In relation to my cryptic comments a page or two back, I will say one or two more things about why I think chasing individual viruses may be unfruitful (as others have commented too). There are lots of ifs and buts and different angles to put on this but here goes. My impression is that many of the symptoms of ME are in a sense apparent sensitivities to, or intolerances of, stimuli: including exertion, foodstuffs, light, noise, chemicals etc. Some of these stimuli, like light, impinge so directly on the nervous system that it seems it must be the nervous system itself that is hypersensitive. That suggests that some circulating factor, or maybe a factor like TNF within the brain is making trivial things seem intolerable. An example would be when one feels intense nausea looking at rich delicious food when one has an acute viral illness. It is not that one has become sensitive to that food especially but that one’s brain has become sensitive to almost everything. My suspicion is that the sense of constantly being afflicted by viruses may be part of the same thing. I agree that it is not going to be as simple as that but I think it is worth considering.
The next point is that if infections with particular viruses were to be blamed one would expect to have occasional reports where the presence of that virus became very obvious – if for instance the person with ME was given certain types of immunosuppressive therapy. I appreciate that epidemics of ME do seem to occur but if it was all due to one virus the epidemic pattern ought to be much more general. Again, you can argue against this, but I am trying to redress a balance. There seems to be an assumption that we need a specific environmental trigger, but, as I have been saying, epidemiological theory does not in fact require this if we factor in the dynamics of the immune response.
What we might be left with is that the dominant sense that ME is like constantly suffering from viral symptoms might point us in the direction of thinking that it is a dysregulation of mediators specifically associated with virus infection. As an example, there is a hint that the molecule TRIM21 might be involved in the handling of viruses within cells by the immune system and there is a link between TRIM21 and Sjogren’s syndrome.
This links back to the debate about mediators like TNF and cortisol. Cortisol suppresses certain effector systems in the immune response, including TNF, at least in the bloodstream, but not others. Cortisol, as far as I am aware, has no effect on circulating antibody levels, presumably because it does not affect plasma cells much. So although cortisol makes RA better by suppressing inflammatory mediators, it may be of little use where antibodies are causing trouble without causing inflammation. A clear example would be the exophthalmos (eye protrusion) associated with anti-thyroid peroxidase antibodies. The absence of any benefit from cortisol in ME would tend to suggest that the symptoms are not due to standard inflammatory pathways. This might be because inflammation is within the central nervous system but even then one would expect cortisol to have some benefit.
