It’s interesting they select specifically for Long Covid and not some other theorized to be post viral thing, like chronic fatigue. But I guess it makes sense too, since Long Covid has a far clearer cause/impact than “idk some virus made you disabled”.
Chronic fatigue is a syndrome: a constellation of symptoms of unknown cause. Long covid has a similar description, but with a bright flashing arrow pointing towards a cause. Having experienced year-long brain fog and loss of executive function due to a flu, I'm hoping that a silver lining of covid is that we will have enough data and funding to actually pinpoint and treat the root cause. And, if I allow myself some optimism, it might point us towards drivers behind other syndromes of a similar nature.
I've been struggling with fatigue since earlier this year after I got (what I presume to be) another bout of Rona. It is debilitating fatigue, where I can get 14 hours of sleep and I'm still exhausted, focus and brain power are elusive faint memories. It sucks.
I've found two things that beat back the fatigue into something manageable; nicotine gum (2mg, once a day), and as many carbohydrates from fresh ripe fruit as I can stuff into my face. I'm concerned that a good supply of fruit will be lacking as winter sets in. I'm still not sure what I'm going to do about that.
It's not cheap but you can buy fruit from growers online. Oranges, persimmons, cherimoyas, guavas, kiwis, pomegranates, and some grapes will be harvested in California. South Florida also has year round produce, and you can buy imports from the Caribbean and South America. Join the "fruit 4 sale" Facebook group or search for farms online.
This is probably one of those areas where one symptom cluster (CFS) can be caused by several different things (COVID, autoimmunity, EBV, etc). So original causes may be different but they all converge on the same major symptoms.
I mean sure but that’s like saying “this condition has tumours” and saying “so cancer” like that is a useful diagnosis.
Hell your response is like someone describing the symptoms of chemo or numerous other heavy treatments and saying “oh so CFS”.
1) Clear molecular signals of pathology mean that minimizers' claims that longcovid is just psychosomatic or malingering are unsupported.
2) Seeing high antibody titers against COVID & EBV adds weight to the viral persistence and reactivation hypothesis: longcovid may be due, in part, to ongoing low-level infection elsewhere in the body along with reactivation of other viruses like EBV or HPV.
3) Autoantibodies were found again, but not significantly different than those seen in non-longcovid control groups, which is interesting because it had been suggested that longcovid may induce immune quality control dysfunction and increase overall autoimmune reactivity.
Hopefully these results can help guide better study design and management for longcovid trials.
> Clear molecular signals of pathology mean that minimizers' claims that long covid is just psychosomatic or malingering are unsupported.
Yes. That's clear now. The UK has an organized program to figure out what's going on with long COVID.[1]
It's been known for a year or two now, from MRI scans, that long COVID is associated with brain and lung inflammation. But the underlying mechanism is not yet known.
This UK longitudinal study [2] is especially useful. "Three in five people with long COVID have impairment in at least one organ (seen in MRI scans) and one in four have impairment in two or more organs, in some cases without symptoms." This has been going on long enough now that the longitudinal studies, where the same patients are re-tested, are starting to produce results.
Were the antibodies detected, or was their activity detected? Because if it's just about the presence of autoantibodies, the simple explanation may be that aab quantities may not significantly differ, but their activity/activation might.
Antibodies were detected, not their activity. Here's the assay used: https://www.cell.com/cell-reports-methods/pdf/S2667-2375(22)... Measuring antibody activity is a lot harder than measuring antibodies, just being able to assess antibody targets in a high-throughput manner is a huge and very recent step forward.
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[ 1.4 ms ] story [ 167 ms ] threadSo chronic fatigue syndrome?
I've been struggling with fatigue since earlier this year after I got (what I presume to be) another bout of Rona. It is debilitating fatigue, where I can get 14 hours of sleep and I'm still exhausted, focus and brain power are elusive faint memories. It sucks.
I've found two things that beat back the fatigue into something manageable; nicotine gum (2mg, once a day), and as many carbohydrates from fresh ripe fruit as I can stuff into my face. I'm concerned that a good supply of fruit will be lacking as winter sets in. I'm still not sure what I'm going to do about that.
While there is a ME/CFS long covid subtype, there are many others as well. In other words, not everyone who has long covid suffers from fatigue.
It could be likely that the ME/CFS long covid subtype may share a common pathology with the varying CFS hypothesized pathogens(influenza, etc).
1) Clear molecular signals of pathology mean that minimizers' claims that longcovid is just psychosomatic or malingering are unsupported.
2) Seeing high antibody titers against COVID & EBV adds weight to the viral persistence and reactivation hypothesis: longcovid may be due, in part, to ongoing low-level infection elsewhere in the body along with reactivation of other viruses like EBV or HPV.
3) Autoantibodies were found again, but not significantly different than those seen in non-longcovid control groups, which is interesting because it had been suggested that longcovid may induce immune quality control dysfunction and increase overall autoimmune reactivity.
Hopefully these results can help guide better study design and management for longcovid trials.
Yes. That's clear now. The UK has an organized program to figure out what's going on with long COVID.[1] It's been known for a year or two now, from MRI scans, that long COVID is associated with brain and lung inflammation. But the underlying mechanism is not yet known.
This UK longitudinal study [2] is especially useful. "Three in five people with long COVID have impairment in at least one organ (seen in MRI scans) and one in four have impairment in two or more organs, in some cases without symptoms." This has been going on long enough now that the longitudinal studies, where the same patients are re-tested, are starting to produce results.
[1] https://www.gov.uk/government/news/new-research-into-treatme...
[2] https://journals.sagepub.com/doi/10.1177/01410768231154703
Were the antibodies detected, or was their activity detected? Because if it's just about the presence of autoantibodies, the simple explanation may be that aab quantities may not significantly differ, but their activity/activation might.
https://nitter.net/VirusesImmunity/status/170633296579227272...