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If immune tolerance is at play, odds are nothing would.

Could still be a downstream effect of a virus, just not a flare per se. Acquired channelopathies come to mind (just as an example).

I'm pretty sure we discussed it here. Sorry, my brain can't work the Search function.

It could be a lot of things. My vague recollection is he found NO evidence of ANY pathogen - virus, bacteria, or parasite - in ANY OF HIS COHORT (if I recall correctly, and I may not be). Given that his cohort was in large part from the NY metro (if I recall correctly), that would be quite...

I believe this may apply to me as well. Not clear if it's viral, though. Overall though, in terms of persistence, the more I dig into immune tolerance and it's role in viral reactivation, the more I suspect it may prove relevant.

I recall it well. I was not impressed then either.

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...