Manuel
Senior Member
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Did you know that syndromes such as ๐๐จ๐ง๐ ๐๐๐๐๐, ๐๐/๐๐ ๐ and ๐ข๐ง๐๐๐๐ญ๐ข๐จ๐ฎ๐ฌ ๐ฆ๐จ๐ง๐จ๐ง๐ฎ๐๐ฅ๐๐จ๐ฌ๐ข๐ฌ share a common immune mechanism?


In both Long COVID and ME/CFS, prolonged exposure to viral antigens results in hyperactivation of CD8 T cells. This leads to a chronic immune response that can cause extreme fatigue, sleep disturbances and cognitive problems.

In mononucleosis, ๐๐๐๐ข๐๐ข๐๐ง๐๐ฒ ๐ข๐ง ๐ญ๐ก๐ ๐๐๐ ๐-๐๐๐ฅ๐ฅ ๐ซ๐๐ฌ๐ฉ๐จ๐ง๐ฌ๐, caused by genetic factors such as certain HLA-II alleles, prevents the immune system from correctly recognizing viral antigens. This deficiency leads to an increase in the number of infected cells, resulting in increased activation of CD8 T cells in an attempt to eliminate the affected cells. This ๐ข๐ง๐๐ซ๐๐๐ฌ๐๐ ๐๐๐ ๐-๐๐๐ฅ๐ฅ ๐๐๐ญ๐ข๐ฏ๐๐ญ๐ข๐จ๐ง in response to CD4 T-cell insufficiency can result in ๐จ๐ฏ๐๐ซ๐๐๐ญ๐ข๐ฏ๐๐ญ๐ข๐จ๐ง of the immune system, leading to ๐๐๐ ๐-๐๐๐ฅ๐ฅ ๐๐ฑ๐ก๐๐ฎ๐ฌ๐ญ๐ข๐จ๐ง and increasing the risk of developing ๐๐ฎ๐ญ๐จ๐ข๐ฆ๐ฆ๐ฎ๐ง๐ ๐๐ข๐ฌ๐๐๐ฌ๐๐ฌ, such as multiple sclerosis, due to the persistent presence of viral antigens.

This inefficiency in antigen recognition can lead to a phenomenon of molecular mimicry, where the immune system mistakes viral antigens for self antigens, exacerbating autoimmunity.

Therefore, those patients who after EBV infection develop infectious mononucleosis are more likely to carry these ineffective HLA-II alleles, which could predispose them also to develop ME/CFS and EBV-associated autoimmune diseases, such as lupus or multiple sclerosis.

In ๐๐/๐๐ ๐ and ๐๐จ๐ง๐ ๐๐๐๐๐, some patients develop ๐๐ฎ๐ญ๐จ๐ข๐ฆ๐ฆ๐ฎ๐ง๐ ๐ก๐ฒ๐ฉ๐จ๐ฉ๐ก๐ฒ๐ฌ๐ข๐ญ๐ข๐ฌ. This condition arises as a direct consequence of the inability of susceptible ๐๐๐-๐๐ alleles to effectively control viral infection, as mentioned above. This deficiency not only prolongs inflammation, but can also trigger an autoimmune response through ๐ฆ๐จ๐ฅ๐๐๐ฎ๐ฅ๐๐ซ ๐ฆ๐ข๐ฆ๐ข๐๐ซ๐ฒ.
In this case, viral antigens mimic ๐๐๐๐ (adrenocorticotropic hormone) structures, a key hormone in the regulation of cortisol, leading to an autoimmune attack against the pituitary gland. This process results in ๐ก๐ฒ๐ฉ๐จ๐๐จ๐ซ๐ญ๐ข๐ฌ๐จ๐ฅ๐ข๐ฌ๐ฆ (low cortisol levels), aggravating fatigue, malaise and other symptoms.

