactivations.

Okay.
So now what?

Are there treatments?
Can autoantibodies be removed?
Can this autoimmunity be “switched off”?
Are we close to a cure?

The honest answer is this: we are not facing an immediate cure , although possibly a future one, but we are facing a huge shift in how we think about the disease.

Because if part of Long COVID, and possibly also ME/CFS, has an autoimmune basis, then it would no longer make sense to treat it as a diffuse syndrome with no therapeutic direction. We would need to do the same thing we do in other autoimmune diseases: classify patients properly, identify biomarkers, and design a stepwise treatment approach.

Not all patients would have the same mechanism.
Not all patients would respond in the same way.
And not all patients would need the same level of treatment.

But for the first time, a more logical therapeutic map is starting to emerge.

A clearer logic is beginning to appear: identify which patients have a real autoimmune component and, from there, think about which therapies could make sense.

At present, what is accessible would not be a cure, but treatments already known from other autoimmune diseases that could help reduce autoantibody activity, modulate the immune response, or decrease part of the immunological damage.

In the best-case scenario, these would be treatments to improve, stabilize, or reduce autoimmunity. Not to completely “erase” the disease.

If I had to rank the options in an orientative way, thinking about potential usefulness and safety profile, I would do it like this:

1. IVIG

The most reasonable short-term option would probably be IVIG, meaning intravenous immunoglobulin.

IVIG does not directly eliminate all autoantibodies as such, but it can modulate the immune system, compete with pathogenic autoantibodies, block part of the inflammation, and dampen the immunological attack without requiring such intense immunosuppression.

In many autoimmune diseases, it is used precisely because of this immunomodulatory effect. Among this type of therapy, it is probably one of the options with the best balance between potential usefulness and safety profile.

That said, it is not free of side effects, it is expensive, and access is limited.

2. FcRn inhibitors

Next, I would place FcRn inhibitors.

These drugs are very interesting because they reduce the total amount of circulating IgG and, with it, they can also reduce the burden of pathogenic autoantibodies.

The advantage is that they are quite targeted toward the humoral component of autoimmunity, meaning the antibody-mediated part.

The disadvantage is that they are not yet truly established for Long COVID or ME/CFS, and it would still be necessary to demonstrate very clearly which subgroup of patients would benefit the most.

Even so, conceptually, if we are talking about an autoantibody-mediated disease, this is one of the most promising strategies.

3. Immunoadsorption

At the next level, I would place immunoadsorption.

This technique consists of filtering the blood to remove immunoglobulins, especially those that may be participating in the autoimmune process.

It is a more targeted strategy than systemic immunosuppression and, in diseases mediated by autoantibodies, it can make a lot of sense.

Its main limitation is logistical: it is not a simple therapy, it requires specialized centers, and its effects may not last if the immune system continues producing the same autoantibodies afterwards.

(1/3)

🔵Continued in the next post.👇🏻

[Robert Fusaro @Papatasso33]

@PhillyPhile215 @PerfectFrogName @LCCampaign @SenMarkey @SenTimKaine @SenDuckworth @marksfamof8 @rezexpat @ResearcherNP @mskerajo @hospmom @muzikguy1 @JasonTasoulas @singh_mona71 @Frances17033 @kitschburgh @chrisca70578779 Done. Let’s hope they do something with this, and recognize the vaccine injured as well.

[Robert Fusaro @Papatasso33]

Help us support the cause. https://t.co/Tinwq0BzqR

[Robert Fusaro @Papatasso33]

@PaulRKeeble @DrDan20000 didn’t you find something similar a while ago?

[Robert Fusaro @Papatasso33]

@MJinMidwest @DrinkswDave Would you mind sharing which MaB they had and what their side effects were? It seems that some get significant improvements with them, others nothing, and some develop serious issues. Here is a group for people injured by them.

https://t.co/yt0GcUPAV1

[Robert Fusaro @Papatasso33]

@chydorina @remissionbiome Were you dealing with SIBO issues as well?

[Robert Fusaro @Papatasso33]

@BrainInflCollab @DrDan20000 has been talking about finding exactly this, and treating his Long Haul patients with these issues for the past few years. Some arrogant “experts” dismissed his findings, but yet again, he was right.

