Discussion in 'General ME/CFS News' started by Jon_Tradicionali, Mar 31, 2014.
I was in my 50's.
There is no mention, at least in the abstract of this Russian paper, of the actual mechanism of viral persistence.
That would be very interesting to know.
One might speculate that the viral persistence mechanism may be as a result of the virus and bacteria placing competing and diametrically opposite demands on the immune system, with the virus requiring a Th1 response from the immune system in order to clear the infection, and the bacteria requiring the opposite Th2 (or Th17) response in order to clear the infection.
As the immune system cannot mount both a strong Th1 and Th2 response at the same time (since Th1 and Th2 are mutually inhibitory), you will get only a weak Th1 and Th2 response, which perhaps allows both the viral and bacterial infections to persist.
Epstein-Barr virus also has the genes to make its own fake (homologue) version of the IL-10, a cytokine which promotes the Th2 response.† It is advantageous for EBV to make this fake IL-10 cytokine, since by promoting the Th2 response, it reduces the Th1 response necessary to fight viruses.
Using this little trick, EBV can dodge the immune response. Such tricks are known as immune evasion. Immune evasion is when a pathogens use clever strategies, such as making fake (homologue) versions of cytokines, to alter the functioning of the immune system to the pathogen's advantage.
Indeed! I recently read a research paper listed in the Latest Research section about this very issue.
EBV seems to have a host of tricks to fool and mess up with the immune system for its own survival. It always amazes and terrifies me how brutal evolution can be.
EBV is not unique in this respect. All pathogens seem to use many different immune evasion tactics. They do cunning things to throw a spanner into the workings of the immune system.
Coxsackievirus B has an effective way of evading the immune system: once coxsackievirus B infects a cell, it quickly removes the MCH-I molecules on the cell surface, which makes these infected cells invisible to the CD8 T-cell immune response. So the immune system effectively cannot "see" this infected cell. †
KDM supports this theory; that the viral trigger is just the tipping point to an already overloaded immune system. Maybe the genetic factor is not susceptibility to ME but rather a defect that hinders liver detoxification, methylation or other immune boosting abilities in our body
Memory T cells as an occupying force
Michael J. Bevan
T cells in the intestinal mucosa
Gut-associated memory T cells are also out of equilibrium with the pool of recirculating memory cells . T cells that have been recently activated by antigen in gut draining lymphoid organs such as mesenteric lymph nodes preferentially acquire homing molecules that allow them to enter the lamina propria and intestinal epithelium . In addition, effector T cells activated in the spleen by viral or bacterial infection have the ability to traffic to any organ, including the gut . Thus, it seems that recently activated effector cells can enter these sites, but resting memory cells cannot. The lymphocytes in the gut-associated lymphoid structures show an activated phenotype, including CD69 and granzyme expression and immediate effector function. The gut lumen contains a vast spectrum of microbial and food antigens which are usually ignored by the immune system. Nevertheless, the enormous surface area of the intestine and its exposure to ingested pathogens make it a key location for enhanced security. Despite the huge number of potential peptides in the gut derived from commensals and food, it is difficult to argue that all the resident memory T cells in the gut epithelium and underlying structures meet antigen (or cross-reactive antigen) at this location. Rather it may be that their activated status provides an antigen nonspecific or innate function in maintaining the integrity of the intestine.
Vitamin D receptor expression controls proliferation of naïve CD8+T cells and development of CD8 mediated gastrointestinal inflammation
Jing Chen13, Danny Bruce134 and Margherita T Cantorna125*
In summary, VDR-deficiency results in the generation of pathogenic CD8+ T cells that contributes to the development of IBD. The causes of the VDR KO CD8+ T cell induced IBD was the rapid proliferation of CD8+ T cells in general and naïve CD8+ T cells in particular, and the overproduction and response to IL-2. Expression of the VDR prevents homeostatic proliferation of CD8+ T cells and vitamin D through the VDR maintains gastrointestinal homeostasis.
CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis
Michael P. Pender1,2
CD8+ T-cell deficiency is a feature of many chronic autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren's syndrome, systemic sclerosis, dermatomyositis, primary biliary cirrhosis, primary sclerosing cholangitis, ulcerative colitis, Crohn's disease, psoriasis, vitiligo, bullous pemphigoid, alopecia areata, idiopathic dilated cardiomyopathy, type 1 diabetes mellitus, Graves' disease, Hashimoto's thyroiditis, myasthenia gravis, IgA nephropathy, membranous nephropathy, and pernicious anaemia. It also occurs in healthy blood relatives of patients with autoimmune diseases, suggesting it is genetically determined. Here it is proposed that this CD8+ T-cell deficiency underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of Epstein-Barr virus (EBV) infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells which would otherwise die in the target organ by activation-induced apoptosis. Autoimmunity is postulated to evolve in the following steps: (1) CD8+ T-cell deficiency, (2) primary EBV infection, (3) decreased CD8+ T-cell control of EBV, (4) increased EBV load and increased anti-EBV antibodies, (5) EBV infection in the target organ, (6) clonal expansion of EBV-infected autoreactive B cells in the target organ, (7) infiltration of autoreactive T cells into the target organ, and (8) development of ectopic lymphoid follicles in the target organ. It is also proposed that deprivation of sunlight and vitamin D at higher latitudes facilitates the development of autoimmune diseases by aggravating the CD8+ T-cell deficiency and thereby further impairing control of EBV. The hypothesis makes predictions which can be tested, including the prevention and successful treatment of chronic autoimmune diseases by controlling EBV infection.
Apologies for not commenting each article, but it is quite easy to see the important information contained.
Methylation is also important in the control of inflammation. More and more evidence is piling up that inflammation is a major component of various chronic illnesses. I think Vegas is spot-on about antibiotics, vaccines, toxins in our food supply and environment.
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