📎 I attach in the thread more publications with information about the relationship between ME and Long COVID.

#LongCovid #MECFS #Health

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✔️ Treat the consequences of developed autoimmunities. For example, if hypocortisolism is present, it should be treated with hydrocortisone in replacement doses (not supraphysiological doses that immunosuppress) to prevent immune hyperactivity.

𝐍𝐞𝐰 𝐚𝐫𝐭𝐢𝐜𝐥𝐞: www.pnas.org/doi/epub/10....

✔️ If viruses are the culprits, they should be treated chronically with antivirals until a therapy capable of completely eliminating them is developed.

💊 𝐖𝐡𝐚𝐭 𝐬𝐡𝐨𝐮𝐥𝐝 𝐛𝐞 𝐝𝐨𝐧𝐞?

✔️ Eliminate the underlying cause, i.e. persistent infection and the consequences of autoimmunities.

❌ The use of ICIs in patients with autoimmune diseases increases the risk of aggravating autoimmunity, especially increasing the risk of autoimmune hypophysitis.

❌ This proposal does not take into account the autoimmunity present in these diseases, which also arises as a consequence of infection in patients with HLA-II alleles.

𝐎𝐧 𝐩𝐫𝐨𝐩𝐨𝐬𝐞𝐝 𝐭𝐡𝐞𝐫𝐚𝐩𝐢𝐞𝐬:
We disagree with one of the treatments suggested in the article.
If infection were the sole cause of these pathologies, therapy with checkpoint inhibitors (CPIs) to decrease immune depletion might be useful. However:

5️⃣ 𝐚𝐧𝐝 𝐝𝐨 𝐝𝐢𝐟𝐟𝐞𝐫𝐞𝐧𝐭 𝐩𝐚𝐭𝐡𝐨𝐠𝐞𝐧𝐬 𝐞𝐦𝐩𝐥𝐨𝐲 𝐯𝐚𝐫𝐲𝐢𝐧𝐠 𝐦𝐞𝐜𝐡𝐚𝐧𝐢𝐬𝐦𝐬, 𝐭𝐡𝐞𝐫𝐞𝐛𝐲 𝐢𝐧𝐟𝐥𝐮𝐞𝐧𝐜𝐢𝐧𝐠 𝐭𝐡𝐞𝐢𝐫 𝐩𝐫𝐨𝐩𝐞𝐧𝐬𝐢𝐭𝐲 𝐭𝐨 𝐢𝐧𝐝𝐮𝐜𝐞 𝐓 𝐜𝐞𝐥𝐥 𝐝𝐲𝐬𝐟𝐮𝐧𝐜𝐭𝐢𝐨𝐧?
Exhaustion occurs primarily through chronic persistence of antigens in all of them. Each will have other pathways to evade the immune response.

Another key factor is the development of autoimmune diseases (such as autoimmune hypophysitis) as a consequence of infection. Autoimmune hypophysitis causes a cortisol deficit, which leads to increased immune hyperactivity and consequently aggravates immune exhaustion.

They may even contribute to the development of autoimmune outbreaks.

4️⃣ 𝐖𝐡𝐚𝐭 𝐜𝐨𝐧𝐝𝐢𝐭𝐢𝐨𝐧𝐬 𝐥𝐞𝐚𝐝 𝐭𝐨 𝐥𝐨𝐧𝐠-𝐭𝐞𝐫𝐦 𝐬𝐜𝐚𝐫𝐫𝐢𝐧𝐠 𝐨𝐟 𝐂𝐃𝟖+ 𝐓 𝐜𝐞𝐥𝐥𝐬 𝐚𝐧𝐝 𝐬𝐮𝐛𝐬𝐞𝐪𝐮𝐞𝐧𝐭𝐥𝐲 𝐜𝐨𝐧𝐭𝐫𝐢𝐛𝐮𝐭𝐞 𝐭𝐨 𝐌𝐄 𝐩𝐚𝐭𝐡𝐨𝐠𝐞𝐧𝐞𝐬𝐢𝐬?
Any persistent infection generates immune exhaustion of CD8 T cells due to chronic antigen persistence.

