I think it is important to remember that "many" of us BEGAN our Th1-to Th2 shift in childhood. I was a severe asthmatic with 65 allergies. I am told that this weighted my immune system to Th2 to begin with. You add major life stress and some type of a viral assault (I have a partial empty sella). I read a M.E. Scottish Study that studied children with ME from an early age of kids who missed around a half a year of school and who grew up to have ME. This fits me. XMRV positive in 2010 and Nagalase levels 1.90 in April 2012, I am hoping to begin GcMAF in June. Thank you all who contributed to this thread.This is just my take on the "SHIFT".
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From the Cheny notes on this thread: Researchers have demonstrated that most CFIDS patients end up stuck in Th2 mode. This has several consequences. When the Th2 system activates, it blocks the Th1 system. This suppresses the Th1 weapons, particularly NK function. Accordingly, there is also an increase in the Th2 weapons - the white cells and antibodies. Most notable is increased antibody production. Dr. Cheney said that if you measure antibodies to anything a CFIDS patient has ever been exposed to, they will very likely be elevated. (At this point he drew small arrows beside the "weapons": They pointed down on the left side to indicated suppression / lower levels; and they pointed up on the right side to indicate activation / higher levels.)
Cheney notes that other problems ensue. Patients get into trouble on both sides: they overreact to things on the right side and under-react to those on the left. When they are Th2 activated, they no longer have the defense mechanisms to keep dormant all the things they caught in the past. They cannot suppress or control them anymore, and the EBV, chlamydia pneumonia, CMV, etc. reactivate. The yeast also begins to appear.
The only defense against being eaten alive at this point is RNase L. (For more information about RNase L, see The Three Phases of CFIDS and other articles in the Cheney section of our website.) RNase L cannot kill any of these things. It only stops them from reproducing. According to Cheney, "It's a line in the sand saying 'No more replication', and it waits for Th1 to come and kill them. But Th1 never comes. RNase L sits there and grinds away, possibly going up and down as the pathogens activate and reactivate. But they never get wiped out. RNase L holds the line, waiting for the cavalry that never arrives."
While it is valiantly trying to hold the line, it is also chewing up human messenger RNA, inhibiting all the enzymes in the body, disrupting protein synthesis, and generally making patients miserable. As RNase L grinds away, it eventually shifts into "after-burner" desperation mode - the more powerful and deadly low molecular weight form discovered in CFIDS patients by Suhaldonik.