๐๐ข๐ฅ๐ ๐ฉ๐๐ญ๐ข๐๐ง๐ญ๐ฌ: although they do not develop pituitary autoimmunity, they experience CD8 T-cell hyperactivation and depletion, which also results in fatigue, sleep disturbances and cognitive problems. In addition, they exhibit ๐๐ฅ๐๐ฏ๐๐ญ๐๐ ๐๐จ๐ซ๐ญ๐ข๐ฌ๐จ๐ฅ ๐ฅ๐๐ฏ๐๐ฅ๐ฌ in response to increased ๐ฉ๐ซ๐จ๐ข๐ง๐๐ฅ๐๐ฆ๐ฆ๐๐ญ๐จ๐ซ๐ฒ ๐๐ฒ๐ญ๐จ๐ค๐ข๐ง๐๐ฌ. These patients may recover without sequelae.
๐๐จ๐๐๐ซ๐๐ญ๐/๐ฌ๐๐ฏ๐๐ซ๐ ๐ฉ๐๐ญ๐ข๐๐ง๐ญ๐ฌ: develop ๐๐ฎ๐ญ๐จ๐ข๐ฆ๐ฆ๐ฎ๐ง๐ ๐ก๐ฒ๐ฉ๐จ๐ฉ๐ก๐ฒ๐ฌ๐ข๐ญ๐ข๐ฌ with hypocortisolism due to molecular mimicry between viral antigens and ACTH, leading to more severe symptoms. These patients may have autoimmune sequelae although the infection will be controlled. There is another possibility in some patients: an increase in ๐ ๐ฅ๐ฎ๐๐จ๐๐จ๐ซ๐ญ๐ข๐๐จ๐ข๐ ๐ซ๐๐๐๐ฉ๐ญ๐จ๐ซ ๐ซ๐๐ฌ๐ข๐ฌ๐ญ๐๐ง๐๐, leading to an effect similar to hypocortisolism, as cortisol signaling is ineffective, aggravating symptoms of inflammation and fatigue.

Moreover, the development of autoimmune diseases such as ๐ฅ๐ฎ๐ฉ๐ฎ๐ฌ or ๐ฆ๐ฎ๐ฅ๐ญ๐ข๐ฉ๐ฅ๐ ๐ฌ๐๐ฅ๐๐ซ๐จ๐ฌ๐ข๐ฌ has exactly the same developmental basis as these syndromes. In these diseases, the combination of a ๐ฉ๐๐ซ๐ฌ๐ข๐ฌ๐ญ๐๐ง๐ญ ๐ข๐ง๐๐๐๐ญ๐ข๐จ๐ง together with ๐ฌ๐ฎ๐ฌ๐๐๐ฉ๐ญ๐ข๐๐ฅ๐ ๐๐๐-๐๐ ๐ ๐๐ง๐๐ญ๐ข๐๐ฌ results in the development of autoimmunity. Thus, all these diseases follow the same developmental model (I attach the outline of the model in the next post).
๐๐จ๐ง๐๐ฅ๐ฎ๐ฌ๐ข๐จ๐ง ๐จ๐ ๐ญ๐ซ๐๐๐ญ๐ฆ๐๐ง๐ญ ๐๐จ๐ซ ๐๐ฅ๐ฅ ๐ญ๐ก๐๐ฌ๐ ๐๐ข๐ฌ๐๐๐ฌ๐๐ฌ:
The key is to address both the ๐ฉ๐๐ซ๐ฌ๐ข๐ฌ๐ญ๐๐ง๐ญ ๐ข๐ง๐๐๐๐ญ๐ข๐จ๐ง through the use of specific antivirals, and to treat the ๐ฉ๐๐ซ๐ฆ๐๐ง๐๐ง๐ญ ๐๐๐ฆ๐๐ ๐ caused by autoimmunity.

#LongCOVID #MECFS #health.
Image of the developmental model of autoimmune hypophysitis. This model can be extrapolated to the development of other autoimmune diseases and CD8 T-cell hyperactivation:
- Substitute myelin or any autoimmune disease-associated antigen for ACTH in the scheme.
- Substitute HLA-DR15 for the allele that is susceptible to a deficient response against the antigen.