Research: ME/CFS and Long COVID share similar dysfunctional immune system

Changes to physiological pathways similar in ME/CFS and Long COVID

A small study in New Zealand of the immune cell proteome in Long COVID, ME/CFS and healthy people uncovered “overlapping protein clusters and enriched molecular pathways particularly in immune functions”.

Senior researcher Prof Warren Tate says:

“It highlights within our community there are significant numbers of people debilitated now with disrupted immune systems, dysfunctional energy production, and disturbed brain regulation of their overall physiology that severely disrupts their family lives, ability to work and participate in their communities long-term, and that these people need support from all levels of society.

Therapeutic targeting of the immune response/inflammatory pathways could be effective.

This also means that the conditions can benefit from a coordinated treatment strategy, said the researchers.

“Immunotherapy for treating specific features of a disturbed immune system for many diseases is in a revolutionary phase of development and should have potential for application to ME/CFS and Long Covid patients now the specific changes in their dysfunctional immune systems are being carefully documented,”

A pilot study on the immune cell proteome of long COVID patients shows changes to physiological pathways similar to those in myalgic encephalomyelitis/chronic fatigue syndrome, by Katie Peppercorn,
Christina D Edgar, Torsten Kleffmann & Warren P Tate in Scientific Reports volume 13, no: 22068 (2023)

Research 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.