Immune cell proteomes of Long COVID patients have functional changes similar to those in ME/Chronic Fatigue Syndrome, 2023, Peppercorn, Tate et al.

https://www.researchsquare.com/article/rs-3335919/v1

Article

Immune cell proteomes of Long COVID patients have functional changes similar to those in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Katie Peppercorn1

Christina D. Edgar1

Torsten Kleffmann1

Warren. P Tate1

Email

1 University of Otago

https://doi.org/10.21203/rs.3.rs-3335919/v1



Of those infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), ~ 10% develop the chronic post-viral debilitating condition, Long COVID (LC).

Although LC is a heterogeneous condition, about half of cases have a typical post-viral fatigue condition with onset and symptoms that are very similar to Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

A key question is whether these conditions are closely related. ME/CFS is a post-stressor fatigue condition that arises from multiple triggers.

To investigate the pathophysiology of LC, a pilot study of patients and healthy controls has used quantitative proteomics to discover changes in peripheral blood mononuclear cell (PBMC) proteins.

A principal component analysis separated all Long COVID patients from healthy controls.

Analysis of 3131 proteins identified 162 proteins differentially regulated, of which 37 were related to immune functions, and 21 to mitochondrial functions.

Markov cluster analysis identified clusters involved in immune system processes, and two aspects of gene expression-spliceosome and transcription.

These results were compared with an earlier dataset of 346 differentially regulated proteins in PBMC’s from ME/CFS patients analysed by the same methodology.

There were overlapping protein clusters and enriched molecular pathways particularly in immune functions, suggesting the two conditions have similar immune pathophysiology as a prominent feature, and mitochondrial functions involved in energy production were affected in both conditions.

This is the preprint abstract. The article is now published, see post #7 below.

 

What does that even mean?

This ambiguiity about cognitive behavioural vs immune triggers for ME is apparently not accidental.

From later in the text.

I think this is much more dangerous than it looks.

The ref to justify this statement is by one of the authors. So self justification of prejudice.

Multiple triggers for ME is fuzzy thinking and buys into BPS narrative that stress causes ME.

The more likely scenario where infection is involved along with reports of stress is that immune conditions make people feel stressed.

The term post-viral is also a BPS assumption. Its not post from where I am sitting with multiple PCR diagnoses of recurring virus, definitely not. If they think it is, the burden is on them to prove it.

So in my view this phraseology is a horrible fudge and the small sample size suggests to me the rest of the paper is too.

It says what we want to hear but without rigorous scientific thinking to back it up, which I distrust and it buys into the BPS belief system.

At best this is clumsy fence straddling for purposes of seeking funding and at worst a potential trojan horse for BPS bamboozlement and the funding lobby it serves.

 

I see @Hutan , so you consider Tate's track record indicates he has good intentions as a genuinely enquiring mind as opposed to being employed to manipulate public perceptions of ME/CFS. Fair enough, I can respect that for what it is, while bearing in mind there is an old adage which warns us about good intentions, which I think applies.

Nevertheless I hope Tate's students go on to exercise their critical thinking and gain clinical level experience with PWME so they get a feel for what ME is rather than what it might be based on imaginative interpretation of descriptions and criteria, the latter being too nebulous to offer a definitive diagnosis.

For this reason, to my mind, patient heterogeneity is most logically regarded as due to multiple distinct subtypes, all matching the nebulous criteria rather than assuming it is the same syndrome with many causes, which IMHO amounts to a kind of class error.

Before we can say there are common phenomena between any subtypes we need to understand each subtype and the physiological systems it affects. That is one aspect of what I am seeing as fuzzy thinking.

Once we have identifiable subtypes we can discuss which if any might be genuinely post-viral, which are atypical chronic active infections (ACAI) like my own illness, which subtypes might involve central sensitisation which requires very careful investigation considering the diagnosis of fibromyalgia and comparison of its criteria with the incredibly painful muscle cricks, cramps and pains I have had since onset of ACAI, which I now know are not sensitisation because they can be managed using Mg / Ca balance.

At the heart of all this is a classification error which we hope Decode ME will help us solve.

 

Now published

https://www.nature.com/articles/s41598-023-49402-9

 

A pilot study on the immune cell proteome of long COVID patients shows changes to physiological pathways similar to those in myalgic encephalomyelitis

Abstract
Of those infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), ~ 10% develop the chronic post-viral debilitating condition, long COVID (LC). Although LC is a heterogeneous condition, about half of cases have typical post-viral fatigue with onset and symptoms that are very similar to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). A key question is whether these conditions are closely related. ME/CFS is a post-stressor fatigue condition that arises from multiple triggers.

To investigate the pathophysiology of LC, a pilot study of patients (n = 6) and healthy controls (n = 5) has used quantitative proteomics to discover changes in peripheral blood mononuclear cell (PBMC) proteins. A principal component analysis separated all long COVID patients from healthy controls. Analysis of 3131 proteins identified 162 proteins differentially regulated, of which 37 were related to immune functions, and 21 to mitochondrial functions.

Markov cluster analysis identified clusters involved in immune system processes, and two aspects of gene expression-spliceosome and transcription. These results were compared with an earlier dataset of 346 differentially regulated proteins in PBMC’s from ME/CFS patients (n = 9) analysed by the same methodology.

There were overlapping protein clusters and enriched molecular pathways particularly in immune functions, suggesting the two conditions have similar immune pathophysiology as a prominent feature, and mitochondrial functions involved in energy production were affected in both conditions.

https://www.nature.com/articles/s41598-023-49402-9#:~:text=ME/CFS is a post,that arises from multiple triggers.

 

posts copied from the News from New Zealand thread

Brief intro to some apparently newly published (Dr Warren Tate Otago University) research (will have to check elsewhere to see what it is as the article gives very little info)

Links between Chronic Fatigue Syndrome and Long Covid found
https://www.rnz.co.nz/national/prog...chronic-fatigue-syndrome-and-long-covid-found

(I came here to find out more myself)

 

2-minute video piece plus text that is somewhat similar to a transcript

"Dunedin researchers reveal strong link between #longCOVID & #chronicfatiguesyndrome"

https://www.newshub.co.nz/home/new-...-long-covid-and-chronic-fatigue-syndrome.html

 

Press release that has led to a lot of media coverage in New Zealand
"Strong links found between #LongCOVID and ME/CFS: Otago study"
https://www.eurekalert.org/news-releases/1032051

 

New research using LC samples analysed against their existing ME/CFS data (published previously) to look for similarities and differences.