I found the new paper from Bupesh to be very interesting in how it kind of ties a few things together that have been floating around. I could be totally misunderstanding this, so bear that in mind.
You have the Dauer response as a reaction to, in this case, an induced HHV6 infection in some cell line or other. So Bupesh posits fragmented mitochondria for the disease mechanism - the "purpose" of this disease mechanism being to keep us alive since the triggering infection didn't kill us in the first place.
But only barely alive, as Mary Schweitzer has put it. As it says in the paper, the body pays a big price for staying alive from the HHV6 infection. It doesby keeping you forever sick - with varying degrees of severity. often for the rest of your life.
It's been known anecdotally for a long time that some PWME don't get colds often - so there is that same mechanism -- fighting like crazy against against a rhinovirus, which most people get fairly often and recover from easily
And Bupesh demonstrated the ability to induce the response in the cells in vitro. Which ties in to looking for something in the blood like Ron Davis and OMF are doing, using the nanoneedle device to measure the induced stress in the cell.
So what is missing in Prusty's paper is, I think, the input of the immunologists? Bupesh is a virus guy - on the infection side of the puzzle?
Now, the Australians come at it from looking at the SNP genetic defect on the calcium ion transport system. They use the clamp device. And they have been able to distinguish samples given by patients diagnosed by strict clinical criteria from other neurological diseases. They are the National Centre for Neuroimmune and Emerging Diseases research group. They have also done something with some unknown dose of naltrexone, only in vitro, which they say is reversing the NK cell degradation - the NK cell thing is by now old and well accepted.
Since Ampligen is still hard to come by - as an immune modulator and anti-viral rolled into one - the Aussies are looking at both a calcium channel blocker and also at the readily available immune modulator called naltrexone in terms of treatment. They have been seeking patients to test naltrexone in whatever the dose they are thinking about, taking their samples in the field also, if necessary.
Jarred Younger is looking at another form of naltrexone altogether for the neuroinflammation But first he has to find a supply.
And then we have stalwart John Chia and his enterovirus samples from stomach tissue. And Klimas and Fletcher looking at gender differences.
So we are basically back to "what disease are we studying and from which angle." And who will get to the finish line first?
So bring on the covid-19 funding for, if any comes, for what may be more cases of post-viral ME from this mutated SARS virus. Who knows yet?
Just my armchair observation.