Viral infection driving autoimmunity could explain delayed onset of MIS-V (theory)

This 2013 paper by Getts et al. is very interesting:

MIS-V (Multi system Inflammatory Syndrome after Vaccination) is a vaccine injury that tends to appear weeks after vaccination. One possibility is that it can take time for persistent viral infections to morph into a state where autoimmunity is happening.

An important consideration is the fact that in most cases viruses and other microbes can infect a host without triggering any clear clinical symptoms.
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Recently, a potential link between WNV infection and subsequent development of myasthenia gravis was described (158). In this report, disease development occurred several months after disease resolution, highlighting an important point that autoimmunity development may require significant time to evolve, becoming clinically evident months if not years after the triggering pathogenic infection has been resolved.

Self-targeting immune cells do not cause always disease without active infection

The paper describes animal model experiments where the animals were injected with PLP139-151 mimics, which causes the body to have T cells that are highly responsive to the mimics. These T cells in theory might also be responsible to the body’s own tissues as the mimics were designed to be very similar to the body’s own tissue/antigens.

However, there is no disease unless there is also a TMEV infection.

This would explain why immune suppression is not a great treatment since it does not deal with the underlying infection and weakens the body’s ability to fight infections.

In a number of rodent models, infection is required for overt autoimmunity to be triggered. Indeed this has been shown elegantly using TMEV and PLP139–151 mimics. While both infection with TMEV and parallel immunization with PLP139–151 peptide in complete Freund’s adjuvant rapidly induce CNS de-myelinating disease, immunization with PLP139–151 mimics alone without infection does not induce disease, even though T cells in these mice are highly responsive to PLP139–151 (117, 118, 138). Presumably, TMEV infection results in the expression of critical factors including chemokines and costimulatory and adhesion molecules that are necessary for the induction and migration of pathogenic Th1 and Th17 autoreactive T cells into the CNS (159). The nature of a pathogen clearly has a significant impact on the development of autoimmunity; in fact, it may enhance or may even inhibit the activation of autoreactive T cells.

We know that the REAP auto-antibody test (which tests for thousands of auto-antibodies) and other AAB panels (e.g. Celltrend) finds AABs in healthy people, where the AABs do not seem to cause health problems.

The necessity of a poorly-suppressed viral infection to cause autoimmune disease could explain why AABs are problematic in sick people but not healthy people.

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