Prions and immune deificiency emerging simultaneously. Fungi and viral reactivation. The spike, I believe, is also affecting Heat Shock Proteins.
The fundamental problem of autoimmune diseases is the failure of the immune system to downregulate its own potentially dangerous cells, which leads to destruction of tissue expressing the relevant autoantigens. Current immunosuppressive therapies offer relief but fail to restore the basic condition of self-tolerance. They do not induce long-term physiological regulation resulting in medication-free disease remissions. Heat shock proteins (HSPs) have shown to possess the capacity of inducing lasting protective immune responses in models of experimental autoimmune diseases. Especially mycobacterial HSP60 and HSP70 were shown to induce disease inhibitory IL-10-producing regulatory T cells in many different models.
HSPs Are the Most Frequent Cytosolic/Nuclear MHC Class II Natural Ligand Source!
Prion disease is accelerated in mice lacking stress-induced heat shock protein 70 (HSP70)
Also, HSP are involved in the REACTIVATION OF LATENT VIRUSES!
One condition in which HSP expression is increased in vivo is fever. Many viral diseases cause the development of fever in the host and, while hyperthermia has been implicated in the reactivation of viral replication in latent /chronic infection, the possibility that fever could be beneficial during acute viral infections has been often suggested.