[Manuel Ruiz @manruipa]

🌟 𝐍𝐞𝐰 𝐚𝐫𝐭𝐢𝐜𝐥𝐞: 𝐭𝐡𝐞 𝐜𝐨𝐧𝐧𝐞𝐜𝐭𝐢𝐨𝐧 𝐛𝐞𝐭𝐰𝐞𝐞𝐧 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃, 𝐌𝐲𝐚𝐥𝐠𝐢𝐜 𝐄𝐧𝐜𝐞𝐩𝐡𝐚𝐥𝐨𝐦𝐲𝐞𝐥𝐢𝐭𝐢𝐬 𝐚𝐧𝐝 𝐩𝐨𝐬𝐭-𝐯𝐚𝐜𝐜𝐢𝐧𝐚𝐥 𝐬𝐲𝐧𝐝𝐫𝐨𝐦𝐞𝐬 𝐥𝐢𝐞𝐬 𝐢𝐧 𝐭𝐡𝐞 𝐝𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭 𝐨𝐟 𝐚𝐧 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐞 𝐇𝐲𝐩𝐨𝐜𝐨𝐫𝐭𝐢𝐬𝐨𝐥𝐞𝐦𝐢𝐜 𝐒𝐲𝐧𝐝𝐫𝐨𝐦𝐞🌟

🌐 I am excited to share with you our latest paper entitled "𝐇𝐲𝐩𝐨𝐜𝐨𝐫𝐭𝐢𝐬𝐨𝐥𝐞𝐦𝐢𝐜 𝐀𝐒𝐈𝐀: 𝐀 𝐯𝐚𝐜𝐜𝐢𝐧𝐞- 𝐚𝐧𝐝 𝐜𝐡𝐫𝐨𝐧𝐢𝐜 𝐢𝐧𝐟𝐞𝐜𝐭𝐢𝐨𝐧-𝐢𝐧𝐝𝐮𝐜𝐞𝐝 𝐬𝐲𝐧𝐝𝐫𝐨𝐦𝐞 𝐛𝐞𝐡𝐢𝐧𝐝 𝐭𝐡𝐞 𝐨𝐫𝐢𝐠𝐢𝐧 𝐨𝐟 𝐥𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃 𝐚𝐧𝐝 𝐦𝐲𝐚𝐥𝐠𝐢𝐜 𝐞𝐧𝐜𝐞𝐩𝐡𝐚𝐥𝐨𝐦𝐲𝐞𝐥𝐢𝐭𝐢𝐬". In this paper, we explain the links between Long COVID, Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (ME/CFS) and COVID-19 post-vaccine syndromes. 🤔 Stay reading to the end and you will also find our treatment proposal that could improve symptoms.💊

➡️𝐋𝐢𝐧𝐤 𝐨𝐟 𝐨𝐮𝐫 𝐫𝐞𝐯𝐢𝐞𝐰 𝐚𝐫𝐭𝐢𝐜𝐥𝐞: https://t.co/IZgPn3HhQN

🔍 𝐀𝐛𝐬𝐭𝐫𝐚𝐜𝐭: We present a model for the development of these diseases that involves a complex interplay between immune hyperactivation, autoimmune hypophysitis or pituitary hypofunction, and immune exhaustion. We believe that the starting point is a deficient CD4 T-cell response to viral infections in genetically predisposed individuals (HLA-DRB1). This would follow from an uncontrolled immune response with hyperactivation of CD8 T cells and elevated antibody production, some of which could be directed against self-antigens, triggering autoimmune hypophysitis or direct damage to the pituitary, resulting in decreased production of pituitary hormones, such as ACTH. 🧬

🔬 𝐖𝐡𝐚𝐭'𝐬 𝐭𝐡𝐞 𝐛𝐢𝐠 𝐝𝐞𝐚𝐥?
1️⃣ 𝐑𝐞𝐥𝐚𝐭𝐢𝐨𝐧𝐬𝐡𝐢𝐩 𝐭𝐨 𝐀𝐒𝐈𝐀 𝐒𝐲𝐧𝐝𝐫𝐨𝐦𝐞: We propose that Long COVID, ME/CFS and post-vaccine COVID-19 syndrome could be included in adjuvant-induced autoimmune/inflammatory syndrome (ASIA) due to their similar clinical manifestations and possible relationship to genetic factors, such as polymorphisms in the HLA-DRB1 gene.
2️⃣ 𝐃𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭𝐚𝐥 𝐌𝐨𝐝𝐞𝐥: We suggest that these diseases begin with a deficient immune response and progress to uncontrolled immune hyperactivation, followed by immune exhaustion, exacerbating symptoms and pathology.
3️⃣ 𝐇𝐲𝐩𝐨𝐜𝐨𝐫𝐭𝐢𝐬𝐨𝐥𝐞𝐦𝐢𝐚: We highlight the decrease in ACTH production and its impact on immune function and clinical symptoms, establishing a direct link with pituitary dysfunction.
4️⃣ 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐏𝐫𝐨𝐩𝐨𝐬𝐚𝐥: We propose a treatment approach including antivirals, corticosteroids/ginseng, antioxidants and metabolic precursors to improve symptoms by modulating immune response, pituitary function, inflammation and oxidative stress.

