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If the diagnostic is questionable - and far too many actually are - its significance would be limited. This also holds true for reactivation metrics.

I'm not sure how meaningful this is. Put another way, this is about as meaningful as claiming there is pretty good negative evidence for persistence of Borrelia, Babesia, or Bartonella in ME/CFS - which is not very meaningful.

Thank you, @Hutan. Although the study technically concerns Lyme, it's the scanning technique, and the purported brain inflammation it suggests, that drew my attention. The Johns Hopkins press release seems to focus on that more than Lyme as well, although that is debatable...

The suggested neuroinflammation was what I found intriguing - and how that could translate in ME/CFS TSPO imaging efforts (reminiscent of Nakatomi et al). It sure feels like neuro-inflammation is at play. I noticed the study indicated that neurocognitive exams on the cohort of 12 demonstrated...

Another PET TSPO neuroimaging study suggesting neuroinflammation involving microglia, this time in PTLDS: https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-018-1381-4

No. In most cases, it is not.

Or if your immune system is fooled, e.g., antigenic variation.

Shameful.

Surprise.

How do you define a reactivated infection?

The conventional model, e.g. CDC's, for ME/CFS is exclusionary: You cannot have any infection that can cause ME/CFS symptoms. So, does testing negative for all the usual suspects have to be part of the model? I suspect there is a logical fallacy embedded in that question, but my point is that...

Could it be the quality of the diagnostics? Ok, yes, I can see that. That makes sense. But this is where I need help. So our symptoms attributable to immune responses are irrespective of our immune response vis a vis antibodies? I apologize. I've struggled with the symptom component vs antibody...

As far as I can tell, any theory would have to account for: A myriad of fluctuating symptoms that can be broadly inconsistent among the patient community; Diminished acuity; Inability to register a meaningful and persistent antibody response with conventional metrics to typical pathogens; PEM...

I'd be interested in a very focused look into acquired immune tolerance and how it may relate to pwME. I'm not quite clear on a few things, not the least of which: If our bodies aren't generating the antibodies they should to whatever agent they should be reacting to, then how do we know that...

I read it a couple months back. I got screened by their automated questionnaire back then, flagged due to age. They can over-ride that. I'm curious enough about the integrity of the efforts, and the metrics being used, to try to get in - but I will need to talk to a human with PI authority...

Well, yes and no. There's a bit of confused logic here, at least it seems to my poor thinking. First, medical syndrome terms ascribed by whom and to what end? I try not to lose sight of the mischaracterization that has haunted ME/CFS for decades. Second, yes, we know the root cause of LC, but...

No way? Some inept meds apply sloppy qualifiers on a few diseases, refuse to throw enough reseach $'s to discover what's at play in each, and you claim there's no way these and others like PTLDS could be separate diseases? This is in part why I think patients need to play a larger role in...

Semantics, most of which are rooted in willful inertia. You could use the same logic for PTLDS. And you'd have good argument for three distinct entities that look almost identical. LC is not ME/CFS is not PTLDS/chronic Lyme. Patients who have been around the block could write reams about the...

By this point the whole mouse model would be laughably absurd if it weren't embraced for far darker things like serial passaging of different pathogens to achieve performance and symptoms goals (e.g. gain of function).

What if someone has both? As in has two discrete diseases simultaneously: ME/CFS and LC?