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
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