Discussion in 'Other Health News and Research' started by natasa778, Nov 16, 2014.
Wow, this sounds like a big deal!
Th1/th2 imbalance theory more or less. Th2 cytokines like IL-4 inhibit the production of Th1 cytokines and vice versa. I know a lot of people think poorly of the theory but I really believe there is some truth to it.
And interferon gamma is low in the first years of ME.
There is considerably more to immune modulation and signalling than simple levels of a small number of cytokines. These were only the easiest examples to study in the beginning. We are almost entirely ignorant of rates of change and temporal correlations. Robust signalling cannot be based on simple levels when there are no means of calibration of thresholds. Ratios of rates are much better at carrying signals in complicated environments. There are known examples of biological signalling where these are very important. We are still missing the majority of signalling information.
Elsewhere on this forum we have again heard that EBV can't be causing the problem because billions of people without this illness are infected with EBV. The same logic could be used to deny the role of EBV in Burkitt's lymphoma, other non-Hodgkin's lymphomas and nasopharyngeal carcinomas. The difference is that these are progressive, fatal diseases for which there has been a great deal of research. I have to ask if there is any law of nature which requires that infectious agents produce acute progressive diseases rather than chronic diseases. What I see instead is a set of social conventions among practicing physicians that should not be carried over into research. If we had not researched the examples above we would not know what we do now.
I remind readers that a high percentage of patients with serious ME/CFS do exhibit polyclonal B-cell expansion. This just does not usually become progressive disease. We are in fact ignorant of the correlation between ME/CFS and various lymphomas because official diagnostic criteria for the disease remove any patient who develops such an outcome from any ME/CFS research cohort. By this standard they never had ME/CFS, only a progressive disease which had not yet become obvious. The reasoning involved is circular, and clinically useless, but does serve purposes which are generally not voiced.
Just as another example of EBV and chronic or relapsing-remitting disease I would mention research in MS. It is possible the main difference between this disease and MS lies in the parts of the nervous system affected.
Not sure if I am following the discussion correctly regarding this study, but is it correct that it was the immune system's reaction to fighting a parasite that caused latent herpesviruses to reactivate? See, http://www.sciencedaily.com/releases/2014/06/140626141015.htm
If yes, then is it possible that pathogens carried by ticks could also result in a similar immune response/reactivation of herpesviruses?
I'm afraid I've contributed to the confusion by broadening the discussion. I'll try to compensate by explaining.
Yes, Wally. Tick-borne diseases could change the ability of the immune system to hold previous infections latent. I am especially looking for pathogens which can exploit clonal expansion in response to another infectious agent because they infect the immune cells undergoing such expansion. Since EBV can replicate its DNA inside immune cells without killing them it is one candidate.
There is no reason to believe Nature signed any agreement about obeying Koch's postulates concerning a single unique pathogen for each disease. Those were simply rules he used to prove that some diseases were caused by microbes. We tend to forget that he did this in a context where many doctors refused to believe the germ theory of infectious disease even as applied to such obvious IDs as cholera! Some continued to argue against the idea that TB was a communicable disease after Koch published his research.
Those rules were shaped by this debate, and Koch himself departed from strict application of them in his later years. His ideas about identifying the infectious agent under a microscope did not apply to viral diseases until the electron microscope was invented in the 1930s. His rules about demonstrating infection in laboratory animals do not apply to highly species-specific pathogens that scarcely infect other species at all, and EBV is quite thoroughly adapted to humans.
We are becoming aware that even a relatively simple organism like EBV has a much larger repertoire of behaviors than we would have guessed. Part of this is due to different strains of the microbial species, and part is due to the context in which it is found. Even when we can identify strains causing a disease, as with HPV and uterine cervical cancer, we are still largely in the dark about how, and how often, these strains arise "in the wild". This ignorance has a major effect on our ability to prevent or cure such diseases.
The next level of research will not be easy, but it is certain to reduce the number of presently known diseases listed as "of unknown etiology". Some of these will even be cured. This will not happen unless we investigate situations which previous researchers have ignored because they violated some academic criteria.
Reactivated EBV is responsible for quite a bit of "real disease" and many premature deaths. Here's a reference to a recent paper which probably represents a serious underestimate.
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