💡 𝐈𝐦𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬 𝐚𝐧𝐝 𝐂𝐨𝐧𝐜𝐥𝐮𝐬𝐢𝐨𝐧𝐬:
🔹These disorders could have an autoimmune origin against the adenohypophysis.
🔹Treatment with antivirals and corticosteroid replacement therapy in patients with permanent pituitary damage could improve symptoms by addressing immune and hormonal dysfunction.

🧠 𝐓𝐡𝐞 𝐤𝐞𝐲 𝐢𝐬 𝐩𝐢𝐭𝐮𝐢𝐭𝐚𝐫𝐲 𝐝𝐚𝐦𝐚𝐠𝐞: 𝐡𝐨𝐰 𝐝𝐨𝐞𝐬 𝐭𝐡𝐢𝐬 𝐫𝐞𝐥𝐚𝐭𝐞 𝐭𝐨 𝐭𝐡𝐞 𝐝𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭 𝐨𝐟 𝐌𝐄/𝐂𝐅𝐒, 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃 𝐚𝐧𝐝 𝐨𝐭𝐡𝐞𝐫 𝐩𝐨𝐬𝐭-𝐯𝐢𝐫𝐚𝐥 𝐚𝐧𝐝 𝐩𝐨𝐬𝐭-𝐯𝐚𝐜𝐜𝐢𝐧𝐞 𝐬𝐲𝐧𝐝𝐫𝐨𝐦𝐞𝐬?

💉 Certain viruses (and other pathogens) and vaccines can affect the pituitary gland, interfering with cortisol production and triggering a cascade of complex symptoms. In patients with weak HLA-DRB1 alleles, such as DR15, immune hyperactivation can trigger an autoimmune response against ACTH, crucial for cortisol production. This is exactly analogous to how other autoimmune diseases such as multiple sclerosis or lupus develop, where the immune system attacks other antigens in the body, but in the syndromes we are discussing, the autoimmunity is specifically directed against pituitary ACTH.

🦠 This link explains why patients with chronic infections often experience persistent hypocortisolemia, as the pathogen continues to produce ACTH-mimicking antigens, maintaining the active autoimmune response or generates direct pituitary damage. In contrast, patients without chronic infections and with the same weak alleles treated with immune checkpoint inhibitors (ICIs) may develop temporary hypophysitis and similar cortisol deficits, but discontinuation of treatment usually allows recovery.

This also explains why patients experience chronic fatigue, dysautonomia, orthostatic intolerance, exercise intolerance, intolerance to stressful events and mild hypoglycemia due to low cortisol. Cortisol is crucial in providing the body with needed energy and regulating the stress response. When cortisol levels are low, as they are in these syndromes, the body cannot respond effectively to physical and emotional demands.

🩸Cortisol plays a crucial role in maintaining stable blood sugar levels by promoting gluconeogenesis (glucose production) and stimulating the release of stored glucose in the form of glycogen in the liver. When there is insufficient cortisol, the body faces difficulties in increasing glucose levels in demand situations, such as during physical exercise or in response to stress, which can lead to episodes of mild hypoglycemia. In times of fright or anger, adrenaline release may temporarily improve symptoms by temporarily increasing glucose availability, briefly compensating for cortisol deficiency. However, this response does not adequately replace the long-term regulatory functions of cortisol, so symptoms may return once adrenaline subsides.

🏋️‍♂️ In the case of physical exercise, which naturally increases cortisol levels to mobilize energy and respond to physical exertion, the lack of this hormone limits the body's ability to maintain sustained physical activity. Patients may experience rapid muscle fatigue, feelings of weakness and slower recovery after exercise.

😰 As for stressful events (exams, travel, surgical operations, etc) , cortisol also plays a crucial role in the body's response to emotional or physical stress. When cortisol levels are insufficient, the body has difficulty handling stressful situations effectively. This can manifest itself in an exacerbation of existing symptoms, such as intense fatigue, dizziness, difficulty concentrating and a generalized feeling of malaise.

➡️ For years, many of these patients have been misunderstood and mislabeled as having psychosomatic illness. This is because their symptoms tend to worsen during periods of stress, which has led to the suggestion that the origin of their problems lies in psychological factors. However, the reality is that these patients are not experiencing symptoms due to an underlying psychological disorder, but as a direct result of insufficient cortisol. The lack of this vital hormone prevents the body from adapting and responding appropriately to stress, which perpetuates and aggravates their physical symptoms.

