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Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in ME/CFS - 2020 - Schreiner

Discussion in 'ME/CFS research' started by Kalliope, Apr 24, 2020.

  1. Snow Leopard

    Snow Leopard Senior Member (Voting Rights)

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    The experience will be quite different, since disease of the motor centres will cause proproceptive error, so they'll experience problems such as tremor, ataxia, apraxia. Yet if there is significant undershoot of force/position compared to the motor centre's model, this will be perceived as fatigue in addition to the above symptoms.
     
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  2. obeat

    obeat Senior Member (Voting Rights)

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    Many of us have specific times of the day when the weakness/ fatigue is worse no matter how well we are pacing, so that's another factor to consider in the pattern.
     
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  3. Amw66

    Amw66 Senior Member (Voting Rights)

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    Michelle, sebaaa and sb4 like this.
  4. Trish

    Trish Moderator Staff Member

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  5. Cinders66

    Cinders66 Senior Member (Voting Rights)

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    That’s interesting. It might be a severity thing. When I became fully bedridden I started to loose sensation /awareness of my limbs , so I would move a curtain but could hardly feel the limb doing it.
    Now spasm is a really bad issue that I’ve not found a way to manage it so i. And I usually lie here only partially aware of my limbs. Sensation returns as “fatigue” subsides/recovery happens so I know I’m doing better when I have more awareness of my feet! If I’m really bad I feel sensation disappear in my legs as if they’ve disappeared and I can hardly move them. It is usually sensation weakness increases the further away from the core.

    i don’t know in MS if what @Jonathan Edwards describes is core regardless of severity. For me I do definitely get some type of the symptoms he describes, more spasm than stiffness though, but didn’t until I became bedridden and it might be in m.e that there’s a succession or build up of fatiguing /impacting factors which correlates with severity. So for example many mild-moderate will not have distressing cognitive issues or particularly marked sensitivities but they afaic pretty much define severe M.E. Which is why all severities need study imo.
     
    Last edited by a moderator: Apr 28, 2020
  6. lunarainbows

    lunarainbows Senior Member (Voting Rights)

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    I have severe ME and have at certain times been very severe but haven’t really had those symptoms.. it’s interesting that you have.. I really do wonder if many of us fall into “subsets” of this illness where there’s actually something different going on. (I have had twitches in my body, but I wouldn’t call it spastic weakness).
     
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  7. Sly Saint

    Sly Saint Senior Member (Voting Rights)

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    April 27, 2020 | By Scott LaFee
    For ME/CFS Patients, Viral Immunities Come at a Devastating, Lifelong Cost
    New research shows a connection between a common human herpes virus-6 exposure that leaves a DNA copy of the virus behind and many of the symptoms of a disabling disease called myalgic encephalomyelitis/chronic fatigue syndrome
    https://ucsdnews.ucsd.edu/pressrele...mmunities-come-at-a-devastating-lifelong-cost
     
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  8. John Mac

    John Mac Senior Member (Voting Rights)

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  9. Mij

    Mij Senior Member (Voting Rights)

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    Yes, stiffness/soreness/fatigue can be the result of not moving, but elevated levels of plasma cytokines can cause this too. This is the case for me. I have to find a comfortable balance to try to get out and walk and not overdo myself to get some relief. Sometimes the opposite occurs and I'm bed bound for another month.
     
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  10. Mithriel

    Mithriel Senior Member (Voting Rights)

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    I just want to say that nobody ever tried to replicate this. The study was dismissed by SW because his study found depression was more likely because his percentage was higher than Behan's number for abnormal mitochondria. That was about the time research into ME stopped in the UK and the US scientists were not interested in mitochondria or problems with exercise.

    A lot of interesting results have been found over the years but they are never picked up and explored.

    Even when I had mild ME, I would just stop, unable to move an arm or move my leg. Other times it would be unable to see or unable to remember how to get home. It happened, it passed.

    As the years have passed, major changes have happened but it is the consequence of these small stoppings.
    When they talk about a damaged aerobic respiration in a cell it felt like it matched my experience. Inbetween the times when a bit did not work at all it worked well.

    The nearest analogy is when electricity is coming from a generator; the TV works fine until the fridge turns on, or the computer works until the heater goes on. There is plenty of energy available for one thing but as soon as there is too many things attached everything becomes flaky.
     
  11. Art Vandelay

    Art Vandelay Senior Member (Voting Rights)

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    That's interesting. Over ten years ago, I was feverish and sweating a lot. I noticed a rough patch of skin appear on the back of my neck which was followed by a scaly, itchy rash across my torso. The GP I saw was clueless, but some weeks later I came across very short article in the newspaper that mentioned Pityriasis rosea. The described symptoms matched what I had experienced perfectly.

