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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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And do these ME1 patients suffer from the chronic sore throat of ME/CFS? My own chronic sore throat was caused by the virus that appeared to trigger my ME/CFS; the sore throat was the very first symptom this virus produced when I first caught it (and at the time of course I thought that it was nothing more than just a sore throat that would soon go away). However, my initial sore throat remained, and is still present to a degree even a decade later.
So I wonder whether the chronic or recurring sore throat often found in ME/CFS might be peculiar to the infectious onset-type ME/CFS, and thus be usable as a differential diagnosis between ME1 and the other MEs you enumerate which have infectious associations.
"We have not looked crimson cresent since biopsy of this area usually need more anesthesia and is quite painful. One patient who had 5 biopsies of the throat because of persistent sore throat tested positive for enterovirus protein in the posterior tongue tonsils but negative in all the other ares of the throat including the red areas. This may be good to do but probably more invasive than a stomach biopsy, which does not usually cause much pain afterwards."
You have all these classifications for ME, very similar to the classifications for herpes. Are they the same thing? Dr. K says CFS is in the herpes family. He suggested it was herpes 6, AKA Stealth Virus.
I think it may be more difficult to separate subgroups by history of symptoms than one might think. In rheumatology we see diseases with completely different mechanisms that can be indistinguishable on symptoms, maybe because symptoms are large a manifestation of the way the immune system responds, rather than what it is responding to.
Of course, many PWME don't experience cold symptoms at all, even though they must be catching colds (I didn't either, for about seven years).
Why must we be catching colds?
Good question - I was having second thoughts about that statement even as I was typing it! But I was thinking that we must surely be exposed to lots of cold viruses. It's been suggested that those PWME without cold symptoms have immune systems ramped up that jump all over the new virus and don't let it multiply. I've got no biomedical knowledge and have no clue whether that makes sense as an explanation.
I'm aware of course that many PWME are isolated (as I was during my first illness) so will have less exposure but it's unlikely to be zero exposure - even bedbound PWME will encounter carers or delivery people.
Now I get a sore throat and feeling lousy and it often comes and goes twice or even three times.
I'm wondering why such viruses seem to come and go twice or three times?
I had one of those viruses this year, crazy runny nose, cough etc and I seemed to have the same virus coming and going three times (with maybe 3-4 weeks between each 'infection).
none of us seems to produce a solid long term immunity to noroviruses. Unlike other viruses you can get reinfection with them just as bad as the first time.
Hi, @Jonathan Edwards, you may have answered this elsewhere, but I still don't understand how something like antibodies directed towards a particular cellular receptor would not lead to additional signs, specifically inflammation of a particular type of tissue, along with elevated IL-6/CRP/ESR?
Unless the receptors are expressed only in certain environments - but those environments are generally places where the antibodies won't get to either.
Which leaves mainly antibodies to extracellular signalling proteins as potential targets in ME/CFS?
Also, to get inflammation from antibody binding you need either for the antibody to crosslink at least two Fc receptor by its back end (so you need at least two antibodies next to each other) or engage complement. A single antibody molecule cannot engage complement and it cannot cross link Fc receptors. So if an antibody binds to a receptor and blocks it or activates it there is no reason to get any inflammation. Inflammation only occurs if rafts of antibodies attached to some polyvalent structure cross link FcR or engage complement. So in thyroid disease an antibody can stimulate thyroxine production by binding to a hormone receptor with no trace of inflammation. In myasthenia gravis there is some complement activation at the endplate target but macrophages with Fc receptors cannot get in. Complement activation generates chemotaxins but not cytokines and IL-6.