Paolo's comparison of the Lyme/ME relationship to HIV/AIDS is interesting, and one I lean toward as well (understanding Bb and company are not retroviruses). I also agree with msf that perhaps the best angle to approach this relationship is through Lyme.
I say this because in Lyme we have a known pathogen. We know in large measure how it acts in acute stage. We have many studies that demonstrate how it behaves and reacts in vitro, and we can speculate and debate and slip into polemics over what happens once the disease enters humans and disseminates. That is, we can try to draw inferences from in vitro studies into how the bacteria can morph and survive not only our immune system, but frequently any abx barrage we fire at them; or, if you incline toward the IDSA camp, reflect that in vitro studies demonstrate fairly conclusively that tetracyclines will pretty much eradicate any viable spirochete.
This is where things really gets unwieldy, imo. Because regardless of school, BOTH sides agree that many sick people emerge post-treatment. (Although one group believes far more remain sick than the other is willing to acknowledge) So, one side without Bb, one side with Bb. But both agree a certain amount of Lyme patients don't recover. So, I think where msf and I concur is that because we have a known causative agent - borrelia - and a known end result - either abx refractory Lyme or, for all intents and purposes, ME/CFS - then the NEXT step is obvious and irrespective of camp. The next step is to explore and qualify the end result in all of these people who continue with symptoms and continue to degenerate post-treatment. To accurately characterize their condition and to attempt to provide meaningful therapies.
This seems a pretty straight forward theory: Lyme sometimes results in ME/CFS. Accordingly, if Lyme is in your research purview, you follow that relationship where ever it may take you, and you explore it, and you reveal both its overt manifestations and its slightest nuances. If Lyme is your responsibility, so too is late stage Lyme, and chronic Lyme - and that portion of ME/CFS cases that is caused by the Lyme agent.
Only, this is not happening, at least not in the US. In fact, the opposite seems true. Many vested with the responsibility of characterizing what some call chronic Lyme or PTLDS, others Late Stage Disseminated Lyme, are, for whatever reasons/incentives, downplaying the severity of the symptom clusters reported to them - downplaying their number, downplaying their intensity, and marginalizing their importance (and in doing so, marginalizing the patients).
This is a small number of very influential researchers and clinicians, but their collective bottle-necking efforts are substantive. They are effective, too.
So much so, that this obvious approach to following the disease from a colony of Bb nestled in a tick's midgut, through latching onto a human host, through the various stages of Lyme, and into what may be ME/CFS... Just doggedly following that trail and uncovering the mechanisms at play... And gauging the extent and validity of that relationship... Seems to have been stopped in its tracks.