    It's thought that Pityriasis rosea can also be caused by a reactivation of HHV-6 or HHV-7.
     
    Last edited: Apr 28, 2020
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  12. cassava7

    cassava7 Senior Member (Voting Rights)

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    Not a fan of the hype around this paper. It's a big hypothesis ontop of preliminary data, yet the media/PR person at UCSD who wrote the press release for the article embellished/extrapolated the results.

    Let's not forget that a year ago, the Science Media Centre in the UK was very keen to point out the shortcomings of the paper on the nanoneedle by Rahim Esfandyapour & Ron Davis, which also lacked data despite being promising (few patients, no control groups with other diseases). Maybe the hype helps researchers secure funding and/or boosts their reputation? But it's detrimental to the field of ME research as a whole. We need nuanced/careful interpretations (e.g. this one from the lead author on the HLA study from Fluge and Mella) on pilot studies...
     
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  13. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    I don't think what you are describing would fit with either agnosia or spasticity though.
    In agnosia it is not that you are unaware in a sensory sense but unaware of being unaware. Nobody ever complains of it as lack of awareness. Spasticity includes stiffness and specific types of spasm but there are other reasons for getting spasms in muscles - they are generally much more common lying in bed than ambulant even in normal circumstances.
     
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  14. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    I am not sure that is quite true. I worked on the second floor of the Rayne institute at UCL alongside the team working with Richard Edwards - including Joan Round and David Jones - during the 1980s. They spent several years looking at ME/CFS muscle and failed to find either structural changes or metabolic changes.
     
  15. unicorn7

    unicorn7 Senior Member (Voting Rights)

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    Do you think the technology and knowledge in that time were sufficient to be sure that they didn't find anything?
     
  16. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    Yes, ultrastructural analysis had been going for a good 20 years. Mitochondrial structure would have been clear to see.
     
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  17. unicorn7

    unicorn7 Senior Member (Voting Rights)

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    I'm wondering about two factors where they might have not found anything in the past:

    One factor is the "serum" factor, where they are now seeing things if you keep the cells in the me/cfs serum, I think that is new? If you are looking for structural or functional problems in mitochondria, in the past, you would have looked at the cells and not the cells + serum of the patient, am I correct?

    The other thing I'm wondering about is the abnormality Ron Davis found, only when they stressed the cells to the max with salt. I think that was new as well? Not testing the cells in resting position, but testing them in a "working" situation.

    Should these two factors make us rethink all the experiments done in the past relating to cell-metabolism and mitochondria? I want to know with every experiment done in ME/CFS: were they done on cells in their own serum? And was the cell then stressed or in a resting state?

    Do you know if these factors are normal factors to consider in cell-related research? Or are these "new factors" that are only considered now in ME/CFS research because some positive results have been gained?
     
  18. Perrier

    Perrier Senior Member (Voting Rights)

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    Dear Marky,
    Truer words were Never spoken.
     
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  19. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    You would be looking at cells bathed in the exact amount of plasma (=serum) that you get in real life in a PWME.
    If the structural change does not occur in the patient in real time during the illness then any structural change in cells in vitro is an artefact. It might perhaps be an interesting artefact but you cannot attribute patients' symptoms to something that does not actually occur in patients!

    Excess salt is not a working situation but an artifactual stress. If the response is relevant to ME then we have to assume that some more realistic stress is going on in ME. So the changes should be found in PWME when they are feeling symptoms. So far I don't think we have much idea what changes were responsible for the impedance measurements from the Davis group though.

    These are about as basic factors as there are in cell research - nothing in any way new. But normally you use cell systems to reproduce effects you KNOW to be present in patients - in order to explain those effects. The big if for me here is that so far nobody has shown that there is much wrong with mitochondria structure or function in vivo.

    Observations on mitochondria in vitro may provide a crucial clue. But whatever measurement of mitochondria you choose, adding this or that in is likely to make the measurement go up a bit or down a bit. So measurements going up or down are no great surprise. Science gets meaningful when you can predict precisely which measurements will go up and by how much and which will go down for any given additive. So far the literature seems to be full of things going randomly up or down or both.
     
  20. FMMM1

    FMMM1 Senior Member (Voting Rights)

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    There's a bit about "structured illumination microscopy (SIM)" i.e. techniques used by Bupesh Prusty to measure mitochondrial length ---.

    I've no idea whether anyone did similar/corresponding work in the past.

    I think some of the unknowns here are:
    • is there something which changes mitochondrial length in some people with ME; and
    • as @Jonathan Edwards and other have said, does this occur in a relevant tissue e.g. muscle, liver ---?

    I'm not dismissing Bupesh's studies/findings but I'd like to see a large scale replication (measuring mitochondria or a biomarker for fragmentation) etc. --- done quickly.
     

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