So yes on the cycloferon...isn’t increasing IFN how oxymatrine works though?
My understanding (which is only a limited one) is oxymatrine shifts the Th1-Th2 immune balance in the direction of Th1. Th1 is the immune response which targets intracellular infections (such viral infections, or intracellular bacteria like Chlamydia pneumoniae). Whereas Th2 is the immune mode which targets extracellular pathogens, like bacteria.
There is an old idea that ME/CFS patients may have insufficient Th1 response, so that they find it harder to clear viruses. Some factors can cause a shift away from the desirable antiviral Th1 response, and shift immunity towards Th2. The Th1-Th2 balance is a bit like a seesaw: if you raise one side, the other side will automatically go down (to an extent). So factors which boost Th2 will tend to automatically reduce Th1.
However, this Th1-Th2 hypothesis of ME/CFS is just a theory; there's no solid science that demonstrates a Th1-Th2 imbalance is the cause of ME/CFS. Nevertheless, people like Dr Chia use the Th1-Th2 model to explain how oxymatrine works for ME/CFS patients.
Cytokines which move the immune response to
Th1 are IL-12, IL-2 and interferon gamma. Cytokines which move the immune response to
Th2 include IL-4 and IL-10.
One study found that oxymatrine boosts the
Th1 cytokines interferon gamma and IL-2, and inhibits the
Th2 cytokines IL-4 and IL-10.
So you can see oxymatrine alters the Th1-Th2 seesaw such that Th1 is increased.
It's interesting that when Dr Chia did a cytokine profile of ME/CFS patients given oxymatrine, all the oxymatrine responders showed a definite shift to Th1; whereas in the oxymatrine non-responders, their immune system did not shift; somehow it remained stuck in Th2.
You can see a graph of this cytokine profile of Dr Chia's oxymatrine patients in
this video at timecode 37:05. You might like to watch the whole oxymatrine section of that video, which starts at 25:08.
I am a non-responder to oxymatrine, which may mean my immune system is stuck in Th2, and does not move to Th1 even with high doses of oxymatrine (I've taken 6 tablets daily for months, but saw nothing).
At this point, while I feel like an intelligent person, I’m still trying to line some of these pieces up in my mind. It seems like CVB infections can ‘turn off’ an interferon response that is responsible for destroying viral RNA - so using both IFN stimulators would potentially yield better results?
In these chronic so-called non-cytolytic enterovirus infections, you just get a pure naked viral RNA infection of the cells (this RNA exists in the cell in both the single-stranded and double stranded forms, and it's thought it is the dsRNA form which is hardest to eradicate).
For some reason, the interferon response is being thwarted, and the immune system is unable to clear this enterovirus RNA (even though there are only small amounts in the cells, and it replicates only very slowly).
Dr Chia and others have suggested the enterovirus dsRNA acts like a seed or a spore, which is hard to remove.
However, a different explanation was recently proposed, relating to some genetic mutations that are known to exist in the non-cytolytic enterovirus RNA: it's been suggested these mutations confer resistance to the interferon response.
