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As far as the autoimmune aspect goes, my view is that the presence of low levels of several autoimmune antibodies does not provide evidence that ME/CFS is an autoimmune disease. Rather, I suggest that the oxidative stress causes a lot of damage to cells, and the immune system is working to clean up the resulting debris. In the process, it produces some antibodies that have an autoimmune character.
Rich
I think the main difference between this hypothesis paper and many of the ones that have come before it is a lack of "bias". I know that Gerwyn has researched every corner of this illness thoroughly. While his bias is or was towards the retroviral model because it fit every symptom beautifully; he knows far more than just that area of research. However, in co authoring this paper he left his bias behind. Rather, this paper looks at all the research over the last decade and pulls together the different pieces without prejudice in to a picture that fits the facts as a patient lives and experiences them.
Feel free to send me the manuscript.This is an explanatory model of disease. It is a hypothesis that maps all observations into a consistent whole to foster research into areas not previous considered. Specifically they must be complete. Do not confuse complete with correct. This is a hypothetically explanation for the complete disease. If you would indicate what you have not located within the manuscript I will direct you to the correct section, but you should know this is not for lay persons.
sIL-2R has now been rejected as a marker of autoimmunity. It is only a reflection of a chronically activated immune system.
Feel free to send me the manuscript.
For starters, the abstract seems to indicate that what is called the initial infection is thought to have been cleared. I submit that it is not, and that if it were the mechanisms described in the model would collapse.
Hi Guido, there is ample evidence that the infections are not cleared, though clearly patients are not always viremic. In the case of Q fever for example, no detectable pathogen can be found - but they only look in the blood. In the case of herpes virus then clearance is not expected anyway. In the case of coxsackie virus the vast majority of patients have ample evidence of viral persistance in tissues, a finding that is also made with herpes family viruses. The issue seems to be that these pathogens are not in the blood. However, it is unclear if they are still capable of activity. In the case of herpes family viruses the latent viruses can still distort physiology. One thing Lerner has questioned is whether whole viruses are still present, or only persistent viral fragments. Even viral fragments could do damage as they would modify the immune response.
The classic model of autoimmunity has one or limited targets being substantively attacked - which means high antibody titres. In the case of CFS or ME it appears we have many targets with lower titres. Lower grade attacks on many targets will have more diffuse and more difficult to detect consequences, but there are still consequences.
The cause of the damage leading to autoantibodies being oxidative and nitrosative stress has reasonable evidence. This does not modify the issue with autoantibodies much. What it does tell us is that it is possible that ongoing oxidative and nitrosative stress are drivers of at least some symptoms, if not most - indeed I have elsewhere suggested that Rituximab and a protocol aimed at managing oxidative and nitrosative stress, plus treating inflammation, might be more effective and result in a higher cure rate. This might make Rituximab fully curative for responder patients.
What I have suggested in another thread is that there are two halves to the illness, and treating one without the other may only be minimally effective. One half is immune, the other is oxidative and nitrosative stress. I would be interested in seeing studies combining these two approaches, particularly using newer anti-B drugs - Rituximab is not the only one out there and very hard to find funding for.
With regard to the Morris&Maes paper, I am examing pieces of it one at a time in more depth. There are a number of interesting points worth more investigation.
Bye, Alex
Then why are many patients found to have no current infection?
The percentage of patients with no tissue based infection is under 20% I think, and thats based on only one class of viruses, the coxsackie viruses. Fold in prevalence of all the others and it will probably push it to over 95%.Given the misdiagnosis rate, I think thats pretty good.
Active blood infections seem to be at a relatively low rate. I am not aware of anyone who has surveyed them all and reported the total prevalance rate for current infections, maybe the current Montoya Standford study will do that.
If you look at Herpes class viruses and discount children, the infection rate is probably clost to 100%. Everyone has them.
NO model currently available explains the persistence of viral fragments and unproliferating viruses such as coxsackie, though its possible that these viruses have a natural latent form. Herpes family viruses certainly do. There is some speculation about this but it is not sufficiently detailed to be called a model.
Bye, Alex
Hi user9876, a feedback loop between viral infection and autoimmune disease as the link you posted suggests could be very interesting. I am currently reading the full paper:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065340/pdf/ar1691.pdf
I will write some more when I have finished.
Bye, Alex
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Bye, Alex