3️⃣ 𝐈𝐬 𝐭𝐡𝐞𝐫𝐞 𝐚 𝐫𝐨𝐥𝐞 of 𝐫𝐞𝐚𝐜𝐭𝐢𝐯𝐚𝐭𝐢𝐨𝐧 𝐨𝐟 𝐡𝐞𝐫𝐩𝐞𝐬𝐯𝐢𝐫𝐮𝐬 𝐢𝐧𝐟𝐞𝐜𝐭𝐢𝐨𝐧𝐬 𝐨𝐫 𝐚𝐥𝐭𝐞𝐫𝐞𝐝 𝐚𝐜𝐭𝐢𝐯𝐢𝐭𝐲 𝐨𝐟 𝐞𝐧𝐝𝐨𝐠𝐞𝐧𝐨𝐮𝐬 𝐫𝐞𝐭𝐫𝐨𝐯𝐢𝐫𝐮𝐬𝐞𝐬?
Yes as in any other immunodeficiency. Reactivations of latent pathogens such as herpesviruses or Parvovirus B19, increase immune depletion and generate damage characteristic of these pathogens

Herpesviruses are most associated with the development of ME/CFS because of their ability to generate latency and because some, such as Epstein-Barr virus, infect by binding to HLA-II molecules.

2️⃣ 𝐀𝐫𝐞 𝐦𝐞𝐦𝐛𝐞𝐫𝐬 𝐨𝐟 𝐚 𝐬𝐢𝐧𝐠𝐥𝐞 𝐩𝐚𝐭𝐡𝐨𝐠𝐞𝐧 𝐟𝐚𝐦𝐢𝐥𝐲 𝐫𝐞𝐬𝐩𝐨𝐧𝐬𝐢𝐛𝐥𝐞 𝐟𝐨𝐫 𝐭𝐡𝐞 𝐨𝐧𝐬𝐞𝐭 𝐨𝐟 𝐌𝐄, 𝐨𝐫 𝐜𝐚𝐧 𝐦𝐮𝐥𝐭𝐢𝐩𝐥𝐞 𝐩𝐚𝐭𝐡𝐨𝐠𝐞𝐧𝐬 𝐢𝐧𝐜𝐢𝐭𝐞 𝐭𝐡𝐞 𝐢𝐥𝐥𝐧𝐞𝐬𝐬?
Any intracellular pathogen (viruses, bacteria or parasites).

1️⃣ 𝐖𝐡𝐚𝐭 𝐚𝐫𝐞 𝐭𝐡𝐞 𝐩𝐚𝐭𝐡𝐨𝐠𝐞𝐧𝐬 𝐜𝐚𝐮𝐬𝐢𝐧𝐠 𝐭𝐡𝐞 𝐢𝐧𝐢𝐭𝐢𝐚𝐥 𝐩𝐫𝐢𝐦𝐢𝐧𝐠 𝐞𝐯𝐞𝐧𝐭, 𝐚𝐧𝐝 𝐚𝐫𝐞 𝐩𝐚𝐭𝐢𝐞𝐧𝐭 𝐓 𝐜𝐞𝐥𝐥 𝐜𝐥𝐨𝐧𝐨𝐭𝐲𝐩𝐞𝐬 𝐚𝐥𝐭𝐞𝐫𝐞𝐝 𝐢𝐧 𝐌𝐄?
Any uncontrolled infection in an individual with HLA-II alleles deficient against that infection.

…is responsible.

🧠 The article raises the 𝐟𝐨𝐥𝐥𝐨𝐰𝐢𝐧𝐠 𝐪𝐮𝐞𝐬𝐭𝐢𝐨𝐧𝐬, which I will answer based on what we currently know from our reviews:

Even the similarity between Myalgic Encephalomyelitis and Long COVID was also rejected.

This new article provides further evidence of the similarity between Myalgic Encephalomyelitis and Long COVID. It demonstrates that immune exhaustion occurs in both pathologies and that persistent infection…

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