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Myalgic Encephalomyelitis/Chronic Fatigue syndrome/Long COVID


Professor Tate’s ME/CFS and Long COVID research 2022

(A) The relationship between ME/CFS and Long COVID

Long COVID is a post viral fatigue syndrome disease that has developed in about 30% of those infected with COVID19 after their initial recovery from infection. It mirrors the development of ME/CFS as a post viral fatigue syndrome after a viral infection. In 2021 we began a pilot study to examine the relationship between the two illnesses by examining molecular signatures in the immune cells of Long COVID patients compared with age/gender matched ME/CFS patients and healthy controls. We found the two post-viral fatigue patient groups clustered together quite closely in the dysregulation of their proteins, separated from the healthy controls, with both groups showing similar immune/inflammatory markers and dysregulated synthesis of mitochondrial proteins. It implies ME/CFS and Long COVID are indeed very similar ‘sister’ illnesses as their symptoms have suggested. The second phase of this study in 2022 is examining the regulation of the synthesis of the immune cell proteins at the DNA level occurring via changes in the epigenetic code. We have already shown over the period of a year ME/CFS patients have a much more unstable epigenetic code (disordered regulation) than a healthy control indicating there is not such tight control of molecular homeostasis. We tracked a relapse in two ME subjects and have shown specific changes in gene expression around the on/off switches of genes that affect immune/inflammatory pathways during the relapse. We now are doing a comparative study between ME/CFS patients with Long COVID patients. We are collaborating with Dr Anna Brooks, an immunologist at the University of Auckland who is evaluating the cellular immunology of Long COVID patients. We will study an interesting subgroup of these patients arising from her studies at the molecular level and also their profiles before and after vaccination. Many ME/CFS patients in New Zealand have had severe ongoing adverse reactions to the Pfizer vaccine (1 in 4 patients) that has led to serious deterioration in the health. We wish to investigate this and determine whether there is a specific molecular signature in these patients but absent in those who tolerated the vaccine well that could explain these reactions.

(B) A model centred on mechanisms to link the brain and peripheral body systems to sustain ME/CFS and Long COVID and promote relapses via fluctuating neuroinflammation

At the end of 2018 we published a hypothesis for how ME/CFS might be being sustained as an ongoing illness involving the hypothalamus and the stress centre within it. We have developed new ideas relevant to this hypothesis in 2021 to test an hypothesis that a stress hormone produced in the brain’s stress centre, and a defective receptor for it, causes excessive production of serotonin. Excessive serotonin levels are known to cause the broad scope of ME/CFS-like symptoms. In 2021 we analysed a gene in DNA samples from our ME/CFS patients for evidence of mutations in the enzyme responsible for degrading the tryptophan starting material used for the synthesis of serotonin. That enzyme controls the levels of tryptophan so that serotonin is produced within physiologically normal levels. If the degrading enzyme were inactive it would promote excessive serotonin levels. We have indeed found inactivating mutations in the critical gene in our patients but also in healthy controls, so while this mutation may convey susceptibility to excessive serotonin synthesis that could sustain and prolong the illness in ME/CFS patients , it does not by itself trigger the disease.

(C) Genetic susceptibility for developing ME/CFS and Long COVID

Up to 1 in 10 people who get Epstein Barr virus infections ( glandular fever) go on to develop ME/CFS, and additionally a small percentage of people with other external stressors can develop the illness. Of those with COVID 19 infection about 30 % develop Long COVID. What are the susceptibility factors in people who go on to develop the long term post-viral debilitating conditions? We are doing a quantitative survey in 2022 of 100 ME/CFS patients and 100 Long COVID patients to tease out factors in their family and personal health histories that might be susceptibility factors for developing the diseases. This would be converted in to risk factors for these diseases in the future that may be of significant benefit for use by health practitioners to mitigate and prevent their patients developing the debilitating long term illnesses.

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