🚨 𝐓𝐡𝐞 𝐃𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭 𝐨𝐟 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐢𝐭𝐲 𝐭𝐨 𝐀𝐂𝐓𝐇: 𝐀 𝐏𝐫𝐨𝐜𝐞𝐬𝐬 𝐒𝐢𝐦𝐢𝐥𝐚𝐫 𝐭𝐨 𝐎𝐭𝐡𝐞𝐫 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐞 𝐃𝐢𝐬𝐞𝐚𝐬𝐞𝐬 𝐬𝐮𝐜𝐡 𝐚𝐬 𝐌𝐮𝐥𝐭𝐢𝐩𝐥𝐞 𝐒𝐜𝐥𝐞𝐫𝐨𝐬𝐢𝐬 🚨

This same mechanism occurs in other autoimmune diseases. Some HLA-II alleles, such as the DR15 variant, are associated with an impaired ability to recognize cells infected with certain pathogens, such as Epstein-Barr virus (EBV). In multiple sclerosis this poor recognition ability specifically affects CD4 T cells, which are crucial for coordinating the immune response. When CD4 T cells cannot correctly recognize infected cells, this leads to hyperactivation of CD8 T cells and an increase in antibodies against the pathogen to compensate for the deficient CD4 T cell response. Without the coordinated help of CD4 T cells, CD8 T cells cannot eliminate all EBV-infected cells, thus never effectively eliminating or controlling the infection and resulting in chronic infection. This results in an increase of infected cells, an exhaustion of CD8 T cells and an increased risk of developing autoimmune diseases, since CD4 T cells, by misrecognizing these viral antigens presented on the HLA-II antigen-presenting cells, can confuse them with the body's own proteins, generating an autoimmune disease. In multiple sclerosis, autoimmunity develops when the EBNA-1 antigen of the Epstein-Barr virus is mistaken for myelin, due to a similar amino acid sequence and molecular mimicry in patients with DR15 alleles. The same could occur in patients with Long COVID, myalgic encephalomyelitis and post-vaccinal syndromes, where autoimmunity against ACTH develops.

#LongCovid #MECFS #Vaccines

[Robert Fusaro @Papatasso33]

@alexandrite113 @arianek @katiamek @ProperChels34 Disappointing,but not surprising.That is unfortunately the case the majority of the time.Medicine is a for profit business with a lot of liability,so to find a doctor willing to advocate for strangers gratis is rare.I will still try with him as well.

[Robert Fusaro @Papatasso33]

@arianek @alexandrite113 @katiamek @ProperChels34 And it seems that her family may not be willing to acknowledge the recommendations of anyone,unless they are in a prestigious position of established medicine, so the more “specialists”,the better.Many of us have been through the same situation,so we know the struggle.

[Robert Fusaro @Papatasso33]

@arianek @alexandrite113 @katiamek @ProperChels34 I will send both of you a message,letting you know what he https://t.co/DMf1fhKOHp you know,getting any doctor to advocate for a patient in another country that they don’t even know is a big ask,but we have to try.He may say no,or he may surprise us.

[Robert Fusaro @Papatasso33]

@arianek @alexandrite113 @katiamek @ProperChels34 Yes,I will be seeing him this Friday for my own case,so I will ask on her behalf.He isn’t an”ME Specialist”,just a Research Neurologist who doesn’t see many patients,so he won’t grasp the full context of ME,but may be able to help with the neurological aspects of it.

[Robert Fusaro @Papatasso33]

@arianek @alexandrite113 @katiamek @ProperChels34 We DMed last night,and she was going to send me an email with her case information,but I haven’t received it yet.Maybe she didn’t have a chance before she was moved?If you have the contact information for her family,at least I can share that with the doctor.

[Robert Fusaro @Papatasso33]

@arianek @katiamek @lifeanalytics In addition to being excluded from almost all of the Long Covid or ME studies or having medical professionals acknowledge or treat us,because they won’t accept vaccines as the cause.

[Robert Fusaro @Papatasso33]

@arianek @katiamek @lifeanalytics Not a problem.We have to support one another,as no one else is.I appreciate the sentiment and kind words,but my ME is caused by the vaccines,along with pericarditis,myocarditis,CIDP,and a ton of other diagnoses.We seem to be harder to help than even viral Long Covid or ME.

[Robert Fusaro @Papatasso33]

@arianek @katiamek I will be seeing him again in a few days, and I will absolutely ask on her behalf in my appointment. We all need to help one another. I would need specifics of her case to give him the correct information.

[Cort Johnson @CortJohnson]

RECOVER, however, has produced less with more than initiative in memory. It spent the bulk of its money on limited observational studies that will tell us little about its largest subset - the ME/CFS-like long COVID group.#LongCOVID #RECOVER #MECFS