UK CMRC 2018 Conference held September 19 & 20 at Bristol

Andy said:
Pariante's presentation looks like nonsense to me - he's found a way to make people persistently fatigued so thinks they might be a useful proxy to PwME.
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Actually, people were already being treated with interferon, so he piggy-backed on that. He was looking at the mechanism by which the treatment, while clearing the Hep C virus, simultaneously induced a long-term fatigue state. Now, whether it's the same fatigue as in ME, who knows? But I wouldn't dismiss it as meaningless so quickly--although I understand why it's tempting..
 
dave30th said:
Actually, people were already being treated with interferon, so he piggy-backed on that. He was looking at the mechanism by which the treatment, while clearing the Hep C virus, simultaneously induced a long-term fatigue state. Now, whether it's the same fatigue as in ME, who knows? But I wouldn't dismiss it as meaningless so quickly--although I understand why it's tempting..
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Is he giving them 2 day CPET?
 
dave30th said:
But I wouldn't dismiss it as meaningless so quickly--although I understand why it's tempting..
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I agree. I think there is avery important message in the alpha interferon story - that fatigue can persist long after the triggering signal has gone. Some other signal must then take over. Moreover, there is no need for any specific autoimmune response.

The pity is that Pariente is still as far as I know wedded to a biopsychosocial view, for reasons that are unclear.
 
dave30th said:
Actually, people were already being treated with interferon, so he piggy-backed on that. He was looking at the mechanism by which the treatment, while clearing the Hep C virus, simultaneously induced a long-term fatigue state. Now, whether it's the same fatigue as in ME, who knows? But I wouldn't dismiss it as meaningless so quickly--although I understand why it's tempting..
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How does he know that the interferon induced the fatigue rather than the virus? Was that part of the presentation?
 
dave30th said:
Actually, people were already being treated with interferon, so he piggy-backed on that. He was looking at the mechanism by which the treatment, while clearing the Hep C virus, simultaneously induced a long-term fatigue state. Now, whether it's the same fatigue as in ME, who knows? But I wouldn't dismiss it as meaningless so quickly--although I understand why it's tempting..
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I think its important to characterize fatigue in more detail. There are the people he is looking at, say people with fatigue after cancer, people with RA, Lupus. But its not clear to me that the fatigue would have the same mechanism or if the experience of fatigue is even the same. So something worth doing would be to try to look at whether the fatigue is the same/different as well as potential mechanisms. But to do some of this would mean listening to patients which doesn't seem popular with some groups.
 
dave30th said:
Actually, people were already being treated with interferon, so he piggy-backed on that. He was looking at the mechanism by which the treatment, while clearing the Hep C virus, simultaneously induced a long-term fatigue state. Now, whether it's the same fatigue as in ME, who knows? But I wouldn't dismiss it as meaningless so quickly--although I understand why it's tempting..
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This looks like a quite interesting approach.. Perhaps it will give us some clues.
 
Jonathan Edwards said:
I agree. I think there is avery important message in the alpha interferon story - that fatigue can persist long after the triggering signal has gone. Some other signal must then take over. Moreover, there is no need for any specific autoimmune response.

The pity is that Pariente is still as far as I know wedded to a biopsychosocial view, for reasons that are unclear.
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This work seems to have been going on for a good few years now but I've not seen any results that hint at an interesting mechanism.

Also how long does the interferon last for (as a chemical in the blood) - Could it be a residual levels are remaining as a signal or is it affecting some other process?
 
Andy said:
How does he know that the interferon induced the fatigue rather than the virus? Was that part of the presentation?
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He was looking at the difference between Hep C patients who took interferon and did not end up with a persistent fatigue state, and those who took interferon and did end up with prolonged fatigue. All cleared the Hep C virus but about 30 % of the participants who got interferon and cleared Hep C still ended up fatigued after six months.
 
dave30th said:
Actually, people were already being treated with interferon, so he piggy-backed on that. He was looking at the mechanism by which the treatment, while clearing the Hep C virus, simultaneously induced a long-term fatigue state. Now, whether it's the same fatigue as in ME, who knows? But I wouldn't dismiss it as meaningless so quickly--although I understand why it's tempting..
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It's fine to see basic research on fatigue. In my opinion, all research on fatigue should specify which type(s) of fatigue it is investigating, though: cognitive, "mental", muscle, motor; fatigue/ fatiguability / fatigue as part of PEM. I think, this should be the premise of comparisons between illnesses. Did Parente even bother whether the fatigue symptoms of people with Hepatitis C are comparable to those of people with ME?

[Added: I see @Adrian made a similiar comment. I would like to stress that I think it is both possible and neceessary to differentiate types of fatigue by capturing the symptoms as precisely as possible before investigating the underlying mechanisms]
 
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Adrian said:
This work seems to have been going on for a good few years now but I've not seen any results that hint at an interesting mechanism.

Also how long does the interferon last for (as a chemical in the blood) - Could it be a residual levels are remaining as a signal or is it affecting some other process?
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I agree that not very much insight seems to have emerged from the studies themselves relating to mechanism.

The interferon does not hang around long. I do not think there is any doubt that it is the interferon rather than the virus that causes the fatigue or that the fatigue goes on far longer than there are significant interferon levels present. I have looked after people who have had interferon for hep C. If it makes them feel terrible it tends to be pretty rapid in onset - it just carries on afterwards.

So I guess there is nothing controversial about the model as an instant of a cytokine triggering fatigue for much longer than it is there. The down side is that it is not clear that these studies have taken us any further from that observation made in the original clinical trials